Topical Cannabinoids in Dermatology

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Topical Cannabinoids in Dermatology

The prevalence of topical cannabinoids has risen sharply in recent years. Commercial advertisers promote their usage as a safe means to treat a multitude of skin disorders, including atopic dermatitis (AD), psoriasis, and acne. Topical compounds have garnered interest in laboratory studies, but the purchase of commercial formulations is limited to over-the-counter products from unregulated suppliers. In this article, we review the scientific evidence behind topical cannabinoids and evaluate their role in clinical dermatology.

Background

Cannabis is designated as a Schedule I drug, according to the Controlled Substances Act of 1970. This listing is given to substances with no therapeutic value and a high potential for abuse. However, as of 2017, 29 states and the District of Columbia have laws legalizing cannabis in some capacity. These regulations typically apply to medicinal use, though several states have now legalized recreational use.

Cannabinoids represent a broad class of chemical compounds derived from the cannabis plant. Originally, this class only comprised phytocannabinoids, cannabinoids produced by the cannabis plant. Tetrahydrocannabinol (THC) is the most well-known phytocannabinoid and leads to the psychoactive effects typically associated with cannabis use. Later investigation led to the discovery of endocannabinoids, cannabinoids that are naturally produced by human and animal bodies, as well as synthetic cannabinoids.1 Cannabidiol is a phytocannabinoid that has been investigated in neurologic and anti-inflammatory conditions.2-4

Cannabinoids act as agonists on 2 principal receptors— cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 2 (CB2)—which are both G protein–coupled receptors (Figure).5 Both have distinct distributions throughout different organ systems, to which cannabinoids (eg, THC, cannabidiol, endocannabinoids) show differential binding.6,7 Importantly, the expression of CB1 and CB2 has been identified on sensory nerve fibers, inflammatory cells, and adnexal structures of human skin.8 Based on these associations, topical application of cannabinoids has become a modality of interest for dermatological disorders. These formulations aim to influence cutaneous morphology without producing psychoactive effects.

Signaling pathways associated with cannabinoid receptor activation. CB1 indicates cannabinoid receptor type 1; CB2, cannabinoid receptor type 2; AC, adenylyl cyclase; cAMP, cyclic adenosine monophosphate; PKA, protein kinase A; MAPK, mitogen-activated protein kinase.

Topical Cannabinoids in Inflammatory Disorders

Atopic dermatitis has emerged as an active area of investigation for cannabinoid receptors and topical agonists (Table 1). In an animal model, Kim et al9 examined the effects of CB1 agonism on skin inflammation. Mice treated with topical CB1 agonists showed greater recovery of epidermal barrier function in acutely abrogated skin relative to those treated with a vehicle preparation. In addition, agonism of CB1 led to significant (P<.001) decreases in skin fold thickness among models of acute and chronic skin inflammation.9

Nam et al10 also examined the role of topical CB1 agonists in mice with induced AD-like symptoms. Relative to treatment with vehicle, CB1 agonists significantly reduced the recruitment of mast cells (P<.01) and lowered the blood concentration of histamine (P<.05). Given the noted decrease in the release of inflammatory mediators, the authors speculated that topical agonsim of CB1 may prove useful in several conditions related to mast cell activation, such as AD, contact dermatitis, and psoriasis.10

The anti-inflammatory properties of topical THC were evaluated by Gaffal et al.11 In a mouse model of allergic contact dermatitis, mice treated with topical THC showed decreases in myeloid immune cell infiltration, with these beneficial effects existing even in mice with deficient CB1 and CB2 receptors. These results support a potentially wide anti-inflammatory activity of topical THC.11

Topical Cannabinoids in Pain Management

The effects of smoked cannabis in treating pain have undergone thorough investigation over recent years. Benefits have been noted in treating neuropathic pain, particularly in human immunodeficiency virus–associated sensory neuropathy.12-15 Smoked cannabis also may provide value as a synergistic therapy with opioids, thereby allowing for lower opioid doses.16

In contrast, research into the relationship between topical application of cannabinoids and nociception remains in preliminary stages (Table 2). In a mouse model, Dogrul et al17 assessed the topical antinociceptive potential of a mixed CB1-CB2 agonist. Results showed significant (P<.01) and dose-dependent antinociceptive effects relative to treatment with a vehicle.17 In a related study, Yesilyurt et al18 evaluated whether a mixed CB1-CB2 agonist could enhance the antinociceptive effects of topical opioids. Among mice treated with the combination of a cannabinoid agonist and topical morphine, a significantly (P<.05) greater analgesic effect was demonstrated relative to topical morphine alone.18

Studies in humans have been far more limited. Phan et al19 conducted a small, nonrandomized, open-label trial of a topical cannabinoid cream in patients with facial postherpetic neuralgia. Of 8 patients treated, 5 noted a mean pain reduction of 87.8%. No comparison vehicle was used. Based on this narrow study design, it is difficult to extrapolate these positive results to a broader patient population.19

 

 

Commercial Products

Although preliminary models with topical cannabinoids have shown potential, large-scale clinical trials in humans have yet to be performed. Despite this lack of investigation, commercial formulations of topical cannabinoids are available to dermatology patients. These formulations are nonstandardized, and no safety data exists regarding their use. Topical cannabinoids on the market may contain various amounts of active ingredient and may be combined with a range of other compounds.

In dermatology offices, it is not uncommon for patients to express an intention to use topical cannabinoid products following their planned treatment or procedure. Patients also have been known to use topical cannabinoid products prior to dermatologic procedures, sometimes in place of an approved topical anesthetic, without consulting the physician performing the procedure. With interventions that lead to active areas of wound healing, the application of such products may increase the risk for contamination and infection. Therefore, patients should be counseled that the use of commercial topical cannabinoids could jeopardize the success of their planned procedure, put them at risk for infection, and possibly lead to systemic absorption and/or changes in wound-healing capacities.

Conclusion

Based on the results from recent animal models, cannabinoids may have a role in future treatment algorithms for several inflammatory conditions. However, current efficacy and safety data are almost entirely limited to preliminary animal studies in rodents. In addition, the formulation of topical cannabinoid products is nonstandardized and poorly regulated. As such, the present evidence does not support the use of topical cannabinoids in dermatology practices. Dermatologists should ask patients about the use of any cannabinoid products as part of a treatment program, especially given the unsubstantiated claims often made by unscrupulous advertisers. This issue highlights the need for further research and regulation.

References
  1. Pacher P, Batkai S, Kunos G. The endocannabinoid system as an emerging target of pharmacotherapy. Pharmacol Rev. 2006;58:389-462.
  2. Giacoppo S, Galuppo M, Pollastro F, et al. A new formulation of cannabidiol in cream shows therapeutic effects in a mouse model of experimental autoimmune encephalomyelitis. Daru. 2015;23:48.
  3. Hammell DC, Zhang LP, Ma F, et al. Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis. Eur J Pain. 2016;20:936-948.
  4. Schicho R, Storr M. Topical and systemic cannabidiol improves trinitrobenzene sulfonic acid colitis in mice. Pharmacology. 2012;89:149-155.
  5. Howlett AC, Barth F, Bonner TI, et al. International Union of Pharmacology. XXVII. Classification of cannabinoid receptors. Pharmacol Rev. 2002;54:161-202.
  6. Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin. Br J Pharmacol. 2008;153:199-215.
  7. Svizenska I, Dubovy P, Sulcova A. Cannabinoid receptors 1 and 2 (CB1 and CB2), their distribution, ligands and functional involvement in nervous system structures—a short review. Pharmacol Biochem Behav. 2008;90:501-511.
  8. Stander S, Schmelz M, Metze D, et al. Distribution of cannabinoid receptor 1 (CB1) and 2 (CB2) on sensory nerve fibers and adnexal structures in human skin. J Dermatol Sci. 2005;38:177-188.
  9. Kim HJ, Kim B, Park BM, et al. Topical cannabinoid receptor 1 agonist attenuates the cutaneous inflammatory responses in oxazolone-induced atopic dermatitis model. Int J Dermatol. 2015;54:E401-E408.
  10. Nam G, Jeong SK, Park BM, et al. Selective cannabinoid receptor-1 agonists regulate mast cell activation in an oxazolone-induced atopic dermatitis model. Ann Dermatol. 2016;28:22-29.
  11. Gaffal E, Cron M, Glodde N, et al. Anti-inflammatory activity of topical THC in DNFB-mediated mouse allergic contact dermatitis independent of CB1 and CB2 receptors. Allergy. 2013;68:994-1000.
  12. Abrams DI, Jay CA, Shade SB, et al. Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trial. Neurology. 2007;68:515-521.
  13. Ellis RJ, Toperoff W, Vaida F, et al. Smoked medicinal cannabis for neuropathic pain in HIV: a randomized, crossover clinical trial. Neuropsychopharmacology. 2009;34:672-680.
  14. Wilsey B, Marcotte T, Deutsch R, et al. Low-dose vaporized cannabis significantly improves neuropathic pain. J Pain. 2013;14:136-148.
  15. Wilsey B, Marcotte T, Tsodikov A, et al. A randomized, placebo-controlled, crossover trial of cannabis cigarettes in neuropathic pain. J Pain. 2008;9:506-521.
  16. Abrams DI, Couey P, Shade SB, et al. Cannabinoid-opioid interaction in chronic pain. Clin Pharmacol Ther. 2011;90:844-851.
  17. Dogrul A, Gul H, Akar A, et al. Topical cannabinoid antinociception: synergy with spinal sites. Pain. 2003;105:11-16.
  18. Yesilyurt O, Dogrul A, Gul H, et al. Topical cannabinoid enhances topical morphine antinociception. Pain. 2003;105:303-308.
  19. Phan NQ, Siepmann D, Gralow I, et al. Adjuvant topical therapy with a cannabinoid receptor agonist in facial postherpetic neuralgia. J Dtsch Dermatol Ges. 2010;8:88-91.
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Drs. Hashim and Goldenberg are from the Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York. Dr. Cohen is from AboutSkin Dermatology and DermSurgery, both in Englewood, Colorado; the Department of Dermatology, University of Colorado Denver, Aurora; and the Department of Dermatology, University of California at Irvine. Dr. Pompei is from Baruch College, City University of New York, New York.

The authors report no conflict of interest.

Correspondence: Gary Goldenberg, MD, Department of Dermatology, Icahn School of Medicine at Mount Sinai Medical Center, 5 E 98th St, New York, NY 10029 ([email protected]).

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Drs. Hashim and Goldenberg are from the Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York. Dr. Cohen is from AboutSkin Dermatology and DermSurgery, both in Englewood, Colorado; the Department of Dermatology, University of Colorado Denver, Aurora; and the Department of Dermatology, University of California at Irvine. Dr. Pompei is from Baruch College, City University of New York, New York.

The authors report no conflict of interest.

Correspondence: Gary Goldenberg, MD, Department of Dermatology, Icahn School of Medicine at Mount Sinai Medical Center, 5 E 98th St, New York, NY 10029 ([email protected]).

Author and Disclosure Information

Drs. Hashim and Goldenberg are from the Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York. Dr. Cohen is from AboutSkin Dermatology and DermSurgery, both in Englewood, Colorado; the Department of Dermatology, University of Colorado Denver, Aurora; and the Department of Dermatology, University of California at Irvine. Dr. Pompei is from Baruch College, City University of New York, New York.

The authors report no conflict of interest.

Correspondence: Gary Goldenberg, MD, Department of Dermatology, Icahn School of Medicine at Mount Sinai Medical Center, 5 E 98th St, New York, NY 10029 ([email protected]).

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Related Articles

The prevalence of topical cannabinoids has risen sharply in recent years. Commercial advertisers promote their usage as a safe means to treat a multitude of skin disorders, including atopic dermatitis (AD), psoriasis, and acne. Topical compounds have garnered interest in laboratory studies, but the purchase of commercial formulations is limited to over-the-counter products from unregulated suppliers. In this article, we review the scientific evidence behind topical cannabinoids and evaluate their role in clinical dermatology.

Background

Cannabis is designated as a Schedule I drug, according to the Controlled Substances Act of 1970. This listing is given to substances with no therapeutic value and a high potential for abuse. However, as of 2017, 29 states and the District of Columbia have laws legalizing cannabis in some capacity. These regulations typically apply to medicinal use, though several states have now legalized recreational use.

Cannabinoids represent a broad class of chemical compounds derived from the cannabis plant. Originally, this class only comprised phytocannabinoids, cannabinoids produced by the cannabis plant. Tetrahydrocannabinol (THC) is the most well-known phytocannabinoid and leads to the psychoactive effects typically associated with cannabis use. Later investigation led to the discovery of endocannabinoids, cannabinoids that are naturally produced by human and animal bodies, as well as synthetic cannabinoids.1 Cannabidiol is a phytocannabinoid that has been investigated in neurologic and anti-inflammatory conditions.2-4

Cannabinoids act as agonists on 2 principal receptors— cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 2 (CB2)—which are both G protein–coupled receptors (Figure).5 Both have distinct distributions throughout different organ systems, to which cannabinoids (eg, THC, cannabidiol, endocannabinoids) show differential binding.6,7 Importantly, the expression of CB1 and CB2 has been identified on sensory nerve fibers, inflammatory cells, and adnexal structures of human skin.8 Based on these associations, topical application of cannabinoids has become a modality of interest for dermatological disorders. These formulations aim to influence cutaneous morphology without producing psychoactive effects.

Signaling pathways associated with cannabinoid receptor activation. CB1 indicates cannabinoid receptor type 1; CB2, cannabinoid receptor type 2; AC, adenylyl cyclase; cAMP, cyclic adenosine monophosphate; PKA, protein kinase A; MAPK, mitogen-activated protein kinase.

Topical Cannabinoids in Inflammatory Disorders

Atopic dermatitis has emerged as an active area of investigation for cannabinoid receptors and topical agonists (Table 1). In an animal model, Kim et al9 examined the effects of CB1 agonism on skin inflammation. Mice treated with topical CB1 agonists showed greater recovery of epidermal barrier function in acutely abrogated skin relative to those treated with a vehicle preparation. In addition, agonism of CB1 led to significant (P<.001) decreases in skin fold thickness among models of acute and chronic skin inflammation.9

Nam et al10 also examined the role of topical CB1 agonists in mice with induced AD-like symptoms. Relative to treatment with vehicle, CB1 agonists significantly reduced the recruitment of mast cells (P<.01) and lowered the blood concentration of histamine (P<.05). Given the noted decrease in the release of inflammatory mediators, the authors speculated that topical agonsim of CB1 may prove useful in several conditions related to mast cell activation, such as AD, contact dermatitis, and psoriasis.10

The anti-inflammatory properties of topical THC were evaluated by Gaffal et al.11 In a mouse model of allergic contact dermatitis, mice treated with topical THC showed decreases in myeloid immune cell infiltration, with these beneficial effects existing even in mice with deficient CB1 and CB2 receptors. These results support a potentially wide anti-inflammatory activity of topical THC.11

Topical Cannabinoids in Pain Management

The effects of smoked cannabis in treating pain have undergone thorough investigation over recent years. Benefits have been noted in treating neuropathic pain, particularly in human immunodeficiency virus–associated sensory neuropathy.12-15 Smoked cannabis also may provide value as a synergistic therapy with opioids, thereby allowing for lower opioid doses.16

In contrast, research into the relationship between topical application of cannabinoids and nociception remains in preliminary stages (Table 2). In a mouse model, Dogrul et al17 assessed the topical antinociceptive potential of a mixed CB1-CB2 agonist. Results showed significant (P<.01) and dose-dependent antinociceptive effects relative to treatment with a vehicle.17 In a related study, Yesilyurt et al18 evaluated whether a mixed CB1-CB2 agonist could enhance the antinociceptive effects of topical opioids. Among mice treated with the combination of a cannabinoid agonist and topical morphine, a significantly (P<.05) greater analgesic effect was demonstrated relative to topical morphine alone.18

Studies in humans have been far more limited. Phan et al19 conducted a small, nonrandomized, open-label trial of a topical cannabinoid cream in patients with facial postherpetic neuralgia. Of 8 patients treated, 5 noted a mean pain reduction of 87.8%. No comparison vehicle was used. Based on this narrow study design, it is difficult to extrapolate these positive results to a broader patient population.19

 

 

Commercial Products

Although preliminary models with topical cannabinoids have shown potential, large-scale clinical trials in humans have yet to be performed. Despite this lack of investigation, commercial formulations of topical cannabinoids are available to dermatology patients. These formulations are nonstandardized, and no safety data exists regarding their use. Topical cannabinoids on the market may contain various amounts of active ingredient and may be combined with a range of other compounds.

In dermatology offices, it is not uncommon for patients to express an intention to use topical cannabinoid products following their planned treatment or procedure. Patients also have been known to use topical cannabinoid products prior to dermatologic procedures, sometimes in place of an approved topical anesthetic, without consulting the physician performing the procedure. With interventions that lead to active areas of wound healing, the application of such products may increase the risk for contamination and infection. Therefore, patients should be counseled that the use of commercial topical cannabinoids could jeopardize the success of their planned procedure, put them at risk for infection, and possibly lead to systemic absorption and/or changes in wound-healing capacities.

Conclusion

Based on the results from recent animal models, cannabinoids may have a role in future treatment algorithms for several inflammatory conditions. However, current efficacy and safety data are almost entirely limited to preliminary animal studies in rodents. In addition, the formulation of topical cannabinoid products is nonstandardized and poorly regulated. As such, the present evidence does not support the use of topical cannabinoids in dermatology practices. Dermatologists should ask patients about the use of any cannabinoid products as part of a treatment program, especially given the unsubstantiated claims often made by unscrupulous advertisers. This issue highlights the need for further research and regulation.

The prevalence of topical cannabinoids has risen sharply in recent years. Commercial advertisers promote their usage as a safe means to treat a multitude of skin disorders, including atopic dermatitis (AD), psoriasis, and acne. Topical compounds have garnered interest in laboratory studies, but the purchase of commercial formulations is limited to over-the-counter products from unregulated suppliers. In this article, we review the scientific evidence behind topical cannabinoids and evaluate their role in clinical dermatology.

Background

Cannabis is designated as a Schedule I drug, according to the Controlled Substances Act of 1970. This listing is given to substances with no therapeutic value and a high potential for abuse. However, as of 2017, 29 states and the District of Columbia have laws legalizing cannabis in some capacity. These regulations typically apply to medicinal use, though several states have now legalized recreational use.

Cannabinoids represent a broad class of chemical compounds derived from the cannabis plant. Originally, this class only comprised phytocannabinoids, cannabinoids produced by the cannabis plant. Tetrahydrocannabinol (THC) is the most well-known phytocannabinoid and leads to the psychoactive effects typically associated with cannabis use. Later investigation led to the discovery of endocannabinoids, cannabinoids that are naturally produced by human and animal bodies, as well as synthetic cannabinoids.1 Cannabidiol is a phytocannabinoid that has been investigated in neurologic and anti-inflammatory conditions.2-4

Cannabinoids act as agonists on 2 principal receptors— cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 2 (CB2)—which are both G protein–coupled receptors (Figure).5 Both have distinct distributions throughout different organ systems, to which cannabinoids (eg, THC, cannabidiol, endocannabinoids) show differential binding.6,7 Importantly, the expression of CB1 and CB2 has been identified on sensory nerve fibers, inflammatory cells, and adnexal structures of human skin.8 Based on these associations, topical application of cannabinoids has become a modality of interest for dermatological disorders. These formulations aim to influence cutaneous morphology without producing psychoactive effects.

Signaling pathways associated with cannabinoid receptor activation. CB1 indicates cannabinoid receptor type 1; CB2, cannabinoid receptor type 2; AC, adenylyl cyclase; cAMP, cyclic adenosine monophosphate; PKA, protein kinase A; MAPK, mitogen-activated protein kinase.

Topical Cannabinoids in Inflammatory Disorders

Atopic dermatitis has emerged as an active area of investigation for cannabinoid receptors and topical agonists (Table 1). In an animal model, Kim et al9 examined the effects of CB1 agonism on skin inflammation. Mice treated with topical CB1 agonists showed greater recovery of epidermal barrier function in acutely abrogated skin relative to those treated with a vehicle preparation. In addition, agonism of CB1 led to significant (P<.001) decreases in skin fold thickness among models of acute and chronic skin inflammation.9

Nam et al10 also examined the role of topical CB1 agonists in mice with induced AD-like symptoms. Relative to treatment with vehicle, CB1 agonists significantly reduced the recruitment of mast cells (P<.01) and lowered the blood concentration of histamine (P<.05). Given the noted decrease in the release of inflammatory mediators, the authors speculated that topical agonsim of CB1 may prove useful in several conditions related to mast cell activation, such as AD, contact dermatitis, and psoriasis.10

The anti-inflammatory properties of topical THC were evaluated by Gaffal et al.11 In a mouse model of allergic contact dermatitis, mice treated with topical THC showed decreases in myeloid immune cell infiltration, with these beneficial effects existing even in mice with deficient CB1 and CB2 receptors. These results support a potentially wide anti-inflammatory activity of topical THC.11

Topical Cannabinoids in Pain Management

The effects of smoked cannabis in treating pain have undergone thorough investigation over recent years. Benefits have been noted in treating neuropathic pain, particularly in human immunodeficiency virus–associated sensory neuropathy.12-15 Smoked cannabis also may provide value as a synergistic therapy with opioids, thereby allowing for lower opioid doses.16

In contrast, research into the relationship between topical application of cannabinoids and nociception remains in preliminary stages (Table 2). In a mouse model, Dogrul et al17 assessed the topical antinociceptive potential of a mixed CB1-CB2 agonist. Results showed significant (P<.01) and dose-dependent antinociceptive effects relative to treatment with a vehicle.17 In a related study, Yesilyurt et al18 evaluated whether a mixed CB1-CB2 agonist could enhance the antinociceptive effects of topical opioids. Among mice treated with the combination of a cannabinoid agonist and topical morphine, a significantly (P<.05) greater analgesic effect was demonstrated relative to topical morphine alone.18

Studies in humans have been far more limited. Phan et al19 conducted a small, nonrandomized, open-label trial of a topical cannabinoid cream in patients with facial postherpetic neuralgia. Of 8 patients treated, 5 noted a mean pain reduction of 87.8%. No comparison vehicle was used. Based on this narrow study design, it is difficult to extrapolate these positive results to a broader patient population.19

 

 

Commercial Products

Although preliminary models with topical cannabinoids have shown potential, large-scale clinical trials in humans have yet to be performed. Despite this lack of investigation, commercial formulations of topical cannabinoids are available to dermatology patients. These formulations are nonstandardized, and no safety data exists regarding their use. Topical cannabinoids on the market may contain various amounts of active ingredient and may be combined with a range of other compounds.

In dermatology offices, it is not uncommon for patients to express an intention to use topical cannabinoid products following their planned treatment or procedure. Patients also have been known to use topical cannabinoid products prior to dermatologic procedures, sometimes in place of an approved topical anesthetic, without consulting the physician performing the procedure. With interventions that lead to active areas of wound healing, the application of such products may increase the risk for contamination and infection. Therefore, patients should be counseled that the use of commercial topical cannabinoids could jeopardize the success of their planned procedure, put them at risk for infection, and possibly lead to systemic absorption and/or changes in wound-healing capacities.

Conclusion

Based on the results from recent animal models, cannabinoids may have a role in future treatment algorithms for several inflammatory conditions. However, current efficacy and safety data are almost entirely limited to preliminary animal studies in rodents. In addition, the formulation of topical cannabinoid products is nonstandardized and poorly regulated. As such, the present evidence does not support the use of topical cannabinoids in dermatology practices. Dermatologists should ask patients about the use of any cannabinoid products as part of a treatment program, especially given the unsubstantiated claims often made by unscrupulous advertisers. This issue highlights the need for further research and regulation.

References
  1. Pacher P, Batkai S, Kunos G. The endocannabinoid system as an emerging target of pharmacotherapy. Pharmacol Rev. 2006;58:389-462.
  2. Giacoppo S, Galuppo M, Pollastro F, et al. A new formulation of cannabidiol in cream shows therapeutic effects in a mouse model of experimental autoimmune encephalomyelitis. Daru. 2015;23:48.
  3. Hammell DC, Zhang LP, Ma F, et al. Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis. Eur J Pain. 2016;20:936-948.
  4. Schicho R, Storr M. Topical and systemic cannabidiol improves trinitrobenzene sulfonic acid colitis in mice. Pharmacology. 2012;89:149-155.
  5. Howlett AC, Barth F, Bonner TI, et al. International Union of Pharmacology. XXVII. Classification of cannabinoid receptors. Pharmacol Rev. 2002;54:161-202.
  6. Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin. Br J Pharmacol. 2008;153:199-215.
  7. Svizenska I, Dubovy P, Sulcova A. Cannabinoid receptors 1 and 2 (CB1 and CB2), their distribution, ligands and functional involvement in nervous system structures—a short review. Pharmacol Biochem Behav. 2008;90:501-511.
  8. Stander S, Schmelz M, Metze D, et al. Distribution of cannabinoid receptor 1 (CB1) and 2 (CB2) on sensory nerve fibers and adnexal structures in human skin. J Dermatol Sci. 2005;38:177-188.
  9. Kim HJ, Kim B, Park BM, et al. Topical cannabinoid receptor 1 agonist attenuates the cutaneous inflammatory responses in oxazolone-induced atopic dermatitis model. Int J Dermatol. 2015;54:E401-E408.
  10. Nam G, Jeong SK, Park BM, et al. Selective cannabinoid receptor-1 agonists regulate mast cell activation in an oxazolone-induced atopic dermatitis model. Ann Dermatol. 2016;28:22-29.
  11. Gaffal E, Cron M, Glodde N, et al. Anti-inflammatory activity of topical THC in DNFB-mediated mouse allergic contact dermatitis independent of CB1 and CB2 receptors. Allergy. 2013;68:994-1000.
  12. Abrams DI, Jay CA, Shade SB, et al. Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trial. Neurology. 2007;68:515-521.
  13. Ellis RJ, Toperoff W, Vaida F, et al. Smoked medicinal cannabis for neuropathic pain in HIV: a randomized, crossover clinical trial. Neuropsychopharmacology. 2009;34:672-680.
  14. Wilsey B, Marcotte T, Deutsch R, et al. Low-dose vaporized cannabis significantly improves neuropathic pain. J Pain. 2013;14:136-148.
  15. Wilsey B, Marcotte T, Tsodikov A, et al. A randomized, placebo-controlled, crossover trial of cannabis cigarettes in neuropathic pain. J Pain. 2008;9:506-521.
  16. Abrams DI, Couey P, Shade SB, et al. Cannabinoid-opioid interaction in chronic pain. Clin Pharmacol Ther. 2011;90:844-851.
  17. Dogrul A, Gul H, Akar A, et al. Topical cannabinoid antinociception: synergy with spinal sites. Pain. 2003;105:11-16.
  18. Yesilyurt O, Dogrul A, Gul H, et al. Topical cannabinoid enhances topical morphine antinociception. Pain. 2003;105:303-308.
  19. Phan NQ, Siepmann D, Gralow I, et al. Adjuvant topical therapy with a cannabinoid receptor agonist in facial postherpetic neuralgia. J Dtsch Dermatol Ges. 2010;8:88-91.
References
  1. Pacher P, Batkai S, Kunos G. The endocannabinoid system as an emerging target of pharmacotherapy. Pharmacol Rev. 2006;58:389-462.
  2. Giacoppo S, Galuppo M, Pollastro F, et al. A new formulation of cannabidiol in cream shows therapeutic effects in a mouse model of experimental autoimmune encephalomyelitis. Daru. 2015;23:48.
  3. Hammell DC, Zhang LP, Ma F, et al. Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis. Eur J Pain. 2016;20:936-948.
  4. Schicho R, Storr M. Topical and systemic cannabidiol improves trinitrobenzene sulfonic acid colitis in mice. Pharmacology. 2012;89:149-155.
  5. Howlett AC, Barth F, Bonner TI, et al. International Union of Pharmacology. XXVII. Classification of cannabinoid receptors. Pharmacol Rev. 2002;54:161-202.
  6. Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin. Br J Pharmacol. 2008;153:199-215.
  7. Svizenska I, Dubovy P, Sulcova A. Cannabinoid receptors 1 and 2 (CB1 and CB2), their distribution, ligands and functional involvement in nervous system structures—a short review. Pharmacol Biochem Behav. 2008;90:501-511.
  8. Stander S, Schmelz M, Metze D, et al. Distribution of cannabinoid receptor 1 (CB1) and 2 (CB2) on sensory nerve fibers and adnexal structures in human skin. J Dermatol Sci. 2005;38:177-188.
  9. Kim HJ, Kim B, Park BM, et al. Topical cannabinoid receptor 1 agonist attenuates the cutaneous inflammatory responses in oxazolone-induced atopic dermatitis model. Int J Dermatol. 2015;54:E401-E408.
  10. Nam G, Jeong SK, Park BM, et al. Selective cannabinoid receptor-1 agonists regulate mast cell activation in an oxazolone-induced atopic dermatitis model. Ann Dermatol. 2016;28:22-29.
  11. Gaffal E, Cron M, Glodde N, et al. Anti-inflammatory activity of topical THC in DNFB-mediated mouse allergic contact dermatitis independent of CB1 and CB2 receptors. Allergy. 2013;68:994-1000.
  12. Abrams DI, Jay CA, Shade SB, et al. Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trial. Neurology. 2007;68:515-521.
  13. Ellis RJ, Toperoff W, Vaida F, et al. Smoked medicinal cannabis for neuropathic pain in HIV: a randomized, crossover clinical trial. Neuropsychopharmacology. 2009;34:672-680.
  14. Wilsey B, Marcotte T, Deutsch R, et al. Low-dose vaporized cannabis significantly improves neuropathic pain. J Pain. 2013;14:136-148.
  15. Wilsey B, Marcotte T, Tsodikov A, et al. A randomized, placebo-controlled, crossover trial of cannabis cigarettes in neuropathic pain. J Pain. 2008;9:506-521.
  16. Abrams DI, Couey P, Shade SB, et al. Cannabinoid-opioid interaction in chronic pain. Clin Pharmacol Ther. 2011;90:844-851.
  17. Dogrul A, Gul H, Akar A, et al. Topical cannabinoid antinociception: synergy with spinal sites. Pain. 2003;105:11-16.
  18. Yesilyurt O, Dogrul A, Gul H, et al. Topical cannabinoid enhances topical morphine antinociception. Pain. 2003;105:303-308.
  19. Phan NQ, Siepmann D, Gralow I, et al. Adjuvant topical therapy with a cannabinoid receptor agonist in facial postherpetic neuralgia. J Dtsch Dermatol Ges. 2010;8:88-91.
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Practice Points

  • Topical cannabinoids are advertised by companies as treatment options for numerous dermatologic conditions.
  • Despite promising data in rodent models, there have been no rigorous studies to date confirming efficacy or safety in humans.
  • Dermatologists should therefore inquire with patients about the use of any topical cannabinoid products, especially around the time of planned procedures, as they may affect treatment outcomes.
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Trauma Care: The “Golden Hour” Meets the “Golden Years”

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Trauma Care: The “Golden Hour” Meets the “Golden Years”

In Emergency Medicine this month and next, Drs. Tom Scalea (See “The Golden Hourglass,” EM, April 2007), Ashley Menne, Daniel Haase, and Jay Menaker of the University of Maryland’s R Adams Cowley Shock Trauma Center paint a detailed picture of the changing landscape of trauma care over the past two decades.

In his introduction, Dr. Scalea writes “Certainly, the most important change has been the ‘graying’ of trauma patients…[whose evaluation and care] may involve a number of diagnostic tests in the ED…”, and whose care must include dealing with comorbidities, and a large number of medications that might interact with the analgesics, sedatives, and anti-seizure meds needed to treat trauma. These considerations have led many Level I trauma centers to add advanced patient age as an independent determinant for both trauma activations and subsequent ICU admissions, and to include “geriatric” consultants in the initial management. 

The aging trauma patient, however, is not the only factor responsible for major changes in the management of serious trauma, as the Shock Trauma group describes the current difficulties in attempting to rapidly reverse the anticoagulation effects of the novel oral anticoagulants (NOACs) that are increasingly being prescribed instead of warfarin to manage the thromboembolic complications of atrial fibrillation, valve replacement, venous thrombosis, and pulmonary embolism in both younger and older patients. They also explain a major change in thinking regarding the optimal degree of blood pressure control in favor of “permissive hypotension” as part of “damage control resuscitation,” and in the amount and types of volume replacement, optimal blood component ratios for transfusion, monitoring, and faster and less invasive endovascular repair techniques for hemostasis. The authors also note the persistent and rising incidence of penetrating trauma from gunshot and knife wounds. 

But the increasing percentages of elderly trauma victims requiring care for devastating falls and low-speed vehicular injuries in even the busiest “knife and gun club” trauma centers mandate the attention of all health care providers. In recent months, much space in this and other journals has been devoted to the health care issues of the elderly (see “Recognizing and Managing Elder Abuse in the Emergency Department,” and “Elder Abuse: A New Old Problem,” EM, May 2017) that necessitate significantly increased resources and provider time and effort now, and for at least the first half of the 21st century.

The main reason for this seismic demographic shift, dubbed by some “the silver tsunami”, is the aging post World War II “baby boomer” generation that has commanded center stage in western society throughout their development since the late 1940s. As a member of that generation, I often wonder how subsequent generations such as “Gen X” and “Millennials” view this phenomenon. Do they resent the attention, resources, and expenditures now demanded by baby boomers? If so, there is an important lesson to be learned from the changes in trauma care described in the following pages: virtually every measure now employed to enhance recovery of an elderly trauma victim will benefit younger trauma victims, as well. At most, some of the measures may not be absolutely necessary because younger adults have greater functional reserve and are more likely to survive less precise management, even if their posttraumatic courses are longer and more difficult. But younger trauma victims with comorbidities can also benefit from a more inclusive team approach from the start, as well as measures such as permissive hypotension, vascular stents and less invasive endovascular approaches, more precise blood component replacement, more accurate monitoring, and a better approach to anticoagulation and its reversal.

Faster and better quality survival of all trauma victims—including, but not limited to, the elderly—will free up needed and expensive resources for other patients and trauma victims, including those who continue to butt heads, drive two and four wheel vehicles at excessive speeds, and engage in trauma of an “interpersonal nature.” 

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In Emergency Medicine this month and next, Drs. Tom Scalea (See “The Golden Hourglass,” EM, April 2007), Ashley Menne, Daniel Haase, and Jay Menaker of the University of Maryland’s R Adams Cowley Shock Trauma Center paint a detailed picture of the changing landscape of trauma care over the past two decades.

In his introduction, Dr. Scalea writes “Certainly, the most important change has been the ‘graying’ of trauma patients…[whose evaluation and care] may involve a number of diagnostic tests in the ED…”, and whose care must include dealing with comorbidities, and a large number of medications that might interact with the analgesics, sedatives, and anti-seizure meds needed to treat trauma. These considerations have led many Level I trauma centers to add advanced patient age as an independent determinant for both trauma activations and subsequent ICU admissions, and to include “geriatric” consultants in the initial management. 

The aging trauma patient, however, is not the only factor responsible for major changes in the management of serious trauma, as the Shock Trauma group describes the current difficulties in attempting to rapidly reverse the anticoagulation effects of the novel oral anticoagulants (NOACs) that are increasingly being prescribed instead of warfarin to manage the thromboembolic complications of atrial fibrillation, valve replacement, venous thrombosis, and pulmonary embolism in both younger and older patients. They also explain a major change in thinking regarding the optimal degree of blood pressure control in favor of “permissive hypotension” as part of “damage control resuscitation,” and in the amount and types of volume replacement, optimal blood component ratios for transfusion, monitoring, and faster and less invasive endovascular repair techniques for hemostasis. The authors also note the persistent and rising incidence of penetrating trauma from gunshot and knife wounds. 

But the increasing percentages of elderly trauma victims requiring care for devastating falls and low-speed vehicular injuries in even the busiest “knife and gun club” trauma centers mandate the attention of all health care providers. In recent months, much space in this and other journals has been devoted to the health care issues of the elderly (see “Recognizing and Managing Elder Abuse in the Emergency Department,” and “Elder Abuse: A New Old Problem,” EM, May 2017) that necessitate significantly increased resources and provider time and effort now, and for at least the first half of the 21st century.

The main reason for this seismic demographic shift, dubbed by some “the silver tsunami”, is the aging post World War II “baby boomer” generation that has commanded center stage in western society throughout their development since the late 1940s. As a member of that generation, I often wonder how subsequent generations such as “Gen X” and “Millennials” view this phenomenon. Do they resent the attention, resources, and expenditures now demanded by baby boomers? If so, there is an important lesson to be learned from the changes in trauma care described in the following pages: virtually every measure now employed to enhance recovery of an elderly trauma victim will benefit younger trauma victims, as well. At most, some of the measures may not be absolutely necessary because younger adults have greater functional reserve and are more likely to survive less precise management, even if their posttraumatic courses are longer and more difficult. But younger trauma victims with comorbidities can also benefit from a more inclusive team approach from the start, as well as measures such as permissive hypotension, vascular stents and less invasive endovascular approaches, more precise blood component replacement, more accurate monitoring, and a better approach to anticoagulation and its reversal.

Faster and better quality survival of all trauma victims—including, but not limited to, the elderly—will free up needed and expensive resources for other patients and trauma victims, including those who continue to butt heads, drive two and four wheel vehicles at excessive speeds, and engage in trauma of an “interpersonal nature.” 

In Emergency Medicine this month and next, Drs. Tom Scalea (See “The Golden Hourglass,” EM, April 2007), Ashley Menne, Daniel Haase, and Jay Menaker of the University of Maryland’s R Adams Cowley Shock Trauma Center paint a detailed picture of the changing landscape of trauma care over the past two decades.

In his introduction, Dr. Scalea writes “Certainly, the most important change has been the ‘graying’ of trauma patients…[whose evaluation and care] may involve a number of diagnostic tests in the ED…”, and whose care must include dealing with comorbidities, and a large number of medications that might interact with the analgesics, sedatives, and anti-seizure meds needed to treat trauma. These considerations have led many Level I trauma centers to add advanced patient age as an independent determinant for both trauma activations and subsequent ICU admissions, and to include “geriatric” consultants in the initial management. 

The aging trauma patient, however, is not the only factor responsible for major changes in the management of serious trauma, as the Shock Trauma group describes the current difficulties in attempting to rapidly reverse the anticoagulation effects of the novel oral anticoagulants (NOACs) that are increasingly being prescribed instead of warfarin to manage the thromboembolic complications of atrial fibrillation, valve replacement, venous thrombosis, and pulmonary embolism in both younger and older patients. They also explain a major change in thinking regarding the optimal degree of blood pressure control in favor of “permissive hypotension” as part of “damage control resuscitation,” and in the amount and types of volume replacement, optimal blood component ratios for transfusion, monitoring, and faster and less invasive endovascular repair techniques for hemostasis. The authors also note the persistent and rising incidence of penetrating trauma from gunshot and knife wounds. 

But the increasing percentages of elderly trauma victims requiring care for devastating falls and low-speed vehicular injuries in even the busiest “knife and gun club” trauma centers mandate the attention of all health care providers. In recent months, much space in this and other journals has been devoted to the health care issues of the elderly (see “Recognizing and Managing Elder Abuse in the Emergency Department,” and “Elder Abuse: A New Old Problem,” EM, May 2017) that necessitate significantly increased resources and provider time and effort now, and for at least the first half of the 21st century.

The main reason for this seismic demographic shift, dubbed by some “the silver tsunami”, is the aging post World War II “baby boomer” generation that has commanded center stage in western society throughout their development since the late 1940s. As a member of that generation, I often wonder how subsequent generations such as “Gen X” and “Millennials” view this phenomenon. Do they resent the attention, resources, and expenditures now demanded by baby boomers? If so, there is an important lesson to be learned from the changes in trauma care described in the following pages: virtually every measure now employed to enhance recovery of an elderly trauma victim will benefit younger trauma victims, as well. At most, some of the measures may not be absolutely necessary because younger adults have greater functional reserve and are more likely to survive less precise management, even if their posttraumatic courses are longer and more difficult. But younger trauma victims with comorbidities can also benefit from a more inclusive team approach from the start, as well as measures such as permissive hypotension, vascular stents and less invasive endovascular approaches, more precise blood component replacement, more accurate monitoring, and a better approach to anticoagulation and its reversal.

Faster and better quality survival of all trauma victims—including, but not limited to, the elderly—will free up needed and expensive resources for other patients and trauma victims, including those who continue to butt heads, drive two and four wheel vehicles at excessive speeds, and engage in trauma of an “interpersonal nature.” 

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Comparison of Salicylic Acid 30% Peel and Pneumatic Broadband Light in the Treatment of Mild to Moderately Severe Facial Acne Vulgaris

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Comparison of Salicylic Acid 30% Peel and Pneumatic Broadband Light in the Treatment of Mild to Moderately Severe Facial Acne Vulgaris

Facial acne vulgaris is a common skin disease among teenagers and adolescents that may negatively affect self-esteem, perceived facial attractiveness, and social participation.1 Treatments for acne often are multimodal and require the utmost adherence. For these reasons, acne treatments have been challenging to clinicians and patients alike, as patient compliance in maintaining the use of prescribed topical and oral medications remains essential to attain improvement in quality of life (QOL).

Salicylic acid is a popular medicament for acne treatment that frequently is used as monotherapy or as an adjuvant for other acne treatments, especially in patients with oily skin.2 Salicylic acid has a keratolytic effect, causing corneocyte discohesion in clogged pores or congested follicles,2 and it is effective in treating both inflammatory and noninflammatory acne.3,4

Light therapy, particularly with visible light, has been demonstrated to improve acne outcomes.5 Pneumatic broadband light (PBBL) is a therapeutic light treatment in the broadband range (400–1200 nm) that is combined with vacuum suction, which creates a mechanical lysis of thin-walled pustules and dislodges pore impaction. Additionally, the blue light portion of the PBBL spectrum targets endogenous porphyrins in Propionibacterium acnes, resulting in bacterial destruction.6-8

The purpose of this study was to compare the efficacy, tolerability, and safety of salicylic acid 30% peel versus PBBL in the treatment of mild to moderately severe facial acne vulgaris.

METHODS

Study Design

This single-blind, randomized, split-face pilot study was approved by the institutional review board of the University of Pennsylvania (Philadelphia, Pennsylvania). All patients provided informed consent before entering the study. The single-blind evaluation was performed by one dermatologist (C.T.) who examined the participants on every visit prior to PBBL treatment.

Before the study started, participants were randomized for which side of the face was to be treated with PBBL using a number assigned to each participant. Participants received both treatments—salicylic acid 30% peel on one side of the face and PBBL treatment on the other side of the face—once weekly for a total of 6 treatments. They were then asked to return for 2 follow-up evaluations at weeks 3 and 6 following the last treatment session and were instructed not to use any topical or oral acne medications during these follow-up periods.

Inclusion and Exclusion Criteria

Patients aged 18 years and older of any race and sex with noninflammatory papules, some inflammatory papules, and no more than 1 nodule (considered as mild to moderately severe facial acne) were included in the study. Participants had not been on any topical acne medications for at least 1 month and/or oral retinoids for at least 1 year prior to the study period. All women completed urine pregnancy tests prior to the study and were advised to utilize birth control during the study period.

Study Treatments

Salicylic Acid 30% Peel

The participant’s face was cleansed thoroughly before application of salicylic acid 30% (1.5 g/2.5 mL) to half of the face and left on for 5 minutes before being carefully rinsed off by spraying with spring water. Prior to initiating PBBL therapy, the peeled side of the participant’s face was covered with a towel.

Pneumatic Broadband Light

On the other side of the face, PBBL was performed to deliver broadband light within the spectrum range of 400 to 1200 nm at a setting approximately equivalent to a fluence of 4 to 6 J/cm2 and a vacuum setting approximately equivalent to a negative pressure of 3 lb/in2. The power setting was increased on each subsequent visit depending on each participant’s tolerability.

Participants were required to apply a moisturizer and sunscreen to the face and avoid excessive sun exposure between study visits.

Efficacy Evaluation

A comparison of the efficacy of the treatments was determined by clinical evaluation and examining the results of the outcome measurements with the modified Global Acne Grading Score (mGAGS) and Acne QOL Scale during each treatment visit. Facial photographs were taken at each visit.

Modified Global Acne Grading Score

The mGAGS is a modification of the Global Acne Grading Scale (GAGS) that has been used to evaluate acne severity in many studies.9-11 The GAGS considers 6 locations on the face with a grading factor for each location. The local score is obtained by multiplying the factor rated by location with the factor of clinical assessment: local score = factor rated by location × factor rated by clinical assessment. The total score is the sum of the individual local scores (Table 1).

Although the original GAGS incorporated the type and location of the lesions in its calculation, we felt that the number of lesions also was important to add to our grading score. Therefore, we modified the GAGS by adding a factor rated by the number of lesions to improve the accuracy of the test. Accordingly, the local mGAGS scores were calculated by multiplying the location factor by the lesion type and number of lesions factors: local score = location factor × lesion type factor × number of lesions factor.

Acne QOL Questionnaire

Acne QOL was assessed during each visit to demonstrate if the treatment results affected participants’ socialization due to appearance.12 Participants were asked to complete the questionnaire, which consisted of 9 questions with 4 rating answers (0=not affected; 1=mildly affected; 2=moderately affected; 3=markedly affected). A total score of 9 or higher (high score) indicated that acne had a substantial negative impact on the participant, while a total score below 9 (low score) meant acne scarcely impacted social aspects and daily activities of the patient.

Safety Evaluation

The safety of the treatments was evaluated by clinical inspection and by comparing the results of the Wong-Baker FACES Pain Rating Scale (WBPRS)13 after treatment. The WBPRS is used worldwide among researchers to assess pain, particularly in children.14,15 It is composed of 6 faces expressing pain with word descriptions with a corresponding number range reflecting pain severity from 0 to 5 (0=no hurt; 1=hurts little bit; 2=hurts little more; 3=hurts even more; 4=hurts whole lot; 5=hurts worst).13

Statistical Analysis

All variables were presented as the median (range). A Wilcoxon signed rank test was used to compare clinical responses between the salicylic acid 30% peel and PBBL therapies. SPSS software version 12.0 was used for all statistical analysis. A 2-tailed P value of ≤.05 was considered statistically significant.

 

 

RESULTS

Study Population

Twelve participants (2 males, 10 females) aged 17 to 36 years (median age, 22 years; mean age [SD], 23.33 [1.65] years) with both comedonal and inflammatory acne were enrolled into this study for 6 split-face treatments of salicylic acid 30% peel and PBBL at 1-week intervals for 6 weeks, with 2 subsequent follow-up sessions at weeks 3 and 6 posttreatment. Of the 12 participants, 11 were white and 1 was Asian American, with Fitzpatrick skin types II to IV. Nine participants (75%) completed the study. One participant dropped out of the study after the fourth treatment due to a scheduling conflict, and the other 2 participants did not return for follow-up. No participants withdrew from the study because of adverse therapeutic events.

Efficacy Evaluation

Comparisons between the salicylic acid 30% peel and PBBL procedures for mGAGS at each visit are shown in Table 2. There was no significant difference in treatment efficacy between the salicylic acid 30% peel and PBBL therapies during the study’s treatment and follow-up events; however, both procedures contributed to a major improvement in acne symptoms by the third treatment session and through to the last follow-up session (P≤.05). Clinical photographs at baseline, at last treatment visit (week 6), and at last follow-up (week 12) are shown in Figures 1 and 2.

Figure 1. A 19-year-old woman with mild acne who was treated with salicylic acid 30% peel on the right side of the face at baseline (A), week 6 (B), and week 12 (C).

Figure 2. A 19-year-old woman with mild acne who was treated with pneumatic broadband light on the left side of the face at baseline (A), week 6 (B), and week 12 (C).

The results of the acne QOL questionnaire are shown in Table 2. Lower scores reflect a higher QOL. Median QOL scores at each visit ranged from 0.5 to 4.5. There was no significant difference found between the peel agent or PBBL based on the baseline QOL and subsequent visit assessments; however, the differences between the 2 treatments were significant at weeks 3 (P=.05) and 5 (P=.03) of treatment as well as at the last follow-up visit (P=.05).

According to the QOL scores, by the third treatment session participants were more satisfied with their improved acne condition from the PBBL procedure than the salicylic acid 30% peel as demonstrated by a positive range of the QOL assessments between PBBL and salicylic acid 30% peel (as shown in the difference in QOL in Table 2: week 3, 0–6; week 4, 0–3; week 5, 0–7). On the other hand, participants saw more improvement from the salicylic acid 30% peel than from PBBL by the last follow-up evaluation, as the differences in QOL scores between the 2 treatments resulted in a negative range (5–0).

Safety

Pain assessment by the WBPRS at every visit showed a low pain rating associated with both salicylic acid 30% peel (range, 0–0.5) and PBBL (range, 1.0–1.5) treatments. The median pain score of the salicylic acid 30% peel appeared higher compared to the PBBL treatment, yet a significant difference between both treatments was seen only at weeks 1, 3, and 6 of treatment (P≤.05).

There were no unexpected therapeutic reactions reported in our study, and no participants withdrew from the study due to adverse events. Most participants experienced only mild adverse reactions, including redness, stinging, and a burning sensation on the salicylic acid 30% peel side, which were transient and disappeared in minutes; only redness occurred on the PBBL-treated side.

Comment

Facial acne treatment is challenging, as prolonged and/or severe acne contributes to scarring, declining self-confidence, and undesirable financial consequences. Even though salicylic acid peel is a commonly used acne treatment choice, the PBBL methodology was approved by the US Food and Drug Administration6 and has become an alternative procedure for acne treatment.

The pharmacological effects of salicylic acid are related to its corneocyte desquamation and exfoliative actions, thereby reducing corneocyte cohesion and unclogging follicular pores.16 Salicylic acid has been demonstrated to ameliorate inflammatory acne by its effects on the arachidonic acid cascade.2,4,17 In our study, salicylic acid 30% peel met participants’ satisfaction in acne improvement similar to a study showing a 50% improvement in acne scores after just 2 treatments.18 Our data support and corroborate that salicylic acid 30% peel renders an improvement in acne sequelae reported in several other studies.2,17,18

Pneumatic broadband light has been known to treat acne by the mechanism of pneumatic suction combined with photodynamic therapy using broadband-pulsed light (400–1200 nm).6-8 By applying the pneumatic device, a vacuum is created on the skin to remove sebum contents from follicles, whereas broadband light is emitted simultaneously to destroy bacteria and decrease the inflammatory process.7 During the vacuum process, the skin is stretched to reduce pain and avoid competitive chromophores (eg, hemoglobin), while the broadband light is administered.7 Broadband light encompasses 2 main light spectrums: blue light (415 nm) activates coproporphyrin III, which induces reactive free radicals and singlet oxygen species and has been reported to be the cause of bacterial cell death,19 and red light (633 nm), which renders an increase of fibroblast growth factors to work against the inflammatory processes.20 There are numerous studies showing a reduction of acne lesions after photopneumatic therapy with minimal side effects.6-8

In our study, we compared the efficacy of salicylic acid 30% peel with PBBL in the treatment of acne. Both treatments showed significant reduction of mGAGS compared to baseline starting from week 3 and lasting until week 12. Remarkably, although there were some participants who reported acne recurrence after completing all treatments at week 6, which could have happened when the treatments were ended, the final acne score at week 12 was still significantly lower than baseline. It is clear that the participants continued their acne improvement up to the 6-week follow-up period without any topical or oral medication. We do not propose that either salicylic acid peel or PBBL treatment is a solitary option but speculate that the combination of both treatments may initiate a faster resolution in the disappearance of acne.

Although there was no statistically significant difference in efficacy between salicylic acid 30% peel and PBBL procedures at each visit, QOL assessments related to treatment satisfaction did yield significant differences between baseline and the end of treatment. We noticed that participants had more positive attitudes toward the PBBL side at week 3 and week 5 but only mild satisfaction at week 4, as the differences in QOL scores between both treatments showed positive ranging values. This finding is most likely related to the immediate reduction of acne pustules by the PBBL vacuum lysis of these lesions. The differences in the QOL scores between both treatments at week 12 (the last follow-up evaluation) provided opposite findings, which meant patients had nearly even improvement in both PBBL method and salicylic acid 30% peel. Therefore, according to QOL data, acne disappeared quickly with the application of PBBL therapy but reappeared on the PBBL-treated side by the follow-up evaluations, though the acne score between both sides showed no statistically significant difference.

We reason that the PBBL therapy works better than salicylic acid 30% peel because the pneumatic system may help to unclog the pores through mechanical debridement via suctioning versus desquamation from salicylic acid 30% peel. Nonetheless, salicylic acid 30% peel sustained improvement when compared to PBBL through the follow-up periods. Both salicylic acid 30% peel and PBBL treatments are well tolerated and may initiate a faster resolution in the improvement of acne when incorporated with a medical program.

Because of the recurrence of acne after treatments were stopped, additional medical therapies are advised to be used along with this study’s clinical treatments to help mitigate the acne symptoms. These treatments should be considered in patients concerned about antibiotic resistance or those who cannot take oral antibiotics or retinoids. Salicylic acid peel is more accessible and affordable than PBBL, whereas PBBL is slightly more tolerable and less irritating than salicylic acid peel. Nevertheless, the cost of investment in PBBL is quite high—as much as $70,000—and does not include disposable, single-use tips, which cost $30 each. The machine is easy to set up, weighs about 40 lb, and requires little space to store. The average cost per visit of PBBL treatment in office is $150.00 and $75.00 for salicylic acid peel (unpublished data, Hospital of the University of Pennsylvania, 2010). Most patients may select salicylic acid peel over PBBL due to the cost and convenience of the treatment. Neither procedure should be considered as a solitary treatment option but rather as adjunctive procedures combined with oral and/or topical acne medications. After this study’s treatments were stopped and without other medications to maintain treatment effectiveness, the lesions reappeared, trending back toward baseline.

 

 

Conclusion

Both salicylic acid 30% peel and PBBL procedures are effective, safe, and well tolerated in treating acne. Although there was no significant difference in the efficacy between both treatments in this study, the small sample size and short follow-up intervals warrant further studies to support the observed outstanding outcomes and should be considered in combination with other medical treatment options. These procedures may be beneficial in holding the patient compliant until their medical therapies have an opportunity to work.

Acknowledgment

The authors would like to thank Joyce Okawa, RN (Philadelphia, Pennsylvania), for her assistance in the submission to the institutional review board of the University of Pennsylvania.

References
  1. Rapp DA, Brenes GA, Feldman SR, et al. Anger and acne: implications for quality of life, patient satisfaction and clinical care. Br J Dermatol. 2004;151:183-189.
  2. Zakopoulou N, Kontochristopoulos G. Superficial chemical peels. J Cosmet Dermatol. 2006;5:246-253.
  3. Berson DS, Cohen JL, Rendon MI, et al. Clinical role and application of superficial chemical peels in today’s practice. J Drugs Dermatol. 2009;8:803-811.
  4. Shalita AR. Treatment of mild and moderate acne vulgaris with salicylic acid in an alcohol-detergent vehicle. Cutis. 1981;28:556-558, 561.
  5. Sakamoto FH, Lopes JD, Anderson RR. Photodynamic therapy for acne vulgaris: a critical review from basics to clinical practice: part I. acne vulgaris: when and why consider photodynamic therapy? J Am Acad Dermatol. 2010;63:183-193; quiz 93-94.
  6. Gold MH, Biron J. Efficacy of a novel combination of pneumatic energy and broadband light for the treatment of acne. J Drugs Dermatol. 2008;7:639-642.
  7. Shamban AT, Enokibori M, Narurkar V, et al. Photopneumatic technology for the treatment of acne vulgaris. J Drugs Dermatol. 2008;7:139-145.
  8. Wanitphakdeedecha R, Tanzi EL, Alster TS. Photopneumatic therapy for the treatment of acne. J Drugs Dermatol. 2009;8:239-241.
  9. Doshi A, Zaheer A, Stiller MJ. A comparison of current acne grading systems and proposal of a novel system. Int J Dermatol. 1997;36:416-418.
  10. Weiss JW, Shavin J, Davis M. Preliminary results of a nonrandomized, multicenter, open-label study of patient satisfaction after treatment with combination benzoyl peroxide/clindamycin topical gel for mild to moderate acne. Clin Ther. 2002;24:1706-1717.
  11. Demircay Z, Kus S, Sur H. Predictive factors for acne flare during isotretinoin treatment. Eur J Dermatol. 2008;18:452-456.
  12. Gupta MA, Johnson AM, Gupta AK. The development of an Acne Quality of Life scale: reliability, validity, and relation to subjective acne severity in mild to moderate acne vulgaris. Acta Derm Venereol. 1998;78:451-456.
  13. Wong DL, Baker CM. Pain in children: comparison of assessment scales. Pediatr Nurs. 1988;14:9-17.
  14. Wong DL, Hockenberry-Eaton M, Wilson D, et al. Wong’s Essentials of Pediatric Nursing. 6th ed. St. Louis, MO: Mosby; 2001:1301.
  15. Zempsky WT, Robbins B, McKay K. Reduction of topical anesthetic onset time using ultrasound: a randomized controlled trial prior to venipuncture in young children. Pain Med. 2008;9:795-802.
  16. Imayama S, Ueda S, Isoda M. Histologic changes in the skin of hairless mice following peeling with salicylic acid. Arch Dermatol. 2000;136:1390-1395.
  17. Lee H, Kim I. Salicylic acid peels for the treatment of acne vulgaris in Asian patients. Dermatol Surg. 2003;29:1196-1199.
  18. Kessler E, Flanagan K, Chia C, et al. Comparison of alpha- and beta-hydroxy acid chemical peels in the treatment of mild to moderately severe facial acne vulgaris. Dermatol Surg. 2008;34:45-50.
  19. Omi T, Munavalli GS, Kawana S, et al. Ultrastructural evidencefor thermal injury to pilosebaceous units during the treatment of acne using photopneumatic (PPX) therapy. J Cosmet Laser Ther. 2008;10:7-11.
  20. Papageorgiou P, Katsambas A, Chu A. Phototherapy with blue (415 nm) and red (660 nm) light in the treatment of acne vulgaris. Br J Dermatol. 2000;142:973-978.
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Author and Disclosure Information

Drs. Thuangtong and Rattanaumpawan are from the Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand. Dr. Thuangtong is from the Department of Dermatology, and Dr. Rattanaumpawan is from the Department of Medicine. Dr. Tangjaturonrusamee is from the Institute of Dermatology, Department of Medical Services, Ministry of Public Health, Bangkok. Dr. Ditre is from the Department of Dermatology, Perelman School of Medicine at University of Pennsylvania, Philadelphia, and Penn Medicine Radnor, Pennsylvania.

The authors report no conflict of interest.

Correspondence: Chérie M. Ditre, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 250 King of Prussia Rd, Radnor, PA 19087 ([email protected]).

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Drs. Thuangtong and Rattanaumpawan are from the Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand. Dr. Thuangtong is from the Department of Dermatology, and Dr. Rattanaumpawan is from the Department of Medicine. Dr. Tangjaturonrusamee is from the Institute of Dermatology, Department of Medical Services, Ministry of Public Health, Bangkok. Dr. Ditre is from the Department of Dermatology, Perelman School of Medicine at University of Pennsylvania, Philadelphia, and Penn Medicine Radnor, Pennsylvania.

The authors report no conflict of interest.

Correspondence: Chérie M. Ditre, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 250 King of Prussia Rd, Radnor, PA 19087 ([email protected]).

Author and Disclosure Information

Drs. Thuangtong and Rattanaumpawan are from the Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand. Dr. Thuangtong is from the Department of Dermatology, and Dr. Rattanaumpawan is from the Department of Medicine. Dr. Tangjaturonrusamee is from the Institute of Dermatology, Department of Medical Services, Ministry of Public Health, Bangkok. Dr. Ditre is from the Department of Dermatology, Perelman School of Medicine at University of Pennsylvania, Philadelphia, and Penn Medicine Radnor, Pennsylvania.

The authors report no conflict of interest.

Correspondence: Chérie M. Ditre, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 250 King of Prussia Rd, Radnor, PA 19087 ([email protected]).

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Facial acne vulgaris is a common skin disease among teenagers and adolescents that may negatively affect self-esteem, perceived facial attractiveness, and social participation.1 Treatments for acne often are multimodal and require the utmost adherence. For these reasons, acne treatments have been challenging to clinicians and patients alike, as patient compliance in maintaining the use of prescribed topical and oral medications remains essential to attain improvement in quality of life (QOL).

Salicylic acid is a popular medicament for acne treatment that frequently is used as monotherapy or as an adjuvant for other acne treatments, especially in patients with oily skin.2 Salicylic acid has a keratolytic effect, causing corneocyte discohesion in clogged pores or congested follicles,2 and it is effective in treating both inflammatory and noninflammatory acne.3,4

Light therapy, particularly with visible light, has been demonstrated to improve acne outcomes.5 Pneumatic broadband light (PBBL) is a therapeutic light treatment in the broadband range (400–1200 nm) that is combined with vacuum suction, which creates a mechanical lysis of thin-walled pustules and dislodges pore impaction. Additionally, the blue light portion of the PBBL spectrum targets endogenous porphyrins in Propionibacterium acnes, resulting in bacterial destruction.6-8

The purpose of this study was to compare the efficacy, tolerability, and safety of salicylic acid 30% peel versus PBBL in the treatment of mild to moderately severe facial acne vulgaris.

METHODS

Study Design

This single-blind, randomized, split-face pilot study was approved by the institutional review board of the University of Pennsylvania (Philadelphia, Pennsylvania). All patients provided informed consent before entering the study. The single-blind evaluation was performed by one dermatologist (C.T.) who examined the participants on every visit prior to PBBL treatment.

Before the study started, participants were randomized for which side of the face was to be treated with PBBL using a number assigned to each participant. Participants received both treatments—salicylic acid 30% peel on one side of the face and PBBL treatment on the other side of the face—once weekly for a total of 6 treatments. They were then asked to return for 2 follow-up evaluations at weeks 3 and 6 following the last treatment session and were instructed not to use any topical or oral acne medications during these follow-up periods.

Inclusion and Exclusion Criteria

Patients aged 18 years and older of any race and sex with noninflammatory papules, some inflammatory papules, and no more than 1 nodule (considered as mild to moderately severe facial acne) were included in the study. Participants had not been on any topical acne medications for at least 1 month and/or oral retinoids for at least 1 year prior to the study period. All women completed urine pregnancy tests prior to the study and were advised to utilize birth control during the study period.

Study Treatments

Salicylic Acid 30% Peel

The participant’s face was cleansed thoroughly before application of salicylic acid 30% (1.5 g/2.5 mL) to half of the face and left on for 5 minutes before being carefully rinsed off by spraying with spring water. Prior to initiating PBBL therapy, the peeled side of the participant’s face was covered with a towel.

Pneumatic Broadband Light

On the other side of the face, PBBL was performed to deliver broadband light within the spectrum range of 400 to 1200 nm at a setting approximately equivalent to a fluence of 4 to 6 J/cm2 and a vacuum setting approximately equivalent to a negative pressure of 3 lb/in2. The power setting was increased on each subsequent visit depending on each participant’s tolerability.

Participants were required to apply a moisturizer and sunscreen to the face and avoid excessive sun exposure between study visits.

Efficacy Evaluation

A comparison of the efficacy of the treatments was determined by clinical evaluation and examining the results of the outcome measurements with the modified Global Acne Grading Score (mGAGS) and Acne QOL Scale during each treatment visit. Facial photographs were taken at each visit.

Modified Global Acne Grading Score

The mGAGS is a modification of the Global Acne Grading Scale (GAGS) that has been used to evaluate acne severity in many studies.9-11 The GAGS considers 6 locations on the face with a grading factor for each location. The local score is obtained by multiplying the factor rated by location with the factor of clinical assessment: local score = factor rated by location × factor rated by clinical assessment. The total score is the sum of the individual local scores (Table 1).

Although the original GAGS incorporated the type and location of the lesions in its calculation, we felt that the number of lesions also was important to add to our grading score. Therefore, we modified the GAGS by adding a factor rated by the number of lesions to improve the accuracy of the test. Accordingly, the local mGAGS scores were calculated by multiplying the location factor by the lesion type and number of lesions factors: local score = location factor × lesion type factor × number of lesions factor.

Acne QOL Questionnaire

Acne QOL was assessed during each visit to demonstrate if the treatment results affected participants’ socialization due to appearance.12 Participants were asked to complete the questionnaire, which consisted of 9 questions with 4 rating answers (0=not affected; 1=mildly affected; 2=moderately affected; 3=markedly affected). A total score of 9 or higher (high score) indicated that acne had a substantial negative impact on the participant, while a total score below 9 (low score) meant acne scarcely impacted social aspects and daily activities of the patient.

Safety Evaluation

The safety of the treatments was evaluated by clinical inspection and by comparing the results of the Wong-Baker FACES Pain Rating Scale (WBPRS)13 after treatment. The WBPRS is used worldwide among researchers to assess pain, particularly in children.14,15 It is composed of 6 faces expressing pain with word descriptions with a corresponding number range reflecting pain severity from 0 to 5 (0=no hurt; 1=hurts little bit; 2=hurts little more; 3=hurts even more; 4=hurts whole lot; 5=hurts worst).13

Statistical Analysis

All variables were presented as the median (range). A Wilcoxon signed rank test was used to compare clinical responses between the salicylic acid 30% peel and PBBL therapies. SPSS software version 12.0 was used for all statistical analysis. A 2-tailed P value of ≤.05 was considered statistically significant.

 

 

RESULTS

Study Population

Twelve participants (2 males, 10 females) aged 17 to 36 years (median age, 22 years; mean age [SD], 23.33 [1.65] years) with both comedonal and inflammatory acne were enrolled into this study for 6 split-face treatments of salicylic acid 30% peel and PBBL at 1-week intervals for 6 weeks, with 2 subsequent follow-up sessions at weeks 3 and 6 posttreatment. Of the 12 participants, 11 were white and 1 was Asian American, with Fitzpatrick skin types II to IV. Nine participants (75%) completed the study. One participant dropped out of the study after the fourth treatment due to a scheduling conflict, and the other 2 participants did not return for follow-up. No participants withdrew from the study because of adverse therapeutic events.

Efficacy Evaluation

Comparisons between the salicylic acid 30% peel and PBBL procedures for mGAGS at each visit are shown in Table 2. There was no significant difference in treatment efficacy between the salicylic acid 30% peel and PBBL therapies during the study’s treatment and follow-up events; however, both procedures contributed to a major improvement in acne symptoms by the third treatment session and through to the last follow-up session (P≤.05). Clinical photographs at baseline, at last treatment visit (week 6), and at last follow-up (week 12) are shown in Figures 1 and 2.

Figure 1. A 19-year-old woman with mild acne who was treated with salicylic acid 30% peel on the right side of the face at baseline (A), week 6 (B), and week 12 (C).

Figure 2. A 19-year-old woman with mild acne who was treated with pneumatic broadband light on the left side of the face at baseline (A), week 6 (B), and week 12 (C).

The results of the acne QOL questionnaire are shown in Table 2. Lower scores reflect a higher QOL. Median QOL scores at each visit ranged from 0.5 to 4.5. There was no significant difference found between the peel agent or PBBL based on the baseline QOL and subsequent visit assessments; however, the differences between the 2 treatments were significant at weeks 3 (P=.05) and 5 (P=.03) of treatment as well as at the last follow-up visit (P=.05).

According to the QOL scores, by the third treatment session participants were more satisfied with their improved acne condition from the PBBL procedure than the salicylic acid 30% peel as demonstrated by a positive range of the QOL assessments between PBBL and salicylic acid 30% peel (as shown in the difference in QOL in Table 2: week 3, 0–6; week 4, 0–3; week 5, 0–7). On the other hand, participants saw more improvement from the salicylic acid 30% peel than from PBBL by the last follow-up evaluation, as the differences in QOL scores between the 2 treatments resulted in a negative range (5–0).

Safety

Pain assessment by the WBPRS at every visit showed a low pain rating associated with both salicylic acid 30% peel (range, 0–0.5) and PBBL (range, 1.0–1.5) treatments. The median pain score of the salicylic acid 30% peel appeared higher compared to the PBBL treatment, yet a significant difference between both treatments was seen only at weeks 1, 3, and 6 of treatment (P≤.05).

There were no unexpected therapeutic reactions reported in our study, and no participants withdrew from the study due to adverse events. Most participants experienced only mild adverse reactions, including redness, stinging, and a burning sensation on the salicylic acid 30% peel side, which were transient and disappeared in minutes; only redness occurred on the PBBL-treated side.

Comment

Facial acne treatment is challenging, as prolonged and/or severe acne contributes to scarring, declining self-confidence, and undesirable financial consequences. Even though salicylic acid peel is a commonly used acne treatment choice, the PBBL methodology was approved by the US Food and Drug Administration6 and has become an alternative procedure for acne treatment.

The pharmacological effects of salicylic acid are related to its corneocyte desquamation and exfoliative actions, thereby reducing corneocyte cohesion and unclogging follicular pores.16 Salicylic acid has been demonstrated to ameliorate inflammatory acne by its effects on the arachidonic acid cascade.2,4,17 In our study, salicylic acid 30% peel met participants’ satisfaction in acne improvement similar to a study showing a 50% improvement in acne scores after just 2 treatments.18 Our data support and corroborate that salicylic acid 30% peel renders an improvement in acne sequelae reported in several other studies.2,17,18

Pneumatic broadband light has been known to treat acne by the mechanism of pneumatic suction combined with photodynamic therapy using broadband-pulsed light (400–1200 nm).6-8 By applying the pneumatic device, a vacuum is created on the skin to remove sebum contents from follicles, whereas broadband light is emitted simultaneously to destroy bacteria and decrease the inflammatory process.7 During the vacuum process, the skin is stretched to reduce pain and avoid competitive chromophores (eg, hemoglobin), while the broadband light is administered.7 Broadband light encompasses 2 main light spectrums: blue light (415 nm) activates coproporphyrin III, which induces reactive free radicals and singlet oxygen species and has been reported to be the cause of bacterial cell death,19 and red light (633 nm), which renders an increase of fibroblast growth factors to work against the inflammatory processes.20 There are numerous studies showing a reduction of acne lesions after photopneumatic therapy with minimal side effects.6-8

In our study, we compared the efficacy of salicylic acid 30% peel with PBBL in the treatment of acne. Both treatments showed significant reduction of mGAGS compared to baseline starting from week 3 and lasting until week 12. Remarkably, although there were some participants who reported acne recurrence after completing all treatments at week 6, which could have happened when the treatments were ended, the final acne score at week 12 was still significantly lower than baseline. It is clear that the participants continued their acne improvement up to the 6-week follow-up period without any topical or oral medication. We do not propose that either salicylic acid peel or PBBL treatment is a solitary option but speculate that the combination of both treatments may initiate a faster resolution in the disappearance of acne.

Although there was no statistically significant difference in efficacy between salicylic acid 30% peel and PBBL procedures at each visit, QOL assessments related to treatment satisfaction did yield significant differences between baseline and the end of treatment. We noticed that participants had more positive attitudes toward the PBBL side at week 3 and week 5 but only mild satisfaction at week 4, as the differences in QOL scores between both treatments showed positive ranging values. This finding is most likely related to the immediate reduction of acne pustules by the PBBL vacuum lysis of these lesions. The differences in the QOL scores between both treatments at week 12 (the last follow-up evaluation) provided opposite findings, which meant patients had nearly even improvement in both PBBL method and salicylic acid 30% peel. Therefore, according to QOL data, acne disappeared quickly with the application of PBBL therapy but reappeared on the PBBL-treated side by the follow-up evaluations, though the acne score between both sides showed no statistically significant difference.

We reason that the PBBL therapy works better than salicylic acid 30% peel because the pneumatic system may help to unclog the pores through mechanical debridement via suctioning versus desquamation from salicylic acid 30% peel. Nonetheless, salicylic acid 30% peel sustained improvement when compared to PBBL through the follow-up periods. Both salicylic acid 30% peel and PBBL treatments are well tolerated and may initiate a faster resolution in the improvement of acne when incorporated with a medical program.

Because of the recurrence of acne after treatments were stopped, additional medical therapies are advised to be used along with this study’s clinical treatments to help mitigate the acne symptoms. These treatments should be considered in patients concerned about antibiotic resistance or those who cannot take oral antibiotics or retinoids. Salicylic acid peel is more accessible and affordable than PBBL, whereas PBBL is slightly more tolerable and less irritating than salicylic acid peel. Nevertheless, the cost of investment in PBBL is quite high—as much as $70,000—and does not include disposable, single-use tips, which cost $30 each. The machine is easy to set up, weighs about 40 lb, and requires little space to store. The average cost per visit of PBBL treatment in office is $150.00 and $75.00 for salicylic acid peel (unpublished data, Hospital of the University of Pennsylvania, 2010). Most patients may select salicylic acid peel over PBBL due to the cost and convenience of the treatment. Neither procedure should be considered as a solitary treatment option but rather as adjunctive procedures combined with oral and/or topical acne medications. After this study’s treatments were stopped and without other medications to maintain treatment effectiveness, the lesions reappeared, trending back toward baseline.

 

 

Conclusion

Both salicylic acid 30% peel and PBBL procedures are effective, safe, and well tolerated in treating acne. Although there was no significant difference in the efficacy between both treatments in this study, the small sample size and short follow-up intervals warrant further studies to support the observed outstanding outcomes and should be considered in combination with other medical treatment options. These procedures may be beneficial in holding the patient compliant until their medical therapies have an opportunity to work.

Acknowledgment

The authors would like to thank Joyce Okawa, RN (Philadelphia, Pennsylvania), for her assistance in the submission to the institutional review board of the University of Pennsylvania.

Facial acne vulgaris is a common skin disease among teenagers and adolescents that may negatively affect self-esteem, perceived facial attractiveness, and social participation.1 Treatments for acne often are multimodal and require the utmost adherence. For these reasons, acne treatments have been challenging to clinicians and patients alike, as patient compliance in maintaining the use of prescribed topical and oral medications remains essential to attain improvement in quality of life (QOL).

Salicylic acid is a popular medicament for acne treatment that frequently is used as monotherapy or as an adjuvant for other acne treatments, especially in patients with oily skin.2 Salicylic acid has a keratolytic effect, causing corneocyte discohesion in clogged pores or congested follicles,2 and it is effective in treating both inflammatory and noninflammatory acne.3,4

Light therapy, particularly with visible light, has been demonstrated to improve acne outcomes.5 Pneumatic broadband light (PBBL) is a therapeutic light treatment in the broadband range (400–1200 nm) that is combined with vacuum suction, which creates a mechanical lysis of thin-walled pustules and dislodges pore impaction. Additionally, the blue light portion of the PBBL spectrum targets endogenous porphyrins in Propionibacterium acnes, resulting in bacterial destruction.6-8

The purpose of this study was to compare the efficacy, tolerability, and safety of salicylic acid 30% peel versus PBBL in the treatment of mild to moderately severe facial acne vulgaris.

METHODS

Study Design

This single-blind, randomized, split-face pilot study was approved by the institutional review board of the University of Pennsylvania (Philadelphia, Pennsylvania). All patients provided informed consent before entering the study. The single-blind evaluation was performed by one dermatologist (C.T.) who examined the participants on every visit prior to PBBL treatment.

Before the study started, participants were randomized for which side of the face was to be treated with PBBL using a number assigned to each participant. Participants received both treatments—salicylic acid 30% peel on one side of the face and PBBL treatment on the other side of the face—once weekly for a total of 6 treatments. They were then asked to return for 2 follow-up evaluations at weeks 3 and 6 following the last treatment session and were instructed not to use any topical or oral acne medications during these follow-up periods.

Inclusion and Exclusion Criteria

Patients aged 18 years and older of any race and sex with noninflammatory papules, some inflammatory papules, and no more than 1 nodule (considered as mild to moderately severe facial acne) were included in the study. Participants had not been on any topical acne medications for at least 1 month and/or oral retinoids for at least 1 year prior to the study period. All women completed urine pregnancy tests prior to the study and were advised to utilize birth control during the study period.

Study Treatments

Salicylic Acid 30% Peel

The participant’s face was cleansed thoroughly before application of salicylic acid 30% (1.5 g/2.5 mL) to half of the face and left on for 5 minutes before being carefully rinsed off by spraying with spring water. Prior to initiating PBBL therapy, the peeled side of the participant’s face was covered with a towel.

Pneumatic Broadband Light

On the other side of the face, PBBL was performed to deliver broadband light within the spectrum range of 400 to 1200 nm at a setting approximately equivalent to a fluence of 4 to 6 J/cm2 and a vacuum setting approximately equivalent to a negative pressure of 3 lb/in2. The power setting was increased on each subsequent visit depending on each participant’s tolerability.

Participants were required to apply a moisturizer and sunscreen to the face and avoid excessive sun exposure between study visits.

Efficacy Evaluation

A comparison of the efficacy of the treatments was determined by clinical evaluation and examining the results of the outcome measurements with the modified Global Acne Grading Score (mGAGS) and Acne QOL Scale during each treatment visit. Facial photographs were taken at each visit.

Modified Global Acne Grading Score

The mGAGS is a modification of the Global Acne Grading Scale (GAGS) that has been used to evaluate acne severity in many studies.9-11 The GAGS considers 6 locations on the face with a grading factor for each location. The local score is obtained by multiplying the factor rated by location with the factor of clinical assessment: local score = factor rated by location × factor rated by clinical assessment. The total score is the sum of the individual local scores (Table 1).

Although the original GAGS incorporated the type and location of the lesions in its calculation, we felt that the number of lesions also was important to add to our grading score. Therefore, we modified the GAGS by adding a factor rated by the number of lesions to improve the accuracy of the test. Accordingly, the local mGAGS scores were calculated by multiplying the location factor by the lesion type and number of lesions factors: local score = location factor × lesion type factor × number of lesions factor.

Acne QOL Questionnaire

Acne QOL was assessed during each visit to demonstrate if the treatment results affected participants’ socialization due to appearance.12 Participants were asked to complete the questionnaire, which consisted of 9 questions with 4 rating answers (0=not affected; 1=mildly affected; 2=moderately affected; 3=markedly affected). A total score of 9 or higher (high score) indicated that acne had a substantial negative impact on the participant, while a total score below 9 (low score) meant acne scarcely impacted social aspects and daily activities of the patient.

Safety Evaluation

The safety of the treatments was evaluated by clinical inspection and by comparing the results of the Wong-Baker FACES Pain Rating Scale (WBPRS)13 after treatment. The WBPRS is used worldwide among researchers to assess pain, particularly in children.14,15 It is composed of 6 faces expressing pain with word descriptions with a corresponding number range reflecting pain severity from 0 to 5 (0=no hurt; 1=hurts little bit; 2=hurts little more; 3=hurts even more; 4=hurts whole lot; 5=hurts worst).13

Statistical Analysis

All variables were presented as the median (range). A Wilcoxon signed rank test was used to compare clinical responses between the salicylic acid 30% peel and PBBL therapies. SPSS software version 12.0 was used for all statistical analysis. A 2-tailed P value of ≤.05 was considered statistically significant.

 

 

RESULTS

Study Population

Twelve participants (2 males, 10 females) aged 17 to 36 years (median age, 22 years; mean age [SD], 23.33 [1.65] years) with both comedonal and inflammatory acne were enrolled into this study for 6 split-face treatments of salicylic acid 30% peel and PBBL at 1-week intervals for 6 weeks, with 2 subsequent follow-up sessions at weeks 3 and 6 posttreatment. Of the 12 participants, 11 were white and 1 was Asian American, with Fitzpatrick skin types II to IV. Nine participants (75%) completed the study. One participant dropped out of the study after the fourth treatment due to a scheduling conflict, and the other 2 participants did not return for follow-up. No participants withdrew from the study because of adverse therapeutic events.

Efficacy Evaluation

Comparisons between the salicylic acid 30% peel and PBBL procedures for mGAGS at each visit are shown in Table 2. There was no significant difference in treatment efficacy between the salicylic acid 30% peel and PBBL therapies during the study’s treatment and follow-up events; however, both procedures contributed to a major improvement in acne symptoms by the third treatment session and through to the last follow-up session (P≤.05). Clinical photographs at baseline, at last treatment visit (week 6), and at last follow-up (week 12) are shown in Figures 1 and 2.

Figure 1. A 19-year-old woman with mild acne who was treated with salicylic acid 30% peel on the right side of the face at baseline (A), week 6 (B), and week 12 (C).

Figure 2. A 19-year-old woman with mild acne who was treated with pneumatic broadband light on the left side of the face at baseline (A), week 6 (B), and week 12 (C).

The results of the acne QOL questionnaire are shown in Table 2. Lower scores reflect a higher QOL. Median QOL scores at each visit ranged from 0.5 to 4.5. There was no significant difference found between the peel agent or PBBL based on the baseline QOL and subsequent visit assessments; however, the differences between the 2 treatments were significant at weeks 3 (P=.05) and 5 (P=.03) of treatment as well as at the last follow-up visit (P=.05).

According to the QOL scores, by the third treatment session participants were more satisfied with their improved acne condition from the PBBL procedure than the salicylic acid 30% peel as demonstrated by a positive range of the QOL assessments between PBBL and salicylic acid 30% peel (as shown in the difference in QOL in Table 2: week 3, 0–6; week 4, 0–3; week 5, 0–7). On the other hand, participants saw more improvement from the salicylic acid 30% peel than from PBBL by the last follow-up evaluation, as the differences in QOL scores between the 2 treatments resulted in a negative range (5–0).

Safety

Pain assessment by the WBPRS at every visit showed a low pain rating associated with both salicylic acid 30% peel (range, 0–0.5) and PBBL (range, 1.0–1.5) treatments. The median pain score of the salicylic acid 30% peel appeared higher compared to the PBBL treatment, yet a significant difference between both treatments was seen only at weeks 1, 3, and 6 of treatment (P≤.05).

There were no unexpected therapeutic reactions reported in our study, and no participants withdrew from the study due to adverse events. Most participants experienced only mild adverse reactions, including redness, stinging, and a burning sensation on the salicylic acid 30% peel side, which were transient and disappeared in minutes; only redness occurred on the PBBL-treated side.

Comment

Facial acne treatment is challenging, as prolonged and/or severe acne contributes to scarring, declining self-confidence, and undesirable financial consequences. Even though salicylic acid peel is a commonly used acne treatment choice, the PBBL methodology was approved by the US Food and Drug Administration6 and has become an alternative procedure for acne treatment.

The pharmacological effects of salicylic acid are related to its corneocyte desquamation and exfoliative actions, thereby reducing corneocyte cohesion and unclogging follicular pores.16 Salicylic acid has been demonstrated to ameliorate inflammatory acne by its effects on the arachidonic acid cascade.2,4,17 In our study, salicylic acid 30% peel met participants’ satisfaction in acne improvement similar to a study showing a 50% improvement in acne scores after just 2 treatments.18 Our data support and corroborate that salicylic acid 30% peel renders an improvement in acne sequelae reported in several other studies.2,17,18

Pneumatic broadband light has been known to treat acne by the mechanism of pneumatic suction combined with photodynamic therapy using broadband-pulsed light (400–1200 nm).6-8 By applying the pneumatic device, a vacuum is created on the skin to remove sebum contents from follicles, whereas broadband light is emitted simultaneously to destroy bacteria and decrease the inflammatory process.7 During the vacuum process, the skin is stretched to reduce pain and avoid competitive chromophores (eg, hemoglobin), while the broadband light is administered.7 Broadband light encompasses 2 main light spectrums: blue light (415 nm) activates coproporphyrin III, which induces reactive free radicals and singlet oxygen species and has been reported to be the cause of bacterial cell death,19 and red light (633 nm), which renders an increase of fibroblast growth factors to work against the inflammatory processes.20 There are numerous studies showing a reduction of acne lesions after photopneumatic therapy with minimal side effects.6-8

In our study, we compared the efficacy of salicylic acid 30% peel with PBBL in the treatment of acne. Both treatments showed significant reduction of mGAGS compared to baseline starting from week 3 and lasting until week 12. Remarkably, although there were some participants who reported acne recurrence after completing all treatments at week 6, which could have happened when the treatments were ended, the final acne score at week 12 was still significantly lower than baseline. It is clear that the participants continued their acne improvement up to the 6-week follow-up period without any topical or oral medication. We do not propose that either salicylic acid peel or PBBL treatment is a solitary option but speculate that the combination of both treatments may initiate a faster resolution in the disappearance of acne.

Although there was no statistically significant difference in efficacy between salicylic acid 30% peel and PBBL procedures at each visit, QOL assessments related to treatment satisfaction did yield significant differences between baseline and the end of treatment. We noticed that participants had more positive attitudes toward the PBBL side at week 3 and week 5 but only mild satisfaction at week 4, as the differences in QOL scores between both treatments showed positive ranging values. This finding is most likely related to the immediate reduction of acne pustules by the PBBL vacuum lysis of these lesions. The differences in the QOL scores between both treatments at week 12 (the last follow-up evaluation) provided opposite findings, which meant patients had nearly even improvement in both PBBL method and salicylic acid 30% peel. Therefore, according to QOL data, acne disappeared quickly with the application of PBBL therapy but reappeared on the PBBL-treated side by the follow-up evaluations, though the acne score between both sides showed no statistically significant difference.

We reason that the PBBL therapy works better than salicylic acid 30% peel because the pneumatic system may help to unclog the pores through mechanical debridement via suctioning versus desquamation from salicylic acid 30% peel. Nonetheless, salicylic acid 30% peel sustained improvement when compared to PBBL through the follow-up periods. Both salicylic acid 30% peel and PBBL treatments are well tolerated and may initiate a faster resolution in the improvement of acne when incorporated with a medical program.

Because of the recurrence of acne after treatments were stopped, additional medical therapies are advised to be used along with this study’s clinical treatments to help mitigate the acne symptoms. These treatments should be considered in patients concerned about antibiotic resistance or those who cannot take oral antibiotics or retinoids. Salicylic acid peel is more accessible and affordable than PBBL, whereas PBBL is slightly more tolerable and less irritating than salicylic acid peel. Nevertheless, the cost of investment in PBBL is quite high—as much as $70,000—and does not include disposable, single-use tips, which cost $30 each. The machine is easy to set up, weighs about 40 lb, and requires little space to store. The average cost per visit of PBBL treatment in office is $150.00 and $75.00 for salicylic acid peel (unpublished data, Hospital of the University of Pennsylvania, 2010). Most patients may select salicylic acid peel over PBBL due to the cost and convenience of the treatment. Neither procedure should be considered as a solitary treatment option but rather as adjunctive procedures combined with oral and/or topical acne medications. After this study’s treatments were stopped and without other medications to maintain treatment effectiveness, the lesions reappeared, trending back toward baseline.

 

 

Conclusion

Both salicylic acid 30% peel and PBBL procedures are effective, safe, and well tolerated in treating acne. Although there was no significant difference in the efficacy between both treatments in this study, the small sample size and short follow-up intervals warrant further studies to support the observed outstanding outcomes and should be considered in combination with other medical treatment options. These procedures may be beneficial in holding the patient compliant until their medical therapies have an opportunity to work.

Acknowledgment

The authors would like to thank Joyce Okawa, RN (Philadelphia, Pennsylvania), for her assistance in the submission to the institutional review board of the University of Pennsylvania.

References
  1. Rapp DA, Brenes GA, Feldman SR, et al. Anger and acne: implications for quality of life, patient satisfaction and clinical care. Br J Dermatol. 2004;151:183-189.
  2. Zakopoulou N, Kontochristopoulos G. Superficial chemical peels. J Cosmet Dermatol. 2006;5:246-253.
  3. Berson DS, Cohen JL, Rendon MI, et al. Clinical role and application of superficial chemical peels in today’s practice. J Drugs Dermatol. 2009;8:803-811.
  4. Shalita AR. Treatment of mild and moderate acne vulgaris with salicylic acid in an alcohol-detergent vehicle. Cutis. 1981;28:556-558, 561.
  5. Sakamoto FH, Lopes JD, Anderson RR. Photodynamic therapy for acne vulgaris: a critical review from basics to clinical practice: part I. acne vulgaris: when and why consider photodynamic therapy? J Am Acad Dermatol. 2010;63:183-193; quiz 93-94.
  6. Gold MH, Biron J. Efficacy of a novel combination of pneumatic energy and broadband light for the treatment of acne. J Drugs Dermatol. 2008;7:639-642.
  7. Shamban AT, Enokibori M, Narurkar V, et al. Photopneumatic technology for the treatment of acne vulgaris. J Drugs Dermatol. 2008;7:139-145.
  8. Wanitphakdeedecha R, Tanzi EL, Alster TS. Photopneumatic therapy for the treatment of acne. J Drugs Dermatol. 2009;8:239-241.
  9. Doshi A, Zaheer A, Stiller MJ. A comparison of current acne grading systems and proposal of a novel system. Int J Dermatol. 1997;36:416-418.
  10. Weiss JW, Shavin J, Davis M. Preliminary results of a nonrandomized, multicenter, open-label study of patient satisfaction after treatment with combination benzoyl peroxide/clindamycin topical gel for mild to moderate acne. Clin Ther. 2002;24:1706-1717.
  11. Demircay Z, Kus S, Sur H. Predictive factors for acne flare during isotretinoin treatment. Eur J Dermatol. 2008;18:452-456.
  12. Gupta MA, Johnson AM, Gupta AK. The development of an Acne Quality of Life scale: reliability, validity, and relation to subjective acne severity in mild to moderate acne vulgaris. Acta Derm Venereol. 1998;78:451-456.
  13. Wong DL, Baker CM. Pain in children: comparison of assessment scales. Pediatr Nurs. 1988;14:9-17.
  14. Wong DL, Hockenberry-Eaton M, Wilson D, et al. Wong’s Essentials of Pediatric Nursing. 6th ed. St. Louis, MO: Mosby; 2001:1301.
  15. Zempsky WT, Robbins B, McKay K. Reduction of topical anesthetic onset time using ultrasound: a randomized controlled trial prior to venipuncture in young children. Pain Med. 2008;9:795-802.
  16. Imayama S, Ueda S, Isoda M. Histologic changes in the skin of hairless mice following peeling with salicylic acid. Arch Dermatol. 2000;136:1390-1395.
  17. Lee H, Kim I. Salicylic acid peels for the treatment of acne vulgaris in Asian patients. Dermatol Surg. 2003;29:1196-1199.
  18. Kessler E, Flanagan K, Chia C, et al. Comparison of alpha- and beta-hydroxy acid chemical peels in the treatment of mild to moderately severe facial acne vulgaris. Dermatol Surg. 2008;34:45-50.
  19. Omi T, Munavalli GS, Kawana S, et al. Ultrastructural evidencefor thermal injury to pilosebaceous units during the treatment of acne using photopneumatic (PPX) therapy. J Cosmet Laser Ther. 2008;10:7-11.
  20. Papageorgiou P, Katsambas A, Chu A. Phototherapy with blue (415 nm) and red (660 nm) light in the treatment of acne vulgaris. Br J Dermatol. 2000;142:973-978.
References
  1. Rapp DA, Brenes GA, Feldman SR, et al. Anger and acne: implications for quality of life, patient satisfaction and clinical care. Br J Dermatol. 2004;151:183-189.
  2. Zakopoulou N, Kontochristopoulos G. Superficial chemical peels. J Cosmet Dermatol. 2006;5:246-253.
  3. Berson DS, Cohen JL, Rendon MI, et al. Clinical role and application of superficial chemical peels in today’s practice. J Drugs Dermatol. 2009;8:803-811.
  4. Shalita AR. Treatment of mild and moderate acne vulgaris with salicylic acid in an alcohol-detergent vehicle. Cutis. 1981;28:556-558, 561.
  5. Sakamoto FH, Lopes JD, Anderson RR. Photodynamic therapy for acne vulgaris: a critical review from basics to clinical practice: part I. acne vulgaris: when and why consider photodynamic therapy? J Am Acad Dermatol. 2010;63:183-193; quiz 93-94.
  6. Gold MH, Biron J. Efficacy of a novel combination of pneumatic energy and broadband light for the treatment of acne. J Drugs Dermatol. 2008;7:639-642.
  7. Shamban AT, Enokibori M, Narurkar V, et al. Photopneumatic technology for the treatment of acne vulgaris. J Drugs Dermatol. 2008;7:139-145.
  8. Wanitphakdeedecha R, Tanzi EL, Alster TS. Photopneumatic therapy for the treatment of acne. J Drugs Dermatol. 2009;8:239-241.
  9. Doshi A, Zaheer A, Stiller MJ. A comparison of current acne grading systems and proposal of a novel system. Int J Dermatol. 1997;36:416-418.
  10. Weiss JW, Shavin J, Davis M. Preliminary results of a nonrandomized, multicenter, open-label study of patient satisfaction after treatment with combination benzoyl peroxide/clindamycin topical gel for mild to moderate acne. Clin Ther. 2002;24:1706-1717.
  11. Demircay Z, Kus S, Sur H. Predictive factors for acne flare during isotretinoin treatment. Eur J Dermatol. 2008;18:452-456.
  12. Gupta MA, Johnson AM, Gupta AK. The development of an Acne Quality of Life scale: reliability, validity, and relation to subjective acne severity in mild to moderate acne vulgaris. Acta Derm Venereol. 1998;78:451-456.
  13. Wong DL, Baker CM. Pain in children: comparison of assessment scales. Pediatr Nurs. 1988;14:9-17.
  14. Wong DL, Hockenberry-Eaton M, Wilson D, et al. Wong’s Essentials of Pediatric Nursing. 6th ed. St. Louis, MO: Mosby; 2001:1301.
  15. Zempsky WT, Robbins B, McKay K. Reduction of topical anesthetic onset time using ultrasound: a randomized controlled trial prior to venipuncture in young children. Pain Med. 2008;9:795-802.
  16. Imayama S, Ueda S, Isoda M. Histologic changes in the skin of hairless mice following peeling with salicylic acid. Arch Dermatol. 2000;136:1390-1395.
  17. Lee H, Kim I. Salicylic acid peels for the treatment of acne vulgaris in Asian patients. Dermatol Surg. 2003;29:1196-1199.
  18. Kessler E, Flanagan K, Chia C, et al. Comparison of alpha- and beta-hydroxy acid chemical peels in the treatment of mild to moderately severe facial acne vulgaris. Dermatol Surg. 2008;34:45-50.
  19. Omi T, Munavalli GS, Kawana S, et al. Ultrastructural evidencefor thermal injury to pilosebaceous units during the treatment of acne using photopneumatic (PPX) therapy. J Cosmet Laser Ther. 2008;10:7-11.
  20. Papageorgiou P, Katsambas A, Chu A. Phototherapy with blue (415 nm) and red (660 nm) light in the treatment of acne vulgaris. Br J Dermatol. 2000;142:973-978.
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Comparison of Salicylic Acid 30% Peel and Pneumatic Broadband Light in the Treatment of Mild to Moderately Severe Facial Acne Vulgaris
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Practice Points

  • Salicylic acid peel and pneumatic broadband light (PBBL) are good alternative options in treating acne in addition to regular oral and topical treatments.
  • Both salicylic acid peel and PBBL are effective, safe, and tolerable.
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U.S. goals for earlier HIV diagnosis and treatment may be out of reach

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In 2015, only 66% of U.S. youth who were diagnosed with HIV in a Centers for Disease Control and Prevention program were introduced to proper care within 90 days of diagnosis, falling far short of the 2020 national goal to introduce 85% of HIV-affected youth to proper care within 30 days.

In an analysis of data from a CDC-funded program covering 61 state and local health departments and 123 community-based organizations in the United States, Puerto Rico, and the U.S. Virgin Islands, the CDC looked at HIV tests, new positive diagnoses, and linkage between patient and care within 90 days of diagnosis. Of 2,973 youths who were newly diagnosed with HIV, 1,955 (66%) were connected to care within 90 days, and 1,871 were interviewed for partner services, according to the CDC. Of 1,911 youths who had been previously diagnosed, 1,749 (92%) were not in medical care at the time of CDC testing.

In particular, 83% of those tested in non–health care facilities were young men who have sex with men, who are a high-risk group for HIV infection but who only received 28% of tests. Since 92% of new infections in 2009 were acquired from HIV-positive people who were not in medical care, “improving the number of youths who are tested is of high importance,” according to Renee Stein, PhD, and her coinvestigators, all of the division of HIV/AIDS prevention and the National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention at the CDC.

“A health care provider’s testing recommendation is the most important predictor of testing among adolescents at risk for HIV infection,” the researchers said. “Increasing the number of HIV tests among youths at risk for HIV and increasing regular retesting among these youths is essential for reducing HIV infection in this vulnerable population.”

No conflicts of interest were reported by the authors.

Read more in MMWR (2017 Jun 23. doi: 10.15585/mmwr.mm6624a2).

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In 2015, only 66% of U.S. youth who were diagnosed with HIV in a Centers for Disease Control and Prevention program were introduced to proper care within 90 days of diagnosis, falling far short of the 2020 national goal to introduce 85% of HIV-affected youth to proper care within 30 days.

In an analysis of data from a CDC-funded program covering 61 state and local health departments and 123 community-based organizations in the United States, Puerto Rico, and the U.S. Virgin Islands, the CDC looked at HIV tests, new positive diagnoses, and linkage between patient and care within 90 days of diagnosis. Of 2,973 youths who were newly diagnosed with HIV, 1,955 (66%) were connected to care within 90 days, and 1,871 were interviewed for partner services, according to the CDC. Of 1,911 youths who had been previously diagnosed, 1,749 (92%) were not in medical care at the time of CDC testing.

In particular, 83% of those tested in non–health care facilities were young men who have sex with men, who are a high-risk group for HIV infection but who only received 28% of tests. Since 92% of new infections in 2009 were acquired from HIV-positive people who were not in medical care, “improving the number of youths who are tested is of high importance,” according to Renee Stein, PhD, and her coinvestigators, all of the division of HIV/AIDS prevention and the National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention at the CDC.

“A health care provider’s testing recommendation is the most important predictor of testing among adolescents at risk for HIV infection,” the researchers said. “Increasing the number of HIV tests among youths at risk for HIV and increasing regular retesting among these youths is essential for reducing HIV infection in this vulnerable population.”

No conflicts of interest were reported by the authors.

Read more in MMWR (2017 Jun 23. doi: 10.15585/mmwr.mm6624a2).

 

In 2015, only 66% of U.S. youth who were diagnosed with HIV in a Centers for Disease Control and Prevention program were introduced to proper care within 90 days of diagnosis, falling far short of the 2020 national goal to introduce 85% of HIV-affected youth to proper care within 30 days.

In an analysis of data from a CDC-funded program covering 61 state and local health departments and 123 community-based organizations in the United States, Puerto Rico, and the U.S. Virgin Islands, the CDC looked at HIV tests, new positive diagnoses, and linkage between patient and care within 90 days of diagnosis. Of 2,973 youths who were newly diagnosed with HIV, 1,955 (66%) were connected to care within 90 days, and 1,871 were interviewed for partner services, according to the CDC. Of 1,911 youths who had been previously diagnosed, 1,749 (92%) were not in medical care at the time of CDC testing.

In particular, 83% of those tested in non–health care facilities were young men who have sex with men, who are a high-risk group for HIV infection but who only received 28% of tests. Since 92% of new infections in 2009 were acquired from HIV-positive people who were not in medical care, “improving the number of youths who are tested is of high importance,” according to Renee Stein, PhD, and her coinvestigators, all of the division of HIV/AIDS prevention and the National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention at the CDC.

“A health care provider’s testing recommendation is the most important predictor of testing among adolescents at risk for HIV infection,” the researchers said. “Increasing the number of HIV tests among youths at risk for HIV and increasing regular retesting among these youths is essential for reducing HIV infection in this vulnerable population.”

No conflicts of interest were reported by the authors.

Read more in MMWR (2017 Jun 23. doi: 10.15585/mmwr.mm6624a2).

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Maintenance of Certification: How Physician Self-regulation Can Improve Quality of Care

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QI enthusiast to QI leader: John Bulger, DO

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Start with localized goals, move toward the Triple Aim

 

Editor’s Note: This SHM series highlights the professional pathways of quality improvement leaders. This month features the story of John Bulger, DO, chief medical officer for Geisinger Health Plan.

As chief medical officer for Geisinger Health Plan, John Bulger, DO, MBA, is intimately acquainted with the daily challenges that intersect with the delivery of safe, quality-driven care in the hospital system.

He’s also very familiar with the intricacies of carving out a professional road map. When Dr. Bulger began practicing as an internist at Geisinger Health System in the late 1990s, there wasn’t a formal hospitalist designation. He created one and became director of the hospital medicine program. Years later, when the opportunity arose to become chief quality officer, Dr. Bulger was a natural fit for the position, having led many improvement-centered committees and projects while running the hospital medicine group.

Dr. John Bulger
But the quality know-how did not come without additional training. “While competencies like problem solving and being a good listener and team player are part of the job of being a hospitalist, they don’t make you an expert in QI,” Dr. Bulger said. “There are learned skills that you need to spend time developing.”

Early in his QI immersion, Dr. Bulger sought training where available from sources such as ACP and SHM, while familiarizing himself with methodologies such as PDSA and Lean. There are far more QI training opportunities available to hospitalists today than when Dr. Bulger began his journey, but the fundamentals of success come back to finding the right mentors, team building, and implementing projects built around SMART goals.

Getting started, Dr. Bulger suggests to “pick something within your scope, like medical reconciliation for every patient, or ensuring that every patient who leaves the hospital gets an appointment with their primary physician within 7 days. Early on, we were working on issues like pneumonia core measures and providing discharge instructions.”

He cautions those starting out in QI against viewing unintended outcomes or project setbacks as failure. “If your goal is to take a (scenario) from bad to perfect, you’ll end up getting discouraged. Any effort toward making things better is helpful. If it doesn’t work you try something else.”

While Dr. Bulger is fully supportive of the impact that quality improvement projects make at the institutional level, he encourages clinicians and researchers to always keep the Institute for Healthcare Improvement Triple Aim in sight.

“We need better measures and more discussion about what is best for patients,” Dr. Bulger said. “The things we talk about in (health care) – readmission rates, glycemic control – have a minimal impact on people’s health, but the social determinants of health – the patient’s housing and economic situation – play a bigger role than anything else. As we move from provider- to patient-centric communities by fixing the Triple Aim, the experience will be better for both providers and patients.”
 

Claudia Stahl is content manager for the Society of Hospital Medicine.

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Start with localized goals, move toward the Triple Aim
Start with localized goals, move toward the Triple Aim

 

Editor’s Note: This SHM series highlights the professional pathways of quality improvement leaders. This month features the story of John Bulger, DO, chief medical officer for Geisinger Health Plan.

As chief medical officer for Geisinger Health Plan, John Bulger, DO, MBA, is intimately acquainted with the daily challenges that intersect with the delivery of safe, quality-driven care in the hospital system.

He’s also very familiar with the intricacies of carving out a professional road map. When Dr. Bulger began practicing as an internist at Geisinger Health System in the late 1990s, there wasn’t a formal hospitalist designation. He created one and became director of the hospital medicine program. Years later, when the opportunity arose to become chief quality officer, Dr. Bulger was a natural fit for the position, having led many improvement-centered committees and projects while running the hospital medicine group.

Dr. John Bulger
But the quality know-how did not come without additional training. “While competencies like problem solving and being a good listener and team player are part of the job of being a hospitalist, they don’t make you an expert in QI,” Dr. Bulger said. “There are learned skills that you need to spend time developing.”

Early in his QI immersion, Dr. Bulger sought training where available from sources such as ACP and SHM, while familiarizing himself with methodologies such as PDSA and Lean. There are far more QI training opportunities available to hospitalists today than when Dr. Bulger began his journey, but the fundamentals of success come back to finding the right mentors, team building, and implementing projects built around SMART goals.

Getting started, Dr. Bulger suggests to “pick something within your scope, like medical reconciliation for every patient, or ensuring that every patient who leaves the hospital gets an appointment with their primary physician within 7 days. Early on, we were working on issues like pneumonia core measures and providing discharge instructions.”

He cautions those starting out in QI against viewing unintended outcomes or project setbacks as failure. “If your goal is to take a (scenario) from bad to perfect, you’ll end up getting discouraged. Any effort toward making things better is helpful. If it doesn’t work you try something else.”

While Dr. Bulger is fully supportive of the impact that quality improvement projects make at the institutional level, he encourages clinicians and researchers to always keep the Institute for Healthcare Improvement Triple Aim in sight.

“We need better measures and more discussion about what is best for patients,” Dr. Bulger said. “The things we talk about in (health care) – readmission rates, glycemic control – have a minimal impact on people’s health, but the social determinants of health – the patient’s housing and economic situation – play a bigger role than anything else. As we move from provider- to patient-centric communities by fixing the Triple Aim, the experience will be better for both providers and patients.”
 

Claudia Stahl is content manager for the Society of Hospital Medicine.

 

Editor’s Note: This SHM series highlights the professional pathways of quality improvement leaders. This month features the story of John Bulger, DO, chief medical officer for Geisinger Health Plan.

As chief medical officer for Geisinger Health Plan, John Bulger, DO, MBA, is intimately acquainted with the daily challenges that intersect with the delivery of safe, quality-driven care in the hospital system.

He’s also very familiar with the intricacies of carving out a professional road map. When Dr. Bulger began practicing as an internist at Geisinger Health System in the late 1990s, there wasn’t a formal hospitalist designation. He created one and became director of the hospital medicine program. Years later, when the opportunity arose to become chief quality officer, Dr. Bulger was a natural fit for the position, having led many improvement-centered committees and projects while running the hospital medicine group.

Dr. John Bulger
But the quality know-how did not come without additional training. “While competencies like problem solving and being a good listener and team player are part of the job of being a hospitalist, they don’t make you an expert in QI,” Dr. Bulger said. “There are learned skills that you need to spend time developing.”

Early in his QI immersion, Dr. Bulger sought training where available from sources such as ACP and SHM, while familiarizing himself with methodologies such as PDSA and Lean. There are far more QI training opportunities available to hospitalists today than when Dr. Bulger began his journey, but the fundamentals of success come back to finding the right mentors, team building, and implementing projects built around SMART goals.

Getting started, Dr. Bulger suggests to “pick something within your scope, like medical reconciliation for every patient, or ensuring that every patient who leaves the hospital gets an appointment with their primary physician within 7 days. Early on, we were working on issues like pneumonia core measures and providing discharge instructions.”

He cautions those starting out in QI against viewing unintended outcomes or project setbacks as failure. “If your goal is to take a (scenario) from bad to perfect, you’ll end up getting discouraged. Any effort toward making things better is helpful. If it doesn’t work you try something else.”

While Dr. Bulger is fully supportive of the impact that quality improvement projects make at the institutional level, he encourages clinicians and researchers to always keep the Institute for Healthcare Improvement Triple Aim in sight.

“We need better measures and more discussion about what is best for patients,” Dr. Bulger said. “The things we talk about in (health care) – readmission rates, glycemic control – have a minimal impact on people’s health, but the social determinants of health – the patient’s housing and economic situation – play a bigger role than anything else. As we move from provider- to patient-centric communities by fixing the Triple Aim, the experience will be better for both providers and patients.”
 

Claudia Stahl is content manager for the Society of Hospital Medicine.

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Knotless Arthroscopic Reduction and Internal Fixation of a Displaced Anterior Cruciate Ligament Tibial Eminence Avulsion Fracture

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Knotless Arthroscopic Reduction and Internal Fixation of a Displaced Anterior Cruciate Ligament Tibial Eminence Avulsion Fracture

Take-Home Points

  • Technique provides optimal fixation while simultaneously protecting open growth plates.
  • Self tensioning feature insures both optimal ACL tension and fracture reduction.
  • No need for future hardware removal.
  • 10Cross suture configuration optimizes strength of fixation for highly consistent results.
  • Use fluoroscopy to avoid violation of tibial physis.

Generally occurring in the 8- to 14-year-old population, tibial eminence avulsion (TEA) fractures are a common variant of anterior cruciate ligament (ACL) ruptures and represent 2% to 5% of all knee injuries in skeletally immature individuals.1,2 Compared with adults, children likely experience this anomaly more often because of the weakness of their incompletely ossified tibial plateau relative to the strength of their native ACL.3

The open repair techniques that have been described have multiple disadvantages, including open incisions, difficult visualization of the fracture owing to the location of the fat pad, and increased risk for arthrofibrosis. Arthroscopic fixation is considered the treatment of choice for TEA fractures because it allows for direct visualization of injury, accurate reduction of fracture fragments, removal of loose fragments, and easy treatment of associated soft-tissue injuries.4-6Several fixation techniques for ACL-TEA fractures were recently described: arthroscopic reduction and internal fixation (ARIF) with Kirschner wires,7 cannulated screws,4 the Meniscus Arrow device (Bionx Implants),8 pull-out sutures,9,10 bioabsorbable nails,11 Herbert screws,12 TightRope fixation (Arthrex),13 and various other rotator cuff and meniscal repair systems.14,15 These approaches tend to have good outcomes for TEA fractures, but there are risks associated with ACL tensioning and potential tibial growth plate violation or hardware problems. Likewise, there are no studies with large numbers of patients treated with these new techniques, so the optimal method of reduction and fixation is still unknown.

In this article, we describe a new ARIF technique that involves 2 absorbable anchors with adjustable suture-tensioning technology. This technique optimizes reduction and helps surgeons avoid proximal tibial physeal damage, procedure-related morbidity, and additional surgery.

Case Report

History

The patient, an 8-year-old boy, sustained a noncontact twisting injury of the left knee during a cutting maneuver in a flag football game. He experienced immediate pain and subsequent swelling. Clinical examination revealed a moderate effusion with motion limitations secondary to swelling and irritability. The patient’s Lachman test result was 2+. Pivot shift testing was not possible because of guarding. The knee was stable to varus and valgus stress at 0° and 30° of flexion. Limited knee flexion prohibited placement of the patient in the position needed for anterior and posterior drawer testing. His patella was stable on lateral stress testing at 20° of flexion with no apprehension. Neurovascular status was intact throughout the lower extremity.

Anteroposterior and lateral radiographs showed a minimally displaced Meyers-McKeever type II TEA fracture (Figures 1A, 1B).

Figure 1.
Distal femoral and proximal tibial growth plates were wide open. Magnetic resonance imaging confirmed the displaced type II TEA fracture and showed good signal quality in the attached ACL (Figures 2A, 2B).
Figure 2.
The remaining ligamentous structures appeared without injury or signal change. No tear signal was seen in the imaging sequences of the medial and lateral meniscus.

After discussing potential treatment options with the parents, Dr. Smith proceeded with arthroscopic surgery for definitive reduction and internal fixation of the patient’s left knee displaced ACL-TEA fracture. The new adjustable suture-tensioning fixation technique was used. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Examination Under Anesthesia

Examination with the patient under general anesthesia revealed 3+ Lachman, 2+ pivot shift with foot in internal and external rotation, and 1+ anterior drawer with foot in neutral and internal rotation. The knee was stable to varus and valgus stress testing.

Surgical Technique

Proper patient positioning and padding of bony prominences were ensured, and the limb was sterilely prepared and draped.

Figure 3.
A standard lateral parapatellar portal was established for arthroscope placement; a medial parapatellar working portal was established as well. Thorough joint inspection revealed normal articular surfaces of patella, femur, and tibial plateau. Similarly, both menisci were intact without evidence of injury.
Figure 4.
With use of the probe, the ACL-TEA fracture could be elevated up to 2 cm toward the top of the notch (Figure 3). Further inspection of the ACL fibers revealed minimal hemorrhaging and no frank tearing (Figure 4).

Given the young age of the patient, it was imperative to avoid the open proximal tibial growth plate. The surgical plan for stabilization involved use of two 3.0-mm BioComposite Knotless SutureTak anchors (Arthrex). This anchor configuration is based on a No. 2 FiberWire suture shuttled through itself to create a locking splice mechanism that allows for adjustable tensioning. The anchors were placed on each side of the tibial bony avulsion site with two No. 2 FiberWire sutures and were then crossed about the avulsion fracture fragment in an “x-type” configuration to secure the ACL back down to the bony bed.

First, a curette was used to débride fibrous tissue on the underside of the fracture fragment and on the fracture bed. Minimal amounts of cancellous bone were débrided from the tibial fracture bed to optimize fracture reduction by slightly recessing the fracture fragment to ensure optimal ACL tensioning (Figure 5).

Figure 5.
Next, an 18-gauge needle was used to establish an accessory superior medial percutaneous portal to ensure a satisfactory drilling trajectory just medial to the fracture site. Under fluoroscopic guidance, a drill guide was placed, and a 2.4-mm bit was used to drill to a depth of 16 mm to accommodate the 12.7-mm anchor. Avoidance of the proximal tibial physis was confirmed with fluoroscopy (Figure 6).
Figure 6.
One of the SutureTak anchors was secured in this drill hole along the anteromedial avulsion fracture site. From the anteromedial portal, a curved needle tip suture passer was placed medially through the ACL fibers and bone, with the wire retrieved out of the superior medial accessory portal. Then, the drill guide was introduced through the lateral portal and positioned just lateral to the tibial avulsion site, a hole was drilled 16 mm deep, and fluoroscopy was used to confirm the physis was not violated. The second SutureTak anchor was placed in this anterolateral location. From the anterolateral portal, the curved needle tip suture passer was placed laterally through the ACL fibers and avulsion fragment, and the wire was passed and retrieved out the anteromedial portal and shuttled back to the anterolateral portal.

Next, from the accessory superior medial portal, the end of the wire that had been passed through the medial aspect of the bony avulsion was retrieved through the lateral portal. This wire was used to shuttle the repair suture from the laterally positioned SutureTak anchor over and through the medial aspect of the bony fragment out of the accessory superior medial (Figure 7).
Figure 7.
This suture was passed through the shuttling loop of the medially positioned SutureTak anchor to create the splice in the anchor for the adjustable fixation. This process was repeated through the lateral aspect of the bony fragment—the medial SutureTak repair suture was passed over the bone here. Thus, the lateral suture was over and through the bony fragment secured to the medial SutureTak anchor, and the medial suture was crossed over and through bone to the lateral SutureTak anchor. With the knee held in full extension, the bony avulsion fracture was easily reduced by alternating tension on the SutureTak limbs, which enabled controlled reduction of the TEA fracture (Figures 8A, 8B).
Figure 8.
An arthroscopic knot pusher was used for final tightening of the SutureTak fixation. An arthroscopic probe was used to confirm anatomical reduction of the fracture and restoration of ACL fiber tension (Figure 9).
Figure 9.
The knee was ranged from 0° to 120° of flexion with visual affirmation of the construct and maintenance of the reduction. Fluoroscopy confirmed anatomical reduction of the TEA fracture. The patient was immobilized in a long leg brace locked in 30° of flexion.

 

 

Follow-Up

Two weeks after surgery, the patient returned to clinic for suture removal. Four weeks after surgery, radiographs confirmed anatomical reduction of the TEA fracture, and outpatient physical therapy (range-of-motion exercises as tolerated) and isometric quadriceps strengthening were instituted. Twelve weeks after surgery, examination revealed full knee motion, negative Lachman and pivot shift test results, and residual quadriceps muscle atrophy, and radiographs confirmed complete fracture healing with maintenance of a normal proximal tibial growth plate (Figures 10A, 10B).

Figure 10.
Sixteen weeks after surgery, ligamentous examination findings were normal, and quadriceps muscle mass was good. In addition, on KT-1000 testing, the surgically repaired knee had only 1 more millimeter of laxity at the 30-pound pull, and equal displacement on the manual maximum test. The patient was allowed to return to full activities as tolerated.

Discussion

The highlight of this case is the simplicity of an excellent reduction of a displaced ACL-TEA fracture. Minimally invasive absorbable implants did not violate the proximal tibial physis, and the unique adjustable suture-tensioning technology allowed the degree of reduction and ACL tension to be “dialed in.” SutureTak implants have strong No. 2 FiberWire suture for excellent stability with an overall small suture load, and their small size avoids the risk of violating the proximal tibial physis and avoids potential growth disturbances.

Despite the obvious risks it poses to the open proximal tibial physis, surgical reduction of Meyers-McKeever type II and type III fractures is the norm for restoring ACL stability. Screws and suture fixation are the most common and reliable methods of TEA fracture reduction.16,17 In recent systematic reviews, however, Osti and colleagues17 and Gans and colleagues18 noted there is not enough evidence to warrant a “gold standard” in pediatric tibial avulsion cases.

Other fixation methods for TEA fractures must be investigated. Anderson and colleagues19 described the biomechanics of 4 different physeal-sparing avulsion fracture reduction techniques: an ultra-high-molecular-weight polyethylene (UHMWPE) suture-suture button, a suture anchor, a polydioxanone suture-suture button, and screw fixation. Using techniques described by Kocher and colleagues,4 Berg,20 Mah and colleagues,21 Vega and colleagues,22 and Lu and colleagues,23 Anderson and colleagues19 reduced TEA fractures in skeletally immature porcine knees. Compared with suture anchors, UHMWPE suture-suture buttons provided biomechanically superior cyclic and load-to-failure results as well as more consistent fixation.

Screw fixation has shown good results but has disadvantages. Incorrect positioning of a screw can lead to impingement and articular cartilage damage, and screw removal may be needed if discomfort at the fixation site persists.24,25 Likewise, screws generally are an option only for large fracture fragments, as there is an inherent risk of fracturing small TEA fractures, which can be common in skeletally immature patients.

Brunner and colleagues26 recently found that TEA fracture repair with absorbable sutures and distal bone bridge fixation yielded 3-month radiographic and clinical healing rates similar to those obtained with nonabsorbable sutures tied around a screw. However, other authors have reported growth disturbances with use of a similar technique, owing to a disturbance of the open proximal tibial growth plate.9 In that regard, a major advantage of this new knotless suturing technique is that distal fixation is not necessary.

The minimally invasive TEA fraction reduction technique described in this article has 6 advantages: It provides excellent fixation while avoiding proximal tibial growth plate injury; the degree of tensioning is easily controlled during reduction; it uses strong suture instead of metal screws or pins; the reduction construct is low-profile; distal fixation is unnecessary; and implant removal is unnecessary, thus limiting subsequent surgical intervention. With respect to long-term outcomes, however, it is not known how this procedure will compare with other commonly used ARIF methods in physeal-sparing techniques for TEA fracture fixation.

This case report highlights a novel pediatric displaced ACL-TEA fracture reduction technique that allows for adjustable reduction and resultant ACL tensioning with excellent strong suture fixation without violating the proximal tibial physis, which could make it invaluable in the surgical treatment of this injury in skeletally immature patients.

Am J Orthop. 2017;46(4):203-208. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Eiskjaer S, Larsen ST, Schmidt MB. The significance of hemarthrosis of the knee in children. Arch Orthop Trauma Surg. 1988;107(2):96-98.

2. Luhmann SJ. Acute traumatic knee effusions in children and adolescents. J Pediatr Orthop. 2003;23(2):199-202.

3. Woo SL, Hollis JM, Adams DJ, Lyon RM, Takai S. Tensile properties of the human femur-anterior cruciate ligament-tibia complex. The effects of specimen age and orientation. Am J Sports Med. 1991;19(3):217-225.

4. Kocher MS, Foreman ES, Micheli LJ. Laxity and functional outcome after arthroscopic reduction and internal fixation of displaced tibial spine fractures in children. Arthroscopy. 2003;19(10):1085-1090.

5. Lubowitz JH, Elson WS, Guttmann D. Part II: arthroscopic treatment of tibial plateau fractures: intercondylar eminence avulsion fractures. Arthroscopy. 2005;21(1):86-92.

6. Vargas B, Lutz N, Dutoit M, Zambelli PY. Nonunion after fracture of the anterior tibial spine: case report and review of the literature. J Pediatr Orthop B. 2009;18(2):90-92.

7. Sommerfeldt DW. Arthroscopically assisted internal fixation of avulsion fractures of the anterior cruciate ligament during childhood and adolescence [in German]. Oper Orthop Traumatol. 2008;20(4-5):310-320.

8. Wouters DB, de Graaf JS, Hemmer PH, Burgerhof JG, Kramer WL. The arthroscopic treatment of displaced tibial spine fractures in children and adolescents using Meniscus Arrows®. Knee Surg Sports Traumatol Arthrosc. 2011;19(5):736-739.

9. Ahn JH, Yoo JC. Clinical outcome of arthroscopic reduction and suture for displaced acute and chronic tibial spine fractures. Knee Surg Sports Traumatol Arthrosc. 2005;13(2):116-121.

10. Huang TW, Hsu KY, Cheng CY, et al. Arthroscopic suture fixation of tibial eminence avulsion fractures. Arthroscopy. 2008;24(11):1232-1238.

11. Liljeros K, Werner S, Janarv PM. Arthroscopic fixation of anterior tibial spine fractures with bioabsorbable nails in skeletally immature patients. Am J Sports Med. 2009;37(5):923-928.

12. Wiegand N, Naumov I, Vamhidy L, Not LG. Arthroscopic treatment of tibial spine fracture in children with a cannulated Herbert screw. Knee. 2014;21(2):481-485.

13. Faivre B, Benea H, Klouche S, Lespagnol F, Bauer T, Hardy P. An original arthroscopic fixation of adult’s tibial eminence fractures using the Tightrope® device: a report of 8 cases and review of literature. Knee. 2014;21(4):833-839.

14. Kluemper CT, Snyder GM, Coats AC, Johnson DL, Mair SD. Arthroscopic suture fixation of tibial eminence fractures. Orthopedics. 2013;36(11):e1401-e1406.

15. Ochiai S, Hagino T, Watanabe Y, Senga S, Haro H. One strategy for arthroscopic suture fixation of tibial intercondylar eminence fractures using the Meniscal Viper Repair System. Sports Med Arthrosc Rehabil Ther Technol. 2011;3:17.

16. Bogunovic L, Tarabichi M, Harris D, Wright R. Treatment of tibial eminence fractures: a systematic review. J Knee Surg. 2015;28(3):255-262.

17. Osti L, Buda M, Soldati F, Del Buono A, Osti R, Maffulli N. Arthroscopic treatment of tibial eminence fracture: a systematic review of different fixation methods. Br Med Bull. 2016;118(1):73-90.

18. Gans I, Baldwin KD, Ganley TJ. Treatment and management outcomes of tibial eminence fractures in pediatric patients: a systematic review. Am J Sports Med. 2014;42(7):1743-1750.

19. Anderson CN, Nyman JS, McCullough KA, et al. Biomechanical evaluation of physeal-sparing fixation methods in tibial eminence fractures. Am J Sports Med. 2013;41(7):1586-1594.

20. Berg EE. Pediatric tibial eminence fractures: arthroscopic cannulated screw fixation. Arthroscopy. 1995;11(3):328-331.

21. Mah JY, Otsuka NY, McLean J. An arthroscopic technique for the reduction and fixation of tibial-eminence fractures. J Pediatr Orthop. 1996;16(1):119-121.

22. Vega JR, Irribarra LA, Baar AK, Iniguez M, Salgado M, Gana N. Arthroscopic fixation of displaced tibial eminence fractures: a new growth plate-sparing method. Arthroscopy. 2008;24(11):1239-1243.

23. Lu XW, Hu XP, Jin C, Zhu T, Ding Y, Dai LY. Reduction and fixation of the avulsion fracture of the tibial eminence using mini-open technique. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1476-1480.

24. Bonin N, Jeunet L, Obert L, Dejour D. Adult tibial eminence fracture fixation: arthroscopic procedure using K-wire folded fixation. Knee Surg Sports Traumatol Arthrosc. 2007;15(7):857-862.

25. Senekovic V, Veselko M. Anterograde arthroscopic fixation of avulsion fractures of the tibial eminence with a cannulated screw: five-year results. Arthroscopy. 2003;19(1):54-61.

26. Brunner S, Vavken P, Kilger R, et al. Absorbable and non-absorbable suture fixation results in similar outcomes for tibial eminence fractures in children and adolescents. Knee Surg Sports Traumatol Arthrosc. 2016;24(3):723-729.

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Take-Home Points

  • Technique provides optimal fixation while simultaneously protecting open growth plates.
  • Self tensioning feature insures both optimal ACL tension and fracture reduction.
  • No need for future hardware removal.
  • 10Cross suture configuration optimizes strength of fixation for highly consistent results.
  • Use fluoroscopy to avoid violation of tibial physis.

Generally occurring in the 8- to 14-year-old population, tibial eminence avulsion (TEA) fractures are a common variant of anterior cruciate ligament (ACL) ruptures and represent 2% to 5% of all knee injuries in skeletally immature individuals.1,2 Compared with adults, children likely experience this anomaly more often because of the weakness of their incompletely ossified tibial plateau relative to the strength of their native ACL.3

The open repair techniques that have been described have multiple disadvantages, including open incisions, difficult visualization of the fracture owing to the location of the fat pad, and increased risk for arthrofibrosis. Arthroscopic fixation is considered the treatment of choice for TEA fractures because it allows for direct visualization of injury, accurate reduction of fracture fragments, removal of loose fragments, and easy treatment of associated soft-tissue injuries.4-6Several fixation techniques for ACL-TEA fractures were recently described: arthroscopic reduction and internal fixation (ARIF) with Kirschner wires,7 cannulated screws,4 the Meniscus Arrow device (Bionx Implants),8 pull-out sutures,9,10 bioabsorbable nails,11 Herbert screws,12 TightRope fixation (Arthrex),13 and various other rotator cuff and meniscal repair systems.14,15 These approaches tend to have good outcomes for TEA fractures, but there are risks associated with ACL tensioning and potential tibial growth plate violation or hardware problems. Likewise, there are no studies with large numbers of patients treated with these new techniques, so the optimal method of reduction and fixation is still unknown.

In this article, we describe a new ARIF technique that involves 2 absorbable anchors with adjustable suture-tensioning technology. This technique optimizes reduction and helps surgeons avoid proximal tibial physeal damage, procedure-related morbidity, and additional surgery.

Case Report

History

The patient, an 8-year-old boy, sustained a noncontact twisting injury of the left knee during a cutting maneuver in a flag football game. He experienced immediate pain and subsequent swelling. Clinical examination revealed a moderate effusion with motion limitations secondary to swelling and irritability. The patient’s Lachman test result was 2+. Pivot shift testing was not possible because of guarding. The knee was stable to varus and valgus stress at 0° and 30° of flexion. Limited knee flexion prohibited placement of the patient in the position needed for anterior and posterior drawer testing. His patella was stable on lateral stress testing at 20° of flexion with no apprehension. Neurovascular status was intact throughout the lower extremity.

Anteroposterior and lateral radiographs showed a minimally displaced Meyers-McKeever type II TEA fracture (Figures 1A, 1B).

Figure 1.
Distal femoral and proximal tibial growth plates were wide open. Magnetic resonance imaging confirmed the displaced type II TEA fracture and showed good signal quality in the attached ACL (Figures 2A, 2B).
Figure 2.
The remaining ligamentous structures appeared without injury or signal change. No tear signal was seen in the imaging sequences of the medial and lateral meniscus.

After discussing potential treatment options with the parents, Dr. Smith proceeded with arthroscopic surgery for definitive reduction and internal fixation of the patient’s left knee displaced ACL-TEA fracture. The new adjustable suture-tensioning fixation technique was used. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Examination Under Anesthesia

Examination with the patient under general anesthesia revealed 3+ Lachman, 2+ pivot shift with foot in internal and external rotation, and 1+ anterior drawer with foot in neutral and internal rotation. The knee was stable to varus and valgus stress testing.

Surgical Technique

Proper patient positioning and padding of bony prominences were ensured, and the limb was sterilely prepared and draped.

Figure 3.
A standard lateral parapatellar portal was established for arthroscope placement; a medial parapatellar working portal was established as well. Thorough joint inspection revealed normal articular surfaces of patella, femur, and tibial plateau. Similarly, both menisci were intact without evidence of injury.
Figure 4.
With use of the probe, the ACL-TEA fracture could be elevated up to 2 cm toward the top of the notch (Figure 3). Further inspection of the ACL fibers revealed minimal hemorrhaging and no frank tearing (Figure 4).

Given the young age of the patient, it was imperative to avoid the open proximal tibial growth plate. The surgical plan for stabilization involved use of two 3.0-mm BioComposite Knotless SutureTak anchors (Arthrex). This anchor configuration is based on a No. 2 FiberWire suture shuttled through itself to create a locking splice mechanism that allows for adjustable tensioning. The anchors were placed on each side of the tibial bony avulsion site with two No. 2 FiberWire sutures and were then crossed about the avulsion fracture fragment in an “x-type” configuration to secure the ACL back down to the bony bed.

First, a curette was used to débride fibrous tissue on the underside of the fracture fragment and on the fracture bed. Minimal amounts of cancellous bone were débrided from the tibial fracture bed to optimize fracture reduction by slightly recessing the fracture fragment to ensure optimal ACL tensioning (Figure 5).

Figure 5.
Next, an 18-gauge needle was used to establish an accessory superior medial percutaneous portal to ensure a satisfactory drilling trajectory just medial to the fracture site. Under fluoroscopic guidance, a drill guide was placed, and a 2.4-mm bit was used to drill to a depth of 16 mm to accommodate the 12.7-mm anchor. Avoidance of the proximal tibial physis was confirmed with fluoroscopy (Figure 6).
Figure 6.
One of the SutureTak anchors was secured in this drill hole along the anteromedial avulsion fracture site. From the anteromedial portal, a curved needle tip suture passer was placed medially through the ACL fibers and bone, with the wire retrieved out of the superior medial accessory portal. Then, the drill guide was introduced through the lateral portal and positioned just lateral to the tibial avulsion site, a hole was drilled 16 mm deep, and fluoroscopy was used to confirm the physis was not violated. The second SutureTak anchor was placed in this anterolateral location. From the anterolateral portal, the curved needle tip suture passer was placed laterally through the ACL fibers and avulsion fragment, and the wire was passed and retrieved out the anteromedial portal and shuttled back to the anterolateral portal.

Next, from the accessory superior medial portal, the end of the wire that had been passed through the medial aspect of the bony avulsion was retrieved through the lateral portal. This wire was used to shuttle the repair suture from the laterally positioned SutureTak anchor over and through the medial aspect of the bony fragment out of the accessory superior medial (Figure 7).
Figure 7.
This suture was passed through the shuttling loop of the medially positioned SutureTak anchor to create the splice in the anchor for the adjustable fixation. This process was repeated through the lateral aspect of the bony fragment—the medial SutureTak repair suture was passed over the bone here. Thus, the lateral suture was over and through the bony fragment secured to the medial SutureTak anchor, and the medial suture was crossed over and through bone to the lateral SutureTak anchor. With the knee held in full extension, the bony avulsion fracture was easily reduced by alternating tension on the SutureTak limbs, which enabled controlled reduction of the TEA fracture (Figures 8A, 8B).
Figure 8.
An arthroscopic knot pusher was used for final tightening of the SutureTak fixation. An arthroscopic probe was used to confirm anatomical reduction of the fracture and restoration of ACL fiber tension (Figure 9).
Figure 9.
The knee was ranged from 0° to 120° of flexion with visual affirmation of the construct and maintenance of the reduction. Fluoroscopy confirmed anatomical reduction of the TEA fracture. The patient was immobilized in a long leg brace locked in 30° of flexion.

 

 

Follow-Up

Two weeks after surgery, the patient returned to clinic for suture removal. Four weeks after surgery, radiographs confirmed anatomical reduction of the TEA fracture, and outpatient physical therapy (range-of-motion exercises as tolerated) and isometric quadriceps strengthening were instituted. Twelve weeks after surgery, examination revealed full knee motion, negative Lachman and pivot shift test results, and residual quadriceps muscle atrophy, and radiographs confirmed complete fracture healing with maintenance of a normal proximal tibial growth plate (Figures 10A, 10B).

Figure 10.
Sixteen weeks after surgery, ligamentous examination findings were normal, and quadriceps muscle mass was good. In addition, on KT-1000 testing, the surgically repaired knee had only 1 more millimeter of laxity at the 30-pound pull, and equal displacement on the manual maximum test. The patient was allowed to return to full activities as tolerated.

Discussion

The highlight of this case is the simplicity of an excellent reduction of a displaced ACL-TEA fracture. Minimally invasive absorbable implants did not violate the proximal tibial physis, and the unique adjustable suture-tensioning technology allowed the degree of reduction and ACL tension to be “dialed in.” SutureTak implants have strong No. 2 FiberWire suture for excellent stability with an overall small suture load, and their small size avoids the risk of violating the proximal tibial physis and avoids potential growth disturbances.

Despite the obvious risks it poses to the open proximal tibial physis, surgical reduction of Meyers-McKeever type II and type III fractures is the norm for restoring ACL stability. Screws and suture fixation are the most common and reliable methods of TEA fracture reduction.16,17 In recent systematic reviews, however, Osti and colleagues17 and Gans and colleagues18 noted there is not enough evidence to warrant a “gold standard” in pediatric tibial avulsion cases.

Other fixation methods for TEA fractures must be investigated. Anderson and colleagues19 described the biomechanics of 4 different physeal-sparing avulsion fracture reduction techniques: an ultra-high-molecular-weight polyethylene (UHMWPE) suture-suture button, a suture anchor, a polydioxanone suture-suture button, and screw fixation. Using techniques described by Kocher and colleagues,4 Berg,20 Mah and colleagues,21 Vega and colleagues,22 and Lu and colleagues,23 Anderson and colleagues19 reduced TEA fractures in skeletally immature porcine knees. Compared with suture anchors, UHMWPE suture-suture buttons provided biomechanically superior cyclic and load-to-failure results as well as more consistent fixation.

Screw fixation has shown good results but has disadvantages. Incorrect positioning of a screw can lead to impingement and articular cartilage damage, and screw removal may be needed if discomfort at the fixation site persists.24,25 Likewise, screws generally are an option only for large fracture fragments, as there is an inherent risk of fracturing small TEA fractures, which can be common in skeletally immature patients.

Brunner and colleagues26 recently found that TEA fracture repair with absorbable sutures and distal bone bridge fixation yielded 3-month radiographic and clinical healing rates similar to those obtained with nonabsorbable sutures tied around a screw. However, other authors have reported growth disturbances with use of a similar technique, owing to a disturbance of the open proximal tibial growth plate.9 In that regard, a major advantage of this new knotless suturing technique is that distal fixation is not necessary.

The minimally invasive TEA fraction reduction technique described in this article has 6 advantages: It provides excellent fixation while avoiding proximal tibial growth plate injury; the degree of tensioning is easily controlled during reduction; it uses strong suture instead of metal screws or pins; the reduction construct is low-profile; distal fixation is unnecessary; and implant removal is unnecessary, thus limiting subsequent surgical intervention. With respect to long-term outcomes, however, it is not known how this procedure will compare with other commonly used ARIF methods in physeal-sparing techniques for TEA fracture fixation.

This case report highlights a novel pediatric displaced ACL-TEA fracture reduction technique that allows for adjustable reduction and resultant ACL tensioning with excellent strong suture fixation without violating the proximal tibial physis, which could make it invaluable in the surgical treatment of this injury in skeletally immature patients.

Am J Orthop. 2017;46(4):203-208. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Technique provides optimal fixation while simultaneously protecting open growth plates.
  • Self tensioning feature insures both optimal ACL tension and fracture reduction.
  • No need for future hardware removal.
  • 10Cross suture configuration optimizes strength of fixation for highly consistent results.
  • Use fluoroscopy to avoid violation of tibial physis.

Generally occurring in the 8- to 14-year-old population, tibial eminence avulsion (TEA) fractures are a common variant of anterior cruciate ligament (ACL) ruptures and represent 2% to 5% of all knee injuries in skeletally immature individuals.1,2 Compared with adults, children likely experience this anomaly more often because of the weakness of their incompletely ossified tibial plateau relative to the strength of their native ACL.3

The open repair techniques that have been described have multiple disadvantages, including open incisions, difficult visualization of the fracture owing to the location of the fat pad, and increased risk for arthrofibrosis. Arthroscopic fixation is considered the treatment of choice for TEA fractures because it allows for direct visualization of injury, accurate reduction of fracture fragments, removal of loose fragments, and easy treatment of associated soft-tissue injuries.4-6Several fixation techniques for ACL-TEA fractures were recently described: arthroscopic reduction and internal fixation (ARIF) with Kirschner wires,7 cannulated screws,4 the Meniscus Arrow device (Bionx Implants),8 pull-out sutures,9,10 bioabsorbable nails,11 Herbert screws,12 TightRope fixation (Arthrex),13 and various other rotator cuff and meniscal repair systems.14,15 These approaches tend to have good outcomes for TEA fractures, but there are risks associated with ACL tensioning and potential tibial growth plate violation or hardware problems. Likewise, there are no studies with large numbers of patients treated with these new techniques, so the optimal method of reduction and fixation is still unknown.

In this article, we describe a new ARIF technique that involves 2 absorbable anchors with adjustable suture-tensioning technology. This technique optimizes reduction and helps surgeons avoid proximal tibial physeal damage, procedure-related morbidity, and additional surgery.

Case Report

History

The patient, an 8-year-old boy, sustained a noncontact twisting injury of the left knee during a cutting maneuver in a flag football game. He experienced immediate pain and subsequent swelling. Clinical examination revealed a moderate effusion with motion limitations secondary to swelling and irritability. The patient’s Lachman test result was 2+. Pivot shift testing was not possible because of guarding. The knee was stable to varus and valgus stress at 0° and 30° of flexion. Limited knee flexion prohibited placement of the patient in the position needed for anterior and posterior drawer testing. His patella was stable on lateral stress testing at 20° of flexion with no apprehension. Neurovascular status was intact throughout the lower extremity.

Anteroposterior and lateral radiographs showed a minimally displaced Meyers-McKeever type II TEA fracture (Figures 1A, 1B).

Figure 1.
Distal femoral and proximal tibial growth plates were wide open. Magnetic resonance imaging confirmed the displaced type II TEA fracture and showed good signal quality in the attached ACL (Figures 2A, 2B).
Figure 2.
The remaining ligamentous structures appeared without injury or signal change. No tear signal was seen in the imaging sequences of the medial and lateral meniscus.

After discussing potential treatment options with the parents, Dr. Smith proceeded with arthroscopic surgery for definitive reduction and internal fixation of the patient’s left knee displaced ACL-TEA fracture. The new adjustable suture-tensioning fixation technique was used. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Examination Under Anesthesia

Examination with the patient under general anesthesia revealed 3+ Lachman, 2+ pivot shift with foot in internal and external rotation, and 1+ anterior drawer with foot in neutral and internal rotation. The knee was stable to varus and valgus stress testing.

Surgical Technique

Proper patient positioning and padding of bony prominences were ensured, and the limb was sterilely prepared and draped.

Figure 3.
A standard lateral parapatellar portal was established for arthroscope placement; a medial parapatellar working portal was established as well. Thorough joint inspection revealed normal articular surfaces of patella, femur, and tibial plateau. Similarly, both menisci were intact without evidence of injury.
Figure 4.
With use of the probe, the ACL-TEA fracture could be elevated up to 2 cm toward the top of the notch (Figure 3). Further inspection of the ACL fibers revealed minimal hemorrhaging and no frank tearing (Figure 4).

Given the young age of the patient, it was imperative to avoid the open proximal tibial growth plate. The surgical plan for stabilization involved use of two 3.0-mm BioComposite Knotless SutureTak anchors (Arthrex). This anchor configuration is based on a No. 2 FiberWire suture shuttled through itself to create a locking splice mechanism that allows for adjustable tensioning. The anchors were placed on each side of the tibial bony avulsion site with two No. 2 FiberWire sutures and were then crossed about the avulsion fracture fragment in an “x-type” configuration to secure the ACL back down to the bony bed.

First, a curette was used to débride fibrous tissue on the underside of the fracture fragment and on the fracture bed. Minimal amounts of cancellous bone were débrided from the tibial fracture bed to optimize fracture reduction by slightly recessing the fracture fragment to ensure optimal ACL tensioning (Figure 5).

Figure 5.
Next, an 18-gauge needle was used to establish an accessory superior medial percutaneous portal to ensure a satisfactory drilling trajectory just medial to the fracture site. Under fluoroscopic guidance, a drill guide was placed, and a 2.4-mm bit was used to drill to a depth of 16 mm to accommodate the 12.7-mm anchor. Avoidance of the proximal tibial physis was confirmed with fluoroscopy (Figure 6).
Figure 6.
One of the SutureTak anchors was secured in this drill hole along the anteromedial avulsion fracture site. From the anteromedial portal, a curved needle tip suture passer was placed medially through the ACL fibers and bone, with the wire retrieved out of the superior medial accessory portal. Then, the drill guide was introduced through the lateral portal and positioned just lateral to the tibial avulsion site, a hole was drilled 16 mm deep, and fluoroscopy was used to confirm the physis was not violated. The second SutureTak anchor was placed in this anterolateral location. From the anterolateral portal, the curved needle tip suture passer was placed laterally through the ACL fibers and avulsion fragment, and the wire was passed and retrieved out the anteromedial portal and shuttled back to the anterolateral portal.

Next, from the accessory superior medial portal, the end of the wire that had been passed through the medial aspect of the bony avulsion was retrieved through the lateral portal. This wire was used to shuttle the repair suture from the laterally positioned SutureTak anchor over and through the medial aspect of the bony fragment out of the accessory superior medial (Figure 7).
Figure 7.
This suture was passed through the shuttling loop of the medially positioned SutureTak anchor to create the splice in the anchor for the adjustable fixation. This process was repeated through the lateral aspect of the bony fragment—the medial SutureTak repair suture was passed over the bone here. Thus, the lateral suture was over and through the bony fragment secured to the medial SutureTak anchor, and the medial suture was crossed over and through bone to the lateral SutureTak anchor. With the knee held in full extension, the bony avulsion fracture was easily reduced by alternating tension on the SutureTak limbs, which enabled controlled reduction of the TEA fracture (Figures 8A, 8B).
Figure 8.
An arthroscopic knot pusher was used for final tightening of the SutureTak fixation. An arthroscopic probe was used to confirm anatomical reduction of the fracture and restoration of ACL fiber tension (Figure 9).
Figure 9.
The knee was ranged from 0° to 120° of flexion with visual affirmation of the construct and maintenance of the reduction. Fluoroscopy confirmed anatomical reduction of the TEA fracture. The patient was immobilized in a long leg brace locked in 30° of flexion.

 

 

Follow-Up

Two weeks after surgery, the patient returned to clinic for suture removal. Four weeks after surgery, radiographs confirmed anatomical reduction of the TEA fracture, and outpatient physical therapy (range-of-motion exercises as tolerated) and isometric quadriceps strengthening were instituted. Twelve weeks after surgery, examination revealed full knee motion, negative Lachman and pivot shift test results, and residual quadriceps muscle atrophy, and radiographs confirmed complete fracture healing with maintenance of a normal proximal tibial growth plate (Figures 10A, 10B).

Figure 10.
Sixteen weeks after surgery, ligamentous examination findings were normal, and quadriceps muscle mass was good. In addition, on KT-1000 testing, the surgically repaired knee had only 1 more millimeter of laxity at the 30-pound pull, and equal displacement on the manual maximum test. The patient was allowed to return to full activities as tolerated.

Discussion

The highlight of this case is the simplicity of an excellent reduction of a displaced ACL-TEA fracture. Minimally invasive absorbable implants did not violate the proximal tibial physis, and the unique adjustable suture-tensioning technology allowed the degree of reduction and ACL tension to be “dialed in.” SutureTak implants have strong No. 2 FiberWire suture for excellent stability with an overall small suture load, and their small size avoids the risk of violating the proximal tibial physis and avoids potential growth disturbances.

Despite the obvious risks it poses to the open proximal tibial physis, surgical reduction of Meyers-McKeever type II and type III fractures is the norm for restoring ACL stability. Screws and suture fixation are the most common and reliable methods of TEA fracture reduction.16,17 In recent systematic reviews, however, Osti and colleagues17 and Gans and colleagues18 noted there is not enough evidence to warrant a “gold standard” in pediatric tibial avulsion cases.

Other fixation methods for TEA fractures must be investigated. Anderson and colleagues19 described the biomechanics of 4 different physeal-sparing avulsion fracture reduction techniques: an ultra-high-molecular-weight polyethylene (UHMWPE) suture-suture button, a suture anchor, a polydioxanone suture-suture button, and screw fixation. Using techniques described by Kocher and colleagues,4 Berg,20 Mah and colleagues,21 Vega and colleagues,22 and Lu and colleagues,23 Anderson and colleagues19 reduced TEA fractures in skeletally immature porcine knees. Compared with suture anchors, UHMWPE suture-suture buttons provided biomechanically superior cyclic and load-to-failure results as well as more consistent fixation.

Screw fixation has shown good results but has disadvantages. Incorrect positioning of a screw can lead to impingement and articular cartilage damage, and screw removal may be needed if discomfort at the fixation site persists.24,25 Likewise, screws generally are an option only for large fracture fragments, as there is an inherent risk of fracturing small TEA fractures, which can be common in skeletally immature patients.

Brunner and colleagues26 recently found that TEA fracture repair with absorbable sutures and distal bone bridge fixation yielded 3-month radiographic and clinical healing rates similar to those obtained with nonabsorbable sutures tied around a screw. However, other authors have reported growth disturbances with use of a similar technique, owing to a disturbance of the open proximal tibial growth plate.9 In that regard, a major advantage of this new knotless suturing technique is that distal fixation is not necessary.

The minimally invasive TEA fraction reduction technique described in this article has 6 advantages: It provides excellent fixation while avoiding proximal tibial growth plate injury; the degree of tensioning is easily controlled during reduction; it uses strong suture instead of metal screws or pins; the reduction construct is low-profile; distal fixation is unnecessary; and implant removal is unnecessary, thus limiting subsequent surgical intervention. With respect to long-term outcomes, however, it is not known how this procedure will compare with other commonly used ARIF methods in physeal-sparing techniques for TEA fracture fixation.

This case report highlights a novel pediatric displaced ACL-TEA fracture reduction technique that allows for adjustable reduction and resultant ACL tensioning with excellent strong suture fixation without violating the proximal tibial physis, which could make it invaluable in the surgical treatment of this injury in skeletally immature patients.

Am J Orthop. 2017;46(4):203-208. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Eiskjaer S, Larsen ST, Schmidt MB. The significance of hemarthrosis of the knee in children. Arch Orthop Trauma Surg. 1988;107(2):96-98.

2. Luhmann SJ. Acute traumatic knee effusions in children and adolescents. J Pediatr Orthop. 2003;23(2):199-202.

3. Woo SL, Hollis JM, Adams DJ, Lyon RM, Takai S. Tensile properties of the human femur-anterior cruciate ligament-tibia complex. The effects of specimen age and orientation. Am J Sports Med. 1991;19(3):217-225.

4. Kocher MS, Foreman ES, Micheli LJ. Laxity and functional outcome after arthroscopic reduction and internal fixation of displaced tibial spine fractures in children. Arthroscopy. 2003;19(10):1085-1090.

5. Lubowitz JH, Elson WS, Guttmann D. Part II: arthroscopic treatment of tibial plateau fractures: intercondylar eminence avulsion fractures. Arthroscopy. 2005;21(1):86-92.

6. Vargas B, Lutz N, Dutoit M, Zambelli PY. Nonunion after fracture of the anterior tibial spine: case report and review of the literature. J Pediatr Orthop B. 2009;18(2):90-92.

7. Sommerfeldt DW. Arthroscopically assisted internal fixation of avulsion fractures of the anterior cruciate ligament during childhood and adolescence [in German]. Oper Orthop Traumatol. 2008;20(4-5):310-320.

8. Wouters DB, de Graaf JS, Hemmer PH, Burgerhof JG, Kramer WL. The arthroscopic treatment of displaced tibial spine fractures in children and adolescents using Meniscus Arrows®. Knee Surg Sports Traumatol Arthrosc. 2011;19(5):736-739.

9. Ahn JH, Yoo JC. Clinical outcome of arthroscopic reduction and suture for displaced acute and chronic tibial spine fractures. Knee Surg Sports Traumatol Arthrosc. 2005;13(2):116-121.

10. Huang TW, Hsu KY, Cheng CY, et al. Arthroscopic suture fixation of tibial eminence avulsion fractures. Arthroscopy. 2008;24(11):1232-1238.

11. Liljeros K, Werner S, Janarv PM. Arthroscopic fixation of anterior tibial spine fractures with bioabsorbable nails in skeletally immature patients. Am J Sports Med. 2009;37(5):923-928.

12. Wiegand N, Naumov I, Vamhidy L, Not LG. Arthroscopic treatment of tibial spine fracture in children with a cannulated Herbert screw. Knee. 2014;21(2):481-485.

13. Faivre B, Benea H, Klouche S, Lespagnol F, Bauer T, Hardy P. An original arthroscopic fixation of adult’s tibial eminence fractures using the Tightrope® device: a report of 8 cases and review of literature. Knee. 2014;21(4):833-839.

14. Kluemper CT, Snyder GM, Coats AC, Johnson DL, Mair SD. Arthroscopic suture fixation of tibial eminence fractures. Orthopedics. 2013;36(11):e1401-e1406.

15. Ochiai S, Hagino T, Watanabe Y, Senga S, Haro H. One strategy for arthroscopic suture fixation of tibial intercondylar eminence fractures using the Meniscal Viper Repair System. Sports Med Arthrosc Rehabil Ther Technol. 2011;3:17.

16. Bogunovic L, Tarabichi M, Harris D, Wright R. Treatment of tibial eminence fractures: a systematic review. J Knee Surg. 2015;28(3):255-262.

17. Osti L, Buda M, Soldati F, Del Buono A, Osti R, Maffulli N. Arthroscopic treatment of tibial eminence fracture: a systematic review of different fixation methods. Br Med Bull. 2016;118(1):73-90.

18. Gans I, Baldwin KD, Ganley TJ. Treatment and management outcomes of tibial eminence fractures in pediatric patients: a systematic review. Am J Sports Med. 2014;42(7):1743-1750.

19. Anderson CN, Nyman JS, McCullough KA, et al. Biomechanical evaluation of physeal-sparing fixation methods in tibial eminence fractures. Am J Sports Med. 2013;41(7):1586-1594.

20. Berg EE. Pediatric tibial eminence fractures: arthroscopic cannulated screw fixation. Arthroscopy. 1995;11(3):328-331.

21. Mah JY, Otsuka NY, McLean J. An arthroscopic technique for the reduction and fixation of tibial-eminence fractures. J Pediatr Orthop. 1996;16(1):119-121.

22. Vega JR, Irribarra LA, Baar AK, Iniguez M, Salgado M, Gana N. Arthroscopic fixation of displaced tibial eminence fractures: a new growth plate-sparing method. Arthroscopy. 2008;24(11):1239-1243.

23. Lu XW, Hu XP, Jin C, Zhu T, Ding Y, Dai LY. Reduction and fixation of the avulsion fracture of the tibial eminence using mini-open technique. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1476-1480.

24. Bonin N, Jeunet L, Obert L, Dejour D. Adult tibial eminence fracture fixation: arthroscopic procedure using K-wire folded fixation. Knee Surg Sports Traumatol Arthrosc. 2007;15(7):857-862.

25. Senekovic V, Veselko M. Anterograde arthroscopic fixation of avulsion fractures of the tibial eminence with a cannulated screw: five-year results. Arthroscopy. 2003;19(1):54-61.

26. Brunner S, Vavken P, Kilger R, et al. Absorbable and non-absorbable suture fixation results in similar outcomes for tibial eminence fractures in children and adolescents. Knee Surg Sports Traumatol Arthrosc. 2016;24(3):723-729.

References

1. Eiskjaer S, Larsen ST, Schmidt MB. The significance of hemarthrosis of the knee in children. Arch Orthop Trauma Surg. 1988;107(2):96-98.

2. Luhmann SJ. Acute traumatic knee effusions in children and adolescents. J Pediatr Orthop. 2003;23(2):199-202.

3. Woo SL, Hollis JM, Adams DJ, Lyon RM, Takai S. Tensile properties of the human femur-anterior cruciate ligament-tibia complex. The effects of specimen age and orientation. Am J Sports Med. 1991;19(3):217-225.

4. Kocher MS, Foreman ES, Micheli LJ. Laxity and functional outcome after arthroscopic reduction and internal fixation of displaced tibial spine fractures in children. Arthroscopy. 2003;19(10):1085-1090.

5. Lubowitz JH, Elson WS, Guttmann D. Part II: arthroscopic treatment of tibial plateau fractures: intercondylar eminence avulsion fractures. Arthroscopy. 2005;21(1):86-92.

6. Vargas B, Lutz N, Dutoit M, Zambelli PY. Nonunion after fracture of the anterior tibial spine: case report and review of the literature. J Pediatr Orthop B. 2009;18(2):90-92.

7. Sommerfeldt DW. Arthroscopically assisted internal fixation of avulsion fractures of the anterior cruciate ligament during childhood and adolescence [in German]. Oper Orthop Traumatol. 2008;20(4-5):310-320.

8. Wouters DB, de Graaf JS, Hemmer PH, Burgerhof JG, Kramer WL. The arthroscopic treatment of displaced tibial spine fractures in children and adolescents using Meniscus Arrows®. Knee Surg Sports Traumatol Arthrosc. 2011;19(5):736-739.

9. Ahn JH, Yoo JC. Clinical outcome of arthroscopic reduction and suture for displaced acute and chronic tibial spine fractures. Knee Surg Sports Traumatol Arthrosc. 2005;13(2):116-121.

10. Huang TW, Hsu KY, Cheng CY, et al. Arthroscopic suture fixation of tibial eminence avulsion fractures. Arthroscopy. 2008;24(11):1232-1238.

11. Liljeros K, Werner S, Janarv PM. Arthroscopic fixation of anterior tibial spine fractures with bioabsorbable nails in skeletally immature patients. Am J Sports Med. 2009;37(5):923-928.

12. Wiegand N, Naumov I, Vamhidy L, Not LG. Arthroscopic treatment of tibial spine fracture in children with a cannulated Herbert screw. Knee. 2014;21(2):481-485.

13. Faivre B, Benea H, Klouche S, Lespagnol F, Bauer T, Hardy P. An original arthroscopic fixation of adult’s tibial eminence fractures using the Tightrope® device: a report of 8 cases and review of literature. Knee. 2014;21(4):833-839.

14. Kluemper CT, Snyder GM, Coats AC, Johnson DL, Mair SD. Arthroscopic suture fixation of tibial eminence fractures. Orthopedics. 2013;36(11):e1401-e1406.

15. Ochiai S, Hagino T, Watanabe Y, Senga S, Haro H. One strategy for arthroscopic suture fixation of tibial intercondylar eminence fractures using the Meniscal Viper Repair System. Sports Med Arthrosc Rehabil Ther Technol. 2011;3:17.

16. Bogunovic L, Tarabichi M, Harris D, Wright R. Treatment of tibial eminence fractures: a systematic review. J Knee Surg. 2015;28(3):255-262.

17. Osti L, Buda M, Soldati F, Del Buono A, Osti R, Maffulli N. Arthroscopic treatment of tibial eminence fracture: a systematic review of different fixation methods. Br Med Bull. 2016;118(1):73-90.

18. Gans I, Baldwin KD, Ganley TJ. Treatment and management outcomes of tibial eminence fractures in pediatric patients: a systematic review. Am J Sports Med. 2014;42(7):1743-1750.

19. Anderson CN, Nyman JS, McCullough KA, et al. Biomechanical evaluation of physeal-sparing fixation methods in tibial eminence fractures. Am J Sports Med. 2013;41(7):1586-1594.

20. Berg EE. Pediatric tibial eminence fractures: arthroscopic cannulated screw fixation. Arthroscopy. 1995;11(3):328-331.

21. Mah JY, Otsuka NY, McLean J. An arthroscopic technique for the reduction and fixation of tibial-eminence fractures. J Pediatr Orthop. 1996;16(1):119-121.

22. Vega JR, Irribarra LA, Baar AK, Iniguez M, Salgado M, Gana N. Arthroscopic fixation of displaced tibial eminence fractures: a new growth plate-sparing method. Arthroscopy. 2008;24(11):1239-1243.

23. Lu XW, Hu XP, Jin C, Zhu T, Ding Y, Dai LY. Reduction and fixation of the avulsion fracture of the tibial eminence using mini-open technique. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1476-1480.

24. Bonin N, Jeunet L, Obert L, Dejour D. Adult tibial eminence fracture fixation: arthroscopic procedure using K-wire folded fixation. Knee Surg Sports Traumatol Arthrosc. 2007;15(7):857-862.

25. Senekovic V, Veselko M. Anterograde arthroscopic fixation of avulsion fractures of the tibial eminence with a cannulated screw: five-year results. Arthroscopy. 2003;19(1):54-61.

26. Brunner S, Vavken P, Kilger R, et al. Absorbable and non-absorbable suture fixation results in similar outcomes for tibial eminence fractures in children and adolescents. Knee Surg Sports Traumatol Arthrosc. 2016;24(3):723-729.

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Knotless Arthroscopic Reduction and Internal Fixation of a Displaced Anterior Cruciate Ligament Tibial Eminence Avulsion Fracture
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A New Option for Glenoid Reconstruction in Recurrent Anterior Shoulder Instability

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A New Option for Glenoid Reconstruction in Recurrent Anterior Shoulder Instability

Take-Home Points

  • Repair anterior bone defect on the glenoid related to recurrent anterior instability with preshaped, predrilled allograft.
  • Avoid graft harvest complications related to coracoid (Latarjet) or iliac crest autograft.
  • Simple guide system to allow for appropriate graft and screw placement.
  • Soft tissues can be repaired to the allograft in predrilled suture holes either inside or outside of the graft
  • Position the graft without step at the anterior glenoid.

Anteroinferior glenoid bone loss plays a significant role in recurrent glenohumeral instability. Arthroscopic capsulolabral reconstruction has been associated with a recurrence rate of 4% in the absence of significant glenoid bone loss but 67% in patients with either bone loss of more than 25% of the inferior glenoid diameter or an engaging Hill-Sachs lesion.1,2 Anteroinferior glenoid rim deficiency has been reported in up to 90% of cases of recurrent instability.3 Glenoid reconstruction is therefore recommended in patients with bone loss of more than 25% and in certain revision cases.4 Surgical strategies in these cases include coracoid transfer, iliac crest autograft, and allograft (osteochondral and iliac crest). These procedures all successfully restore stability of the glenohumeral joint. However, they carry the drawbacks of technical complexity with increased operative time or risk of neurovascular damage, or they create a nonanatomical reconstruction, which may contribute to subsequent instability arthropathy. In this article, we introduce a technique in which a preshaped allograft (Glenojet; Arthrosurface, Inc.) is used to match the contour of the glenoid defect. The graft is simple to insert and can reduce operative time.

Graft Preparation

The shaped human tissue cortical bone allograft is usually prepared from proximal or distal tibia or femur. There is no cartilage on the graft. It can be ordered in 2 sizes, 10 mm × 29 mm and 13 mm × 34 mm, for different amounts of bone loss. The more commonly used smaller graft reconstructs defects of 20% to 30% of the glenoid.

Figure 1.
The graft has a flat surface that abuts the glenoid and a concave surface that repairs to the capsule. The graft has predrilled holes for cortical screw placement as well as smaller holes for threading suture for capsule repair. It is shaped to match the contour of the glenoid (Figure 1).

The sutures through this allograft can be prepared on the back table while the rest of the equipment is set up. Start by tying a No. 2 FiberWire (or equivalent) over a small thin object, such as a Freer elevator. Once the knot is secure, remove the Freer and trim the knot tails short. Thread another suture through the loop that has been created and pull to make the 2 tails even. Then thread these tails through one of the small holes of the graft, going from the flat side to the concave side. Pull the suture tails all the way through, including through the loop of the prior suture. The knot of the loop prevents the entire construct from pulling through. The suture tails are then able to slide as if attached to an anchor. Repeat these steps for the other 2 small holes to get a total of 3 sutures exiting the concave side of the graft (Figure 1). Alternatively, pass the suture the opposite way, if tying the capsule inside the graft is preferred.

Surgical Technique

A standard deltopectoral approach is used to expose the anterior glenoid. The subscapularis can either be split in line with its fibers or tenotomized with 1 cm to 2 cm attached to the tuberosity for later repair. In either instance, it is important to separate the muscle from the underlying capsule layer, as the capsule is what is directly repaired to the graft.

The capsule is carefully peeled off the anterior glenoid. A Fukuda or similar retractor may be used on the humerus, and a glenoid retractor is placed on the anterior glenoid, under the capsule and subscapularis, for optimal exposure. Once the anterior glenoid surface is exposed, the drill guide is placed flush against the surface of the glenoid.

Figure 2.
It is important to confirm the guide is seated flush on the glenoid, as this ensures correct positioning, angulation, and alignment of the graft. The laser mark on the guide is positioned in line with the anterior glenoid fracture plane. The guide is securely held while 2 guide pins are drilled in place, until just past the posterior cortex of the glenoid (Figure 2).

The guide is removed. The cannulated reamer is introduced and advanced until the guide pin appears in the viewing window of the reamer and hits the stop—approximating the correct amount of bone to remove. This step is repeated for the second guide pin. Reaming flattens the anterior glenoid and allows for maximal stable apposition of the graft to the glenoid. The allograft is then inserted onto the pins in the correct orientation to match the surface of the native glenoid.

The length of the superior guide pin is measured with the depth gauge device. It is then removed, and the appropriate-length 3.5-mm cortical bone screw is inserted (alternatively, the guide pin is removed, and a standard depth gauge is used to measure screw length). Once the superior guide pin is secure, the process is repeated for the inferior guide pin (Figure 3).
Figure 3.
The screws should have excellent bicortical fixation. Although we have not had any intraoperative graft fractures, overtensioning of the screws could cause the graft to fail at the screw site at follow-up. Therefore, we recommend not overtightening the screws.

Once the graft is secure, the capsule is attached to the graft with the use of a free needle on the suture of the graft (Figure 4).
Figure 4.
The capsule is advanced as necessary for appropriate anterior soft-tissue tensioning. Once the capsular repair is complete, the subscapularis is repaired as necessary.

 

 

Outcomes

Coracoid bone transfer or the Bristow-Latarjet technique has become more popular since bone loss was recognized as an important cause of failure of soft-tissue repair for anterior instability. This procedure, however, is not without complications. In a recent systematic review of 45 studies (1904 shoulders), Griesser and colleagues5 found an overall complication rate of 30% and a reoperation rate of 7%.

Given the potential complications of coracoid bone transfer, allograft reconstruction of the anteroinferior glenoid has become increasingly popular and proved successful at short- and medium-term follow-up. Allograft reconstruction avoids the drawbacks of traditional coracoid bone transfer—namely, high rates of neurovascular injury, and nonanatomical reconstruction with high rates of graft resorption and arthritis.5,6 At average 45-month follow-up after fresh distal tibia allograft reconstruction, Provencher and colleagues7 found an 89% radiographic union rate (average lysis, 3%), significantly improved patient-reported outcomes, and no recurrent instability. Similarly, in a study of iliac crest allograft reconstruction in 10 patients with an average 4-year follow-up, Mascarenhas and colleagues8 found an 80% radiographic union rate at 6 months, significantly improved patient-reported outcomes, and no recurrent shoulder instability.

The advantage of Glenojet over other allografts is that it is preshaped and predrilled and saves the surgeon the time and effort of preparing graft in the operating room. The surgical technologist can place the sutures before the patient enters the room. The 2 allograft sizes (10 mm × 29 mm, 13 mm × 34 mm) accommodate the spectrum of bone loss in glenoid deficiency, and graft contour fits the native glenoid well. So far we have implanted this allograft in 15 patients, and at short-term follow-up there are no known cases of recurrent instability.

The potential disadvantages of Glenojet are similar to those of other allografts. Care must be taken with retractor placement to avoid damaging the axillary and musculocutaneous nerves. There are concerns about graft union and subsequent resorption, but this will require long-term follow-up to determine. At 9-month follow-up, we had 1 fracture at the superior corner of the graft, which may have resulted from overtightening the screws in the graft, creating a stress concentration. After removal of this fragment arthroscopically, the patient has done very well clinically with no pain, instability and has returned to all activities. Although the graft does not have an articular surface, the capsular repair covers much of the articular side of the graft, and therefore we do not anticipate that the absence of articular cartilage will contribute to glenohumeral arthritis, though long-term follow-up is lacking. The other question many have is related to the lack of the sling effect since there is no conjoined tendon on the graft. Yamamoto and colleagues9 have reported that the conjoined tendon is the major stabilizing force at time zero in a cadaver model. However, other authors7,8 have successfully reconstructed glenoid defects in these difficult cases without the “sling effect” of the conjoined tendon with excellent clinical results. Our experience has been similar. It is likely that long-term studies will be necessary to answer this question. We have also done some cases with the tendon attached after releasing it from the coracoid, but the series is too small to make any comment about whether this is important or not.

The main limitation of this allograft technique is the lack of long-term outcome studies. However, short-term results are promising, and the ease of the procedure makes it an attractive option for either glenoid reconstruction of bony Bankart lesions or failed bone reconstruction, such as Bristow-Latarjet reconstruction.

Glenojetallograft is a new glenoid reconstruction option that is technically easy and simple to perform in cases of glenoid bone loss, while still creating an anatomical buttress with less surgical dissection than traditional coracoid bone transfer. Short-term outcomes are reassuring, though more research is needed for long-term graft follow-up and recurrent instability.

Am J Orthop. 2017;46(4):199-202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.

2. Rowe CR, Sakellarides HT. Factors related to recurrences of anterior dislocations of the shoulder. Clin Orthop. 1961;(20):40-48.

3. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

4. Sayegh ET, Mascarenhas R, Chalmers PN, Cole BJ, Verma NN, Romeo AA. Allograft reconstruction for glenoid bone loss in glenohumeral instability: a systematic review. Arthroscopy. 2014;30(12):1642-1649.

5. Griesser MJ, Harris JD, McCoy BW, et al. Complications and re-operati ons after Bristow-Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-292.

6. Young DC, Rockwood CA Jr. Complications of a failed Bristow procedure and their management. J Bone Joint Surg Am. 1991;73(7):969-981.

7. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

8. Mascarenhas R, Raleigh E, McRae S, Leiter J, Saltzman B, MacDonald PB. Iliac crest allograft glenoid reconstruction for recurrent anterior shoulder instability in athletes: surgical technique and results. Int J Shoulder Surg. 2014;8(4):127-132.

9. Yamamoto N, Muraki T, An KN, et al. The stabilizing mechanism of the Latarjet procedure: a cadaveric study. J Bone Joint Surg Am. 2013;95(15):1390-1397.

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Take-Home Points

  • Repair anterior bone defect on the glenoid related to recurrent anterior instability with preshaped, predrilled allograft.
  • Avoid graft harvest complications related to coracoid (Latarjet) or iliac crest autograft.
  • Simple guide system to allow for appropriate graft and screw placement.
  • Soft tissues can be repaired to the allograft in predrilled suture holes either inside or outside of the graft
  • Position the graft without step at the anterior glenoid.

Anteroinferior glenoid bone loss plays a significant role in recurrent glenohumeral instability. Arthroscopic capsulolabral reconstruction has been associated with a recurrence rate of 4% in the absence of significant glenoid bone loss but 67% in patients with either bone loss of more than 25% of the inferior glenoid diameter or an engaging Hill-Sachs lesion.1,2 Anteroinferior glenoid rim deficiency has been reported in up to 90% of cases of recurrent instability.3 Glenoid reconstruction is therefore recommended in patients with bone loss of more than 25% and in certain revision cases.4 Surgical strategies in these cases include coracoid transfer, iliac crest autograft, and allograft (osteochondral and iliac crest). These procedures all successfully restore stability of the glenohumeral joint. However, they carry the drawbacks of technical complexity with increased operative time or risk of neurovascular damage, or they create a nonanatomical reconstruction, which may contribute to subsequent instability arthropathy. In this article, we introduce a technique in which a preshaped allograft (Glenojet; Arthrosurface, Inc.) is used to match the contour of the glenoid defect. The graft is simple to insert and can reduce operative time.

Graft Preparation

The shaped human tissue cortical bone allograft is usually prepared from proximal or distal tibia or femur. There is no cartilage on the graft. It can be ordered in 2 sizes, 10 mm × 29 mm and 13 mm × 34 mm, for different amounts of bone loss. The more commonly used smaller graft reconstructs defects of 20% to 30% of the glenoid.

Figure 1.
The graft has a flat surface that abuts the glenoid and a concave surface that repairs to the capsule. The graft has predrilled holes for cortical screw placement as well as smaller holes for threading suture for capsule repair. It is shaped to match the contour of the glenoid (Figure 1).

The sutures through this allograft can be prepared on the back table while the rest of the equipment is set up. Start by tying a No. 2 FiberWire (or equivalent) over a small thin object, such as a Freer elevator. Once the knot is secure, remove the Freer and trim the knot tails short. Thread another suture through the loop that has been created and pull to make the 2 tails even. Then thread these tails through one of the small holes of the graft, going from the flat side to the concave side. Pull the suture tails all the way through, including through the loop of the prior suture. The knot of the loop prevents the entire construct from pulling through. The suture tails are then able to slide as if attached to an anchor. Repeat these steps for the other 2 small holes to get a total of 3 sutures exiting the concave side of the graft (Figure 1). Alternatively, pass the suture the opposite way, if tying the capsule inside the graft is preferred.

Surgical Technique

A standard deltopectoral approach is used to expose the anterior glenoid. The subscapularis can either be split in line with its fibers or tenotomized with 1 cm to 2 cm attached to the tuberosity for later repair. In either instance, it is important to separate the muscle from the underlying capsule layer, as the capsule is what is directly repaired to the graft.

The capsule is carefully peeled off the anterior glenoid. A Fukuda or similar retractor may be used on the humerus, and a glenoid retractor is placed on the anterior glenoid, under the capsule and subscapularis, for optimal exposure. Once the anterior glenoid surface is exposed, the drill guide is placed flush against the surface of the glenoid.

Figure 2.
It is important to confirm the guide is seated flush on the glenoid, as this ensures correct positioning, angulation, and alignment of the graft. The laser mark on the guide is positioned in line with the anterior glenoid fracture plane. The guide is securely held while 2 guide pins are drilled in place, until just past the posterior cortex of the glenoid (Figure 2).

The guide is removed. The cannulated reamer is introduced and advanced until the guide pin appears in the viewing window of the reamer and hits the stop—approximating the correct amount of bone to remove. This step is repeated for the second guide pin. Reaming flattens the anterior glenoid and allows for maximal stable apposition of the graft to the glenoid. The allograft is then inserted onto the pins in the correct orientation to match the surface of the native glenoid.

The length of the superior guide pin is measured with the depth gauge device. It is then removed, and the appropriate-length 3.5-mm cortical bone screw is inserted (alternatively, the guide pin is removed, and a standard depth gauge is used to measure screw length). Once the superior guide pin is secure, the process is repeated for the inferior guide pin (Figure 3).
Figure 3.
The screws should have excellent bicortical fixation. Although we have not had any intraoperative graft fractures, overtensioning of the screws could cause the graft to fail at the screw site at follow-up. Therefore, we recommend not overtightening the screws.

Once the graft is secure, the capsule is attached to the graft with the use of a free needle on the suture of the graft (Figure 4).
Figure 4.
The capsule is advanced as necessary for appropriate anterior soft-tissue tensioning. Once the capsular repair is complete, the subscapularis is repaired as necessary.

 

 

Outcomes

Coracoid bone transfer or the Bristow-Latarjet technique has become more popular since bone loss was recognized as an important cause of failure of soft-tissue repair for anterior instability. This procedure, however, is not without complications. In a recent systematic review of 45 studies (1904 shoulders), Griesser and colleagues5 found an overall complication rate of 30% and a reoperation rate of 7%.

Given the potential complications of coracoid bone transfer, allograft reconstruction of the anteroinferior glenoid has become increasingly popular and proved successful at short- and medium-term follow-up. Allograft reconstruction avoids the drawbacks of traditional coracoid bone transfer—namely, high rates of neurovascular injury, and nonanatomical reconstruction with high rates of graft resorption and arthritis.5,6 At average 45-month follow-up after fresh distal tibia allograft reconstruction, Provencher and colleagues7 found an 89% radiographic union rate (average lysis, 3%), significantly improved patient-reported outcomes, and no recurrent instability. Similarly, in a study of iliac crest allograft reconstruction in 10 patients with an average 4-year follow-up, Mascarenhas and colleagues8 found an 80% radiographic union rate at 6 months, significantly improved patient-reported outcomes, and no recurrent shoulder instability.

The advantage of Glenojet over other allografts is that it is preshaped and predrilled and saves the surgeon the time and effort of preparing graft in the operating room. The surgical technologist can place the sutures before the patient enters the room. The 2 allograft sizes (10 mm × 29 mm, 13 mm × 34 mm) accommodate the spectrum of bone loss in glenoid deficiency, and graft contour fits the native glenoid well. So far we have implanted this allograft in 15 patients, and at short-term follow-up there are no known cases of recurrent instability.

The potential disadvantages of Glenojet are similar to those of other allografts. Care must be taken with retractor placement to avoid damaging the axillary and musculocutaneous nerves. There are concerns about graft union and subsequent resorption, but this will require long-term follow-up to determine. At 9-month follow-up, we had 1 fracture at the superior corner of the graft, which may have resulted from overtightening the screws in the graft, creating a stress concentration. After removal of this fragment arthroscopically, the patient has done very well clinically with no pain, instability and has returned to all activities. Although the graft does not have an articular surface, the capsular repair covers much of the articular side of the graft, and therefore we do not anticipate that the absence of articular cartilage will contribute to glenohumeral arthritis, though long-term follow-up is lacking. The other question many have is related to the lack of the sling effect since there is no conjoined tendon on the graft. Yamamoto and colleagues9 have reported that the conjoined tendon is the major stabilizing force at time zero in a cadaver model. However, other authors7,8 have successfully reconstructed glenoid defects in these difficult cases without the “sling effect” of the conjoined tendon with excellent clinical results. Our experience has been similar. It is likely that long-term studies will be necessary to answer this question. We have also done some cases with the tendon attached after releasing it from the coracoid, but the series is too small to make any comment about whether this is important or not.

The main limitation of this allograft technique is the lack of long-term outcome studies. However, short-term results are promising, and the ease of the procedure makes it an attractive option for either glenoid reconstruction of bony Bankart lesions or failed bone reconstruction, such as Bristow-Latarjet reconstruction.

Glenojetallograft is a new glenoid reconstruction option that is technically easy and simple to perform in cases of glenoid bone loss, while still creating an anatomical buttress with less surgical dissection than traditional coracoid bone transfer. Short-term outcomes are reassuring, though more research is needed for long-term graft follow-up and recurrent instability.

Am J Orthop. 2017;46(4):199-202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Repair anterior bone defect on the glenoid related to recurrent anterior instability with preshaped, predrilled allograft.
  • Avoid graft harvest complications related to coracoid (Latarjet) or iliac crest autograft.
  • Simple guide system to allow for appropriate graft and screw placement.
  • Soft tissues can be repaired to the allograft in predrilled suture holes either inside or outside of the graft
  • Position the graft without step at the anterior glenoid.

Anteroinferior glenoid bone loss plays a significant role in recurrent glenohumeral instability. Arthroscopic capsulolabral reconstruction has been associated with a recurrence rate of 4% in the absence of significant glenoid bone loss but 67% in patients with either bone loss of more than 25% of the inferior glenoid diameter or an engaging Hill-Sachs lesion.1,2 Anteroinferior glenoid rim deficiency has been reported in up to 90% of cases of recurrent instability.3 Glenoid reconstruction is therefore recommended in patients with bone loss of more than 25% and in certain revision cases.4 Surgical strategies in these cases include coracoid transfer, iliac crest autograft, and allograft (osteochondral and iliac crest). These procedures all successfully restore stability of the glenohumeral joint. However, they carry the drawbacks of technical complexity with increased operative time or risk of neurovascular damage, or they create a nonanatomical reconstruction, which may contribute to subsequent instability arthropathy. In this article, we introduce a technique in which a preshaped allograft (Glenojet; Arthrosurface, Inc.) is used to match the contour of the glenoid defect. The graft is simple to insert and can reduce operative time.

Graft Preparation

The shaped human tissue cortical bone allograft is usually prepared from proximal or distal tibia or femur. There is no cartilage on the graft. It can be ordered in 2 sizes, 10 mm × 29 mm and 13 mm × 34 mm, for different amounts of bone loss. The more commonly used smaller graft reconstructs defects of 20% to 30% of the glenoid.

Figure 1.
The graft has a flat surface that abuts the glenoid and a concave surface that repairs to the capsule. The graft has predrilled holes for cortical screw placement as well as smaller holes for threading suture for capsule repair. It is shaped to match the contour of the glenoid (Figure 1).

The sutures through this allograft can be prepared on the back table while the rest of the equipment is set up. Start by tying a No. 2 FiberWire (or equivalent) over a small thin object, such as a Freer elevator. Once the knot is secure, remove the Freer and trim the knot tails short. Thread another suture through the loop that has been created and pull to make the 2 tails even. Then thread these tails through one of the small holes of the graft, going from the flat side to the concave side. Pull the suture tails all the way through, including through the loop of the prior suture. The knot of the loop prevents the entire construct from pulling through. The suture tails are then able to slide as if attached to an anchor. Repeat these steps for the other 2 small holes to get a total of 3 sutures exiting the concave side of the graft (Figure 1). Alternatively, pass the suture the opposite way, if tying the capsule inside the graft is preferred.

Surgical Technique

A standard deltopectoral approach is used to expose the anterior glenoid. The subscapularis can either be split in line with its fibers or tenotomized with 1 cm to 2 cm attached to the tuberosity for later repair. In either instance, it is important to separate the muscle from the underlying capsule layer, as the capsule is what is directly repaired to the graft.

The capsule is carefully peeled off the anterior glenoid. A Fukuda or similar retractor may be used on the humerus, and a glenoid retractor is placed on the anterior glenoid, under the capsule and subscapularis, for optimal exposure. Once the anterior glenoid surface is exposed, the drill guide is placed flush against the surface of the glenoid.

Figure 2.
It is important to confirm the guide is seated flush on the glenoid, as this ensures correct positioning, angulation, and alignment of the graft. The laser mark on the guide is positioned in line with the anterior glenoid fracture plane. The guide is securely held while 2 guide pins are drilled in place, until just past the posterior cortex of the glenoid (Figure 2).

The guide is removed. The cannulated reamer is introduced and advanced until the guide pin appears in the viewing window of the reamer and hits the stop—approximating the correct amount of bone to remove. This step is repeated for the second guide pin. Reaming flattens the anterior glenoid and allows for maximal stable apposition of the graft to the glenoid. The allograft is then inserted onto the pins in the correct orientation to match the surface of the native glenoid.

The length of the superior guide pin is measured with the depth gauge device. It is then removed, and the appropriate-length 3.5-mm cortical bone screw is inserted (alternatively, the guide pin is removed, and a standard depth gauge is used to measure screw length). Once the superior guide pin is secure, the process is repeated for the inferior guide pin (Figure 3).
Figure 3.
The screws should have excellent bicortical fixation. Although we have not had any intraoperative graft fractures, overtensioning of the screws could cause the graft to fail at the screw site at follow-up. Therefore, we recommend not overtightening the screws.

Once the graft is secure, the capsule is attached to the graft with the use of a free needle on the suture of the graft (Figure 4).
Figure 4.
The capsule is advanced as necessary for appropriate anterior soft-tissue tensioning. Once the capsular repair is complete, the subscapularis is repaired as necessary.

 

 

Outcomes

Coracoid bone transfer or the Bristow-Latarjet technique has become more popular since bone loss was recognized as an important cause of failure of soft-tissue repair for anterior instability. This procedure, however, is not without complications. In a recent systematic review of 45 studies (1904 shoulders), Griesser and colleagues5 found an overall complication rate of 30% and a reoperation rate of 7%.

Given the potential complications of coracoid bone transfer, allograft reconstruction of the anteroinferior glenoid has become increasingly popular and proved successful at short- and medium-term follow-up. Allograft reconstruction avoids the drawbacks of traditional coracoid bone transfer—namely, high rates of neurovascular injury, and nonanatomical reconstruction with high rates of graft resorption and arthritis.5,6 At average 45-month follow-up after fresh distal tibia allograft reconstruction, Provencher and colleagues7 found an 89% radiographic union rate (average lysis, 3%), significantly improved patient-reported outcomes, and no recurrent instability. Similarly, in a study of iliac crest allograft reconstruction in 10 patients with an average 4-year follow-up, Mascarenhas and colleagues8 found an 80% radiographic union rate at 6 months, significantly improved patient-reported outcomes, and no recurrent shoulder instability.

The advantage of Glenojet over other allografts is that it is preshaped and predrilled and saves the surgeon the time and effort of preparing graft in the operating room. The surgical technologist can place the sutures before the patient enters the room. The 2 allograft sizes (10 mm × 29 mm, 13 mm × 34 mm) accommodate the spectrum of bone loss in glenoid deficiency, and graft contour fits the native glenoid well. So far we have implanted this allograft in 15 patients, and at short-term follow-up there are no known cases of recurrent instability.

The potential disadvantages of Glenojet are similar to those of other allografts. Care must be taken with retractor placement to avoid damaging the axillary and musculocutaneous nerves. There are concerns about graft union and subsequent resorption, but this will require long-term follow-up to determine. At 9-month follow-up, we had 1 fracture at the superior corner of the graft, which may have resulted from overtightening the screws in the graft, creating a stress concentration. After removal of this fragment arthroscopically, the patient has done very well clinically with no pain, instability and has returned to all activities. Although the graft does not have an articular surface, the capsular repair covers much of the articular side of the graft, and therefore we do not anticipate that the absence of articular cartilage will contribute to glenohumeral arthritis, though long-term follow-up is lacking. The other question many have is related to the lack of the sling effect since there is no conjoined tendon on the graft. Yamamoto and colleagues9 have reported that the conjoined tendon is the major stabilizing force at time zero in a cadaver model. However, other authors7,8 have successfully reconstructed glenoid defects in these difficult cases without the “sling effect” of the conjoined tendon with excellent clinical results. Our experience has been similar. It is likely that long-term studies will be necessary to answer this question. We have also done some cases with the tendon attached after releasing it from the coracoid, but the series is too small to make any comment about whether this is important or not.

The main limitation of this allograft technique is the lack of long-term outcome studies. However, short-term results are promising, and the ease of the procedure makes it an attractive option for either glenoid reconstruction of bony Bankart lesions or failed bone reconstruction, such as Bristow-Latarjet reconstruction.

Glenojetallograft is a new glenoid reconstruction option that is technically easy and simple to perform in cases of glenoid bone loss, while still creating an anatomical buttress with less surgical dissection than traditional coracoid bone transfer. Short-term outcomes are reassuring, though more research is needed for long-term graft follow-up and recurrent instability.

Am J Orthop. 2017;46(4):199-202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.

2. Rowe CR, Sakellarides HT. Factors related to recurrences of anterior dislocations of the shoulder. Clin Orthop. 1961;(20):40-48.

3. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

4. Sayegh ET, Mascarenhas R, Chalmers PN, Cole BJ, Verma NN, Romeo AA. Allograft reconstruction for glenoid bone loss in glenohumeral instability: a systematic review. Arthroscopy. 2014;30(12):1642-1649.

5. Griesser MJ, Harris JD, McCoy BW, et al. Complications and re-operati ons after Bristow-Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-292.

6. Young DC, Rockwood CA Jr. Complications of a failed Bristow procedure and their management. J Bone Joint Surg Am. 1991;73(7):969-981.

7. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

8. Mascarenhas R, Raleigh E, McRae S, Leiter J, Saltzman B, MacDonald PB. Iliac crest allograft glenoid reconstruction for recurrent anterior shoulder instability in athletes: surgical technique and results. Int J Shoulder Surg. 2014;8(4):127-132.

9. Yamamoto N, Muraki T, An KN, et al. The stabilizing mechanism of the Latarjet procedure: a cadaveric study. J Bone Joint Surg Am. 2013;95(15):1390-1397.

References

1. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.

2. Rowe CR, Sakellarides HT. Factors related to recurrences of anterior dislocations of the shoulder. Clin Orthop. 1961;(20):40-48.

3. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

4. Sayegh ET, Mascarenhas R, Chalmers PN, Cole BJ, Verma NN, Romeo AA. Allograft reconstruction for glenoid bone loss in glenohumeral instability: a systematic review. Arthroscopy. 2014;30(12):1642-1649.

5. Griesser MJ, Harris JD, McCoy BW, et al. Complications and re-operati ons after Bristow-Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-292.

6. Young DC, Rockwood CA Jr. Complications of a failed Bristow procedure and their management. J Bone Joint Surg Am. 1991;73(7):969-981.

7. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

8. Mascarenhas R, Raleigh E, McRae S, Leiter J, Saltzman B, MacDonald PB. Iliac crest allograft glenoid reconstruction for recurrent anterior shoulder instability in athletes: surgical technique and results. Int J Shoulder Surg. 2014;8(4):127-132.

9. Yamamoto N, Muraki T, An KN, et al. The stabilizing mechanism of the Latarjet procedure: a cadaveric study. J Bone Joint Surg Am. 2013;95(15):1390-1397.

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Systematic Review of Novel Synovial Fluid Markers and Polymerase Chain Reaction in the Diagnosis of Prosthetic Joint Infection

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Systematic Review of Novel Synovial Fluid Markers and Polymerase Chain Reaction in the Diagnosis of Prosthetic Joint Infection

Take-Home Points

  • Novel synovial markers and PCR have the potential to improve the detection of PJIs.
  • 10Difficult-to-detect infections of prosthetic joints pose a diagnostic problem to surgeons and can lead to suboptimal outcomes.
  • AD is a highly sensitive and specific synovial fluid marker for detecting PJIs.
  • AD has shown promising results in detecting low virulence organisms.
  • Studies are needed to determine how to best incorporate novel synovial markers and PCR to current diagnostic criteria in order to improve diagnostic accuracy.

Approximately 7 million Americans are living with a hip or knee replacement.1 According to projections, primary hip arthroplasties will increase by 174% and knee arthroplasties by 673% by 2030. Revision arthroplasties are projected to increase by 137% for hips and 601% for knees during the same time period.2 Infection and aseptic loosening are the most common causes of implant failure.3 The literature shows that infection is the most common cause of failure within 2 years after surgery and that aseptic loosening is the most common cause for late revision.3

Recent studies suggest that prosthetic joint infection (PJI) may be underreported because of difficulty making a diagnosis and that cases of aseptic loosening may in fact be attributable to infections with low-virulence organisms.2,3 These findings have led to new efforts to develop uniform criteria for diagnosing PJIs. In 2011, the Musculoskeletal Infection Society (MSIS) offered a new definition for PJI diagnosis, based on clinical and laboratory criteria, to increase the accuracy of PJI diagnosis.4 The MSIS committee acknowledged that PJI may be present even if these criteria are not met, particularly in the case of low-virulence organisms, as patients may not present with clinical signs of infection and may have normal inflammatory markers and joint aspirates. Reports of PJI cases misdiagnosed as aseptic loosening suggest that current screening and diagnostic tools are not sensitive enough to detect all infections and that PJI is likely underdiagnosed.

According to MSIS criteria, the diagnosis of PJI can be made when there is a sinus tract communicating with the prosthesis, when a pathogen is isolated by culture from 2 or more separate tissue or fluid samples obtained from the affected prosthetic joint, or when 4 of 6 criteria are met. The 6 criteria are (1) elevated serum erythrocyte sedimentation rate (ESR) (>30 mm/hour) and elevated C-reactive protein (CRP) level (>10 mg/L); (2) elevated synovial white blood cell (WBC) count (1100-4000 cells/μL); (3) elevated synovial polymorphonuclear leukocytes (>64%); (4) purulence in affected joint; (5) isolation of a microorganism in a culture of periprosthetic tissue or fluid; and (6) more than 5 neutrophils per high-power field in 5 high-power fields observed.

In this review article, we discuss recently developed novel synovial biomarkers and polymerase chain reaction (PCR) technologies that may help increase the sensitivity and specificity of diagnostic guidelines for PJI.

Methods

Using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses), we performed a systematic review of specific synovial fluid markers and PCR used in PJI diagnosis. In May 2016, we searched the PubMed database for these criteria: ((((((PCR[Text Word]) OR IL-6[Text Word]) OR leukocyte esterase[Text Word]) OR alpha defensin[Text Word]) AND ((“infection/diagnosis”[MeSH Terms] OR “infection/surgery”[MeSH Terms])))) AND (prosthetic joint infection[MeSH Terms] OR periprosthetic joint infection[MeSH Terms]).

We included patients who had undergone total hip, knee, or shoulder arthroplasty (THA, TKA, TSA). Index tests were PCR and the synovial fluid markers α-defensin (AD), interleukin 6 (IL-6), and leukocyte esterase (LE). Reference tests included joint fluid/serum analysis or tissue analysis (ESR/CRP level, cell count, culture, frozen section), which defined the MSIS criteria for PJI. Primary outcomes of interest were sensitivity and specificity, and secondary outcomes of interest included positive predictive value (PPV), negative predictive value (NPV), positive likelihood ratio (+LR), and negative likelihood ratio (–LR). Randomized controlled trials and controlled cohort studies in humans published within the past 10 years were included.

Results

Our full-text review yielded 15 papers that met our study inclusion criteria (Figure 1).

α-Defensin

One of the novel synovial biomarkers that has shown significant promise in diagnosing PJIs, even with difficult-to-detect organisms, is AD.

Figure 1.
Frangiamore and colleagues5 conducted a prospective study comparing patients with painful TSAs that required revision (n = 33). Patients were grouped based on objective clinical, laboratory, and histologic criteria of infection, which included preoperative clinical signs (swelling, sinus track, redness, drainage), elevated serum ESR or CRP, intraoperative gross findings (purulence, necrosis) and positive intraoperative frozen section. Synovial fluid aspiration was obtained preoperatively or intraoperatively. Of the 33 patients, 11 patients met the authors criteria for suspected PJI prior to final intraoperative culture results; 22 patients did not. Of the samples taken intraoperatively, Propionibacterium acnes was the most commonly isolated organism (9 cases), followed by coagulase-negative Staphylococcus (4 cases). AD demonstrated a sensitivity of 63%, specificity of 95%, +LR ratio of 12.1, and –LR ratio of 0.38. AD showed a strong association with growth of P acnes in the infected group (median signal-to-cutoff ratio, 4.45) compared with the noninfected group (median signal-to-cutoff ratio, 1.33) as well as strong associations with frozen section histology. Frangiamore and colleagues5 concluded that the use of AD in diagnosing PJIs with difficult-to-detect organisms was promising.

AD has shown even more impressive results as a biomarker for PJI in the hip and knee, where infection with low virulence organism is less common. In 2014, Deirmengian and colleagues6 conducted a prospective clinical study of 149 patients who underwent revision THA or TKA for aseptic loosening (n = 112) or PJI (n = 37) as defined by MSIS criteria. Aseptic loosening was diagnosed when there was no identifiable reason for pain, and MSIS criteria were not met. Synovial fluid aspirates were collected before or during surgery. AD correctly identified 143 of the 149 patients with confirmed infection with sensitivity of 97.3% (95% confidence interval [CI], 85.8%-99.6%) and specificity of 95.5% (95% CI, 89.9%-98.5%). Similarly, Bingham and colleagues7 conducted a retrospective clinical study of 61 assays done on 57 patients who underwent revision arthroplasty for PJI as defined by MSIS criteria. Synovial fluid aspirates were collected before or during surgery. AD correctly identified all 19 PJIs with sensitivity of 100% (95% CI, 79%-100%) and specificity of 95% (95% CI, 83%-99%). Sensitivity and specificity of the AD assay more accurately predicted infection than synovial cell count or serum ESR/CRP level did.

These results are supported by another prospective study by Deirmengian and colleagues8 differentiating aseptic failures and PJIs in THA or TKA. The sensitivity and specificity of AD in diagnosing PJI were 100% (95% CI, 85.05%-100%).

Table 1.
Synovial fluid was collected from 46 patients before and during surgery: 23 with PJI and 23 with aseptic failure as defined by MSIS criteria. All patients were tested for AD or LE. Of the 23 PJI cases, 18 were associated with a positive culture, with the most common organism being Staphylococcus epidermidis (n = 6). AD correctly diagnosed 100% of PJIs, whereas LE correctly diagnosed only 78%; the difference was statistically significant (P < 0.001).

In a prospective study of 102 patients who underwent revision THA or TKA secondary to aseptic loosening or PJI, Frangiamore and colleaguesalso demonstrated the value of AD as a diagnostic for PJI in primary and revision hip and knee arthroplasty.
Figure 2.
Based on MSIS criteria, 54 cases were classified as non-infected first-stage revision, 24 as infected first-stage revision, 35 as non-infected second-stage revision, and 3 as infected second-stage revision. For patients with first-stage revision THA or TKA, AD had sensitivity of 100% (95% CI, 86%-100%), specificity of 98% (95% CI, 90%-100%), PPV of 96% (95% CI, 80%-99%), and NPV of 100% (95% CI, 93%-100%). +LR was 54 (95% CI, 8-376), and –LR was 0. When combining all patients, AD outperformed serum ESR and CRP and synovial cell count as a biomarker for predicting PJI.

Table 1 and Figure 2 provide a concise review of the findings of each study.

Interleukin 6

Another synovial fluid biomarker that has shown promise in PJI diagnosis is IL-6. In 2015, Frangiamore and colleagues10 conducted a prospective clinical study of 32 patients who underwent revision TSA. Synovial fluid aspiration was obtained before or during surgery. MSIS criteria were used to establish the diagnosis of PJI. IL-6 had sensitivity of 87% and specificity of 90%, with +LR of 8.45 and –LR of 0.15 in predicting PJI. Synovial fluid IL-6 had strong associations with frozen section histology and growth of P acnes. Frangiamore and colleagues10 recommended an ideal IL-6 cutoff of 359.1 pg/mL and reported that, though not as accurate as AD, synovial fluid IL-6 levels can help predict positive cultures in patients who undergo revision TSA.

Lenski and Scherer11 conducted another retrospective clinical study of the diagnostic value of IL-6 in PJI.

Table 2.
Revision total joint arthroplasty (TJA) was performed for aseptic loosening (38 patients) or PJI (31 patients) based on criteria modeled after MSIS criteria. All joints were aspirated for synovial fluid IL-6, synovial fluid lactate dehydrogenase, synovial fluid glucose, synovial fluid lactate, synovial fluid WBCs, and serum CRP. IL-6 had sensitivity of 90.9%, specificity of 94.7%, +LR of 17.27, and –LR of 0.10. An optimal IL-6 cutoff value of 30,750 pg/mL was determined.

Randau and colleagues12 conducted a prospective clinical study of 120 patients who presented with painful THA or TKA and underwent revision for PJI, aseptic failure, or aseptic revision without signs of infection or loosening. Synovial fluid aspirate was collected before or during surgery.
Figure 3.
PJI was diagnosed with the modified MSIS criteria. IL-6 sensitivity and specificity depended on the cutoff value. A cutoff of >2100 pg/mL yielded sensitivity of 62.5% (95% CI, 43.69%-78.9%) and specificity of 85.71% (95% CI, 71.46%-94.57%), and a cutoff of >9000 pg/mL yielded sensitivity of 46.9% (95% CI, 29.09%-65.26%) and specificity of 97.62% (95% CI, 87.43%-99.94%). The authors concluded that synovial IL-6 is a more accurate marker than synovial WBC count.

Table 2 and Figure 3 provide a concise review of the findings of each study.

Leukocyte Esterase

LE strips are an inexpensive screening tool for PJI, according to some studies. In a prospective clinical study of 364 endoprosthetic joint (hip, knee, shoulder) interventions, Guenther and colleagues13 collected synovial fluid before surgery. Samples were tested with graded LE strips using PJI criteria set by the authors. Results were correlated with preoperative synovial fluid aspirations, serum CRP level, serum WBC count, and intraoperative histopathologic and microbiological findings. Whereas 293 (93.31%) of the 314 aseptic cases had negative test strip readings, 100% of the 50 infected cases were positive. LE had sensitivity of 100%, specificity of 96.5%, PPV of 82%, and NPV of 100%.

Wetters et al14 performed a prospective clinical study on 223 patients who underwent TKAs and THAs for suspected PJI based on having criteria defined by the authors of the study. Synovial fluid samples were collected either preoperatively or intraoperatively.

Table 3.
Using a synovial fluid WBC >3k WBC per microliter, the sensitivity, specificity, PPV, and NPV were 92.9%, 88.8%, 75%, and 97.2%, respectively. Using positive cultures or the presence of a draining sinus tract, the sensitivity, specificity, PPV, and NPV were 93.3%, 77%, 37.8%, and 98.7%, respectively. Of note, the most common organism found at the time of revision for infection was coagulase-negative Staphylococcus (6 out of 39).

Other authors have reported different findings that LE is an unreliable marker in PJI diagnosis. In one prospective clinical study of 85 patients who underwent primary or revision TSA, synovial fluid was collected during surgery.15 According to MSIS criteria, only 5 positive LE results predicted PJI among 21 primary and revision patients with positive cultures. Of the 7 revision patients who met the MSIS criteria for PJI, only 2 had a positive LE test. LE had sensitivity of 28.6%, specificity of 63.6%, PPV of 28.6%, and NPV of 87.5%. Six of the 7 revision patients grew P acnes. These results showed that LE was unreliable in detecting shoulder PJI.15

In another prospective clinical study, Tischler and colleagues16 enrolled 189 patients who underwent revision TKA or THA for aseptic failure or PJI as defined by the MSIS criteria. Synovial fluid was collected intraoperatively.
Figure 4.
Fifteen of the 52 patients with a MSIS defined PJI had positive cultures with the most common organism being coagulase-negative Staphylococcus (7). Two thresholds were used to consider a positive LE test. When using the first threshold that had a lower acceptance level for positivity, the sensitivity, specificity, PPV, and NPV were 79.2% (95% CI, 65.9%-89.2%), 80.8 (95% CI, 73.3%-87.1%), 61.8% (95% CI, 49.2%-73.3%), and 90.1% (95% CI, 84.3%-95.4%), respectively. When using the higher threshold, the sensitivity, specificity, PPV, and NPV were 66% (95% CI, 51.7%-78.5%), 97.1% (95% CI, 92.6%-99.2%), 89.7% (95% CI, 75.8%-97.1%), and 88% (95% CI, 81.7%-92.7%), respectively. Once again, these results were in line with LE not being a reliable marker in diagnosing PJI.

Table 3 and Figure 4 provide a concise review of the findings of each study.

 

 

Polymerase Chain Reaction

Studies have found that PCR analysis of synovial fluid is effective in detecting bacteria on the surface of implants removed during revision arthroplasties. Comparison of the 16S rRNA gene sequences of bacterial genomes showed a diverse range of bacterial species within biofilms on the surface of clinical and subclinical infections.17 These findings, along with those of other studies, suggest that PCR analysis of synovial fluid is useful in diagnosing PJI and identifying organisms and their sensitivities to antibiotics.

Gallo and colleagues18 performed a prospective clinical study on 115 patients who underwent revision TKAs or THAs. Synovial fluid was collected intraoperatively. PCR assays targeting the 16S rDNA were carried out on 101 patients. PJIs were classified based on criteria of the authors of this study, of which there were 42. The sensitivity, specificity, PPV, NPV, +LR, and -LR for PCR were 71.4% (95% CI, 61.5%-75.5%), 97% (95% CI, 91.7%-99.1%), 92.6% (95% CI, 79.8%-97.9%), 86.5% (95% CI, 81.8%-88.4%), 23.6 (95% CI, 5.9%-93.8%), and 0.29 (95% CI, 0.17%-0.49%), respectively. Of note the most common organism detected in 42 PJIs was coagulase-negative Staphylococcus.

Marin and colleagues19 conducted a prospective study of 122 patients who underwent arthroplasty for suspected infection or aseptic loosening as defined by the authors’ clinicohistopathologic criteria. Synovial fluid and biopsy specimens were collected during surgery, and 40 patients met the infection criteria. The authors concluded that 16S PCR is more specific and has better PPV than culture does as one positive 16S PCR resulted in a specificity and PPV of PJI of 96.3% and 91.7%, respectively. However, they noted that culture was more sensitive in diagnosing PJI.

Jacovides and colleagues20 conducted a prospective study on 82 patients undergoing primary TKA, revision TKA, and revision THA.

Table 4.
The synovial fluid aspirate was collected intraoperatively. PJI was diagnosed based on study specific criteria, which was a combination of clinical suspicion and standard laboratory tests (ESR, CRP, cell count and tissue culture). Using the study’s criteria, PJI was diagnosed in 23 samples, and 57 samples were diagnosed as uninfected. When 1 or more species were present, the PCR-Electrospray Ionization Mass Spectrometry (PCR-ESI/MS) yielded a sensitivity, specificity, PPV, and NPV value of 95.7%, 12.3%, 30.6%, and 87.5%, respectively.

The low PCR sensitivities reported in the literature were explained in a review by Hartley and Harris.21 They wrote that BR 16S rDNA and sequencing of PJI samples inherently have low sensitivity because of the contamination that can occur from the PCR reagents themselves or from sample mishandling. Techniques that address contaminant (extraneous DNA) removal, such as ultraviolet irradiation and DNase treatment, reduce Taq DNA polymerase activity, which reduces PCR sensitivity.
Figure 5.
The simplest way to avoid the effects of “low-level contaminants” is to decrease the number of PCR cycles, which also reduces sensitivity. However, loss of contaminants has resulted in increased specificities in studies that have used BR 16S rDNA PCR. The authors also stated that, when PCR incorporates cloning and sequencing, mass spectroscopic detection, or species-specific PCR, sensitivity is higher with increased contamination.

Table 4 and Figure 5 provide a concise review of the findings of each study.

Discussion

Although there is no gold standard for the diagnosis of PJIs, several clinical and laboratory criteria guidelines are currently used to help clinicians diagnose infections of prosthetic joints. However, despite standardization of diagnostic criteria, PJI continue to be a diagnostic challenge.

Table 5.
Diagnosing PJI has been difficult for several reasons, including lack of highly sensitive and specific clinical findings and laboratory tests, as well as difficulty in culturing organisms, particularly fastidious organisms. More effective diagnostic tools are needed to avoid failing to accurately detect infections which lead to poor outcomes in patients who undergo TJA. Moreover, PJIs with low-virulence organisms are especially troublesome, as they can present with normal serum inflammatory markers and negative synovial fluid analysis and cultures from joint aspiration.22

AD is a highly sensitive and specific synovial fluid biomarker in detecting common PJIs.

Table 6.
AD has a higher sensitivity and specificity for detecting PJI, as compared to synovial fluid cell count, culture, ESR, and CRP.15,16,19 Moreover, it has been shown that as many as 38% to 88% of patients diagnosed with aseptic loosening have PJIs with low-grade organisms,23,24 such as Coagulase-negative S acnes and P acnes. Several studies reviewed in this article have demonstrated that AD can detect infections with these low virulence organisms. Our systematic review supports the claim that AD can potentially be used as a screening tool for PJI with common, as well as difficult-to-detect, organisms.
Figure 6.
Our findings also support the claim that novel synovial fluid biomarkers have the potential to become of significant diagnostic use and help improve the ability to diagnose PJIs when combined with current laboratory and clinical diagnostic criteria.

In summary, 5 AD studies5-9 had sensitivity ranging from 63% to 100% and specificity ranging from 95% to 100%; 3 IL-6 studies10-12 had sensitivity ranging from 46.8% to 90.9% and specificity ranging from 85.7% to 97.6%; 4 LE studies13-16 had sensitivity ranging from 28.6% to 100% and specificity ranging from 63.6% to 96.5%; and 3 PCR studies18-20 had sensitivity ranging from 67.1% to 95.7% and specificity ranging from 12.3% to 97.8%. Sensitivity and specificity were consistently higher for AD than for IL-6, LE, and PCR, though there was significant overlap, heterogeneity, and variation across all the included studies.
Figure 7.
Moreover, the outlier study with the lowest sensitivity for AD (63%) was in patients undergoing TSA, where P acnes infection is more common and has been reported to be more difficult to detect by standard diagnostic tools. Tables 5, 6 and Figures 6, 7 provide the data for each of these studies.

Although the overall incidence of PJI is low, infected revisions remain a substantial financial burden to hospitals, as annual costs of infected revisions is estimated to exceed $1.62 billion by 2020.25 The usefulness of novel biomarkers and PCR in diagnosing PJI can be found in their ability to diagnose infections and facilitate appropriate early treatment. Several of these tests are readily available commercially and have the potential to be cost-effective diagnostic tools. The price to perform an AD test from Synovasure TM (Zimmer Biomet) ranges from $93 to $143. LE also provides an economic option for diagnosing PJI, as LE strips are commercially available for the cost of about 25 cents. PCR has also become an economic option, as costs can average $15.50 per sample extraction or PCR assay and $42.50 per amplicon sequence as reported in a study by Vandercam and colleagues.26 Future studies are needed to determine a diagnostic algorithm which incorporates these novel synovial markers to improve diagnostic accuracy of PJI in the most cost effective manner.

The current literature supports that AD can potentially be used to screen for PJI. Our findings suggest novel synovial fluid biomarkers may become of significant diagnostic use when combined with current laboratory and clinical diagnostic criteria. We recommend use of AD in cases in which pain, stiffness, and poor TJA outcome cannot be explained by errors in surgical technique, and infection is suspected despite MSIS criteria not being met.

The studies reviewed in this manuscript were limited in that none presented level I evidence (12 had level II evidence, and 3 had level III evidence), and there was significant heterogeneity (some studies used their own diagnostic standard, and others used the MSIS criteria). Larger scale prospective studies comparing serum ESR/CRP level and synovial fluid analysis to novel synovial markers are needed.

Am J Orthop. 2017;46(4):190-198. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Maradit Kremers H, Larson DR, Crowson CS, et al. Prevalence of total hip and knee replacement in the United States. J Bone Joint Surg Am. 2015;97(17):1386-1397.

2. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785.

3. Sharkey PF, Lichstein PM, Shen C, Tokarski AT, Parvizi J. Why are total knee arthroplasties failing today—has anything changed after 10 years? J Arthroplasty. 2014;29(9):1774-1778.

4. Butler-Wu SM, Burns EM, Pottinger PS, et al. Optimization of periprosthetic culture for diagnosis of Propionibacterium acnes prosthetic joint infection. J Clin Microbiol. 2011;49(7):2490-2495.

5. Frangiamore SJ, Saleh A, Grosso MJ, et al. α-Defensin as a predictor of periprosthetic shoulder infection. J Shoulder Elbow Surg. 2015;24(7):1021-1027.

6. Deirmengian C, Kardos K, Kilmartin P, Cameron A, Schiller K, Parvizi J. Combined measurement of synovial fluid α-defensin and C-reactive protein levels: highly accurate for diagnosing periprosthetic joint infection. J Bone Joint Surg Am. 2014;96(17):1439-1445.

7. Bingham J, Clarke H, Spangehl M, Schwartz A, Beauchamp C, Goldberg B. The alpha defensin-1 biomarker assay can be used to evaluate the potentially infected total joint arthroplasty. Clin Orthop Relat Res. 2014;472(12):4006-4009.

8. Deirmengian C, Kardos K, Kilmartin P, et al. The alpha-defensin test for periprosthetic joint infection outperforms the leukocyte esterase test strip. Clin Orthop Relat Res. 2015;473(1):198-203.

9. Frangiamore SJ, Gajewski ND, Saleh A, Farias-Kovac M, Barsoum WK, Higuera CA. α-Defensin accuracy to diagnose periprosthetic joint infection—best available test? J Arthroplasty. 2016;31(2):456-460.

10. Frangiamore SJ, Saleh A, Kovac MF, et al. Synovial fluid interleukin-6 as a predictor of periprosthetic shoulder infection. J Bone Joint Surg Am. 2015;97(1):63-70.

11. Lenski M, Scherer MA. Synovial IL-6 as inflammatory marker in periprosthetic joint infections. J Arthroplasty. 2014;29(6):1105-1109.

12. Randau TM, Friedrich MJ, Wimmer MD, et al. Interleukin-6 in serum and in synovial fluid enhances the differentiation between periprosthetic joint infection and aseptic loosening. PLoS One. 2014;9(2):e89045.

13. Guenther D, Kokenge T, Jacobs O, et al. Excluding infections in arthroplasty using leucocyte esterase test. Int Orthop. 2014;38(11):2385-2390.

14. Wetters NG, Berend KR, Lombardi AV, Morris MJ, Tucker TL, Della Valle CJ. Leukocyte esterase reagent strips for the rapid diagnosis of periprosthetic joint infection. J Arthroplasty. 2012;27(8 suppl):8-11.

15. Nelson GN, Paxton ES, Narzikul A, Williams G, Lazarus MD, Abboud JA. Leukocyte esterase in the diagnosis of shoulder periprosthetic joint infection. J Shoulder Elbow Surg. 2015;24(9):1421-1426.

16. Tischler EH, Cavanaugh PK, Parvizi J. Leukocyte esterase strip test: matched for Musculoskeletal Infection Society criteria. J Bone Joint Surg Am. 2014;96(22):1917-1920.

17. Dempsey KE, Riggio MP, Lennon A, et al. Identification of bacteria on the surface of clinically infected and non-infected prosthetic hip joints removed during revision arthroplasties by 16S rRNA gene sequencing and by microbiological culture. Arthritis Res Ther. 2007;9(3):R46.

18. Gallo J, Kolar M, Dendis M, et al. Culture and PCR analysis of joint fluid in the diagnosis of prosthetic joint infection. New Microbiol. 2008;31(1):97-104.

19. Marin M, Garcia-Lechuz JM, Alonso P, et al. Role of universal 16S rRNA gene PCR and sequencing in diagnosis of prosthetic joint infection. J Clin Microbiol. 2012;50(3):583-589.

20. Jacovides CL, Kreft R, Adeli B, Hozack B, Ehrlich GD, Parvizi J. Successful identification of pathogens by polymerase chain reaction (PCR)-based electron spray ionization time-of-flight mass spectrometry (ESI-TOF-MS) in culture-negative periprosthetic joint infection. J Bone Joint Surg Am. 2012;94(24):2247-2254.

21. Hartley JC, Harris KA. Molecular techniques for diagnosing prosthetic joint infections. J Antimicrob Chemother. 2014;69(suppl 1):i21-i24.

22. Zappe B, Graf S, Ochsner PE, Zimmerli W, Sendi P. Propionibacterium spp. in prosthetic joint infections: a diagnostic challenge. Arch Orthop Trauma Surg. 2008;128(10):1039-1046.

23. Rasouli MR, Harandi AA, Adeli B, Purtill JJ, Parvizi J. Revision total knee arthroplasty: infection should be ruled out in all cases. J Arthroplasty. 2012;27(6):1239-1243.e1-e2.

24. Hunt RW, Bond MJ, Pater GD. Psychological responses to cancer: a case for cancer support groups. Community Health Stud. 1990;14(1):35-38.

25. Kurtz SM, Lau E, Schmier J, Ong KL, Zhao K, Parvizi J. Infection burden for hip and knee arthroplasty in the United States. J Arthroplasty. 2008;23(7):984-991.

26. Vandercam B, Jeumont S, Cornu O, et al. Amplification-based DNA analysis in the diagnosis of prosthetic joint infection. J Mol Diagn. 2008;10(6):537-543.

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Acknowledgments: This article was presented as a paper at the annual meeting of the Clinical Orthopedic Society, September 29-October 1, 2016, New Orleans, LA, and at the Annual Pan Pacific Orthopaedic Congress, August 10-13, 2016, Waikoloa, HI.

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Take-Home Points

  • Novel synovial markers and PCR have the potential to improve the detection of PJIs.
  • 10Difficult-to-detect infections of prosthetic joints pose a diagnostic problem to surgeons and can lead to suboptimal outcomes.
  • AD is a highly sensitive and specific synovial fluid marker for detecting PJIs.
  • AD has shown promising results in detecting low virulence organisms.
  • Studies are needed to determine how to best incorporate novel synovial markers and PCR to current diagnostic criteria in order to improve diagnostic accuracy.

Approximately 7 million Americans are living with a hip or knee replacement.1 According to projections, primary hip arthroplasties will increase by 174% and knee arthroplasties by 673% by 2030. Revision arthroplasties are projected to increase by 137% for hips and 601% for knees during the same time period.2 Infection and aseptic loosening are the most common causes of implant failure.3 The literature shows that infection is the most common cause of failure within 2 years after surgery and that aseptic loosening is the most common cause for late revision.3

Recent studies suggest that prosthetic joint infection (PJI) may be underreported because of difficulty making a diagnosis and that cases of aseptic loosening may in fact be attributable to infections with low-virulence organisms.2,3 These findings have led to new efforts to develop uniform criteria for diagnosing PJIs. In 2011, the Musculoskeletal Infection Society (MSIS) offered a new definition for PJI diagnosis, based on clinical and laboratory criteria, to increase the accuracy of PJI diagnosis.4 The MSIS committee acknowledged that PJI may be present even if these criteria are not met, particularly in the case of low-virulence organisms, as patients may not present with clinical signs of infection and may have normal inflammatory markers and joint aspirates. Reports of PJI cases misdiagnosed as aseptic loosening suggest that current screening and diagnostic tools are not sensitive enough to detect all infections and that PJI is likely underdiagnosed.

According to MSIS criteria, the diagnosis of PJI can be made when there is a sinus tract communicating with the prosthesis, when a pathogen is isolated by culture from 2 or more separate tissue or fluid samples obtained from the affected prosthetic joint, or when 4 of 6 criteria are met. The 6 criteria are (1) elevated serum erythrocyte sedimentation rate (ESR) (>30 mm/hour) and elevated C-reactive protein (CRP) level (>10 mg/L); (2) elevated synovial white blood cell (WBC) count (1100-4000 cells/μL); (3) elevated synovial polymorphonuclear leukocytes (>64%); (4) purulence in affected joint; (5) isolation of a microorganism in a culture of periprosthetic tissue or fluid; and (6) more than 5 neutrophils per high-power field in 5 high-power fields observed.

In this review article, we discuss recently developed novel synovial biomarkers and polymerase chain reaction (PCR) technologies that may help increase the sensitivity and specificity of diagnostic guidelines for PJI.

Methods

Using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses), we performed a systematic review of specific synovial fluid markers and PCR used in PJI diagnosis. In May 2016, we searched the PubMed database for these criteria: ((((((PCR[Text Word]) OR IL-6[Text Word]) OR leukocyte esterase[Text Word]) OR alpha defensin[Text Word]) AND ((“infection/diagnosis”[MeSH Terms] OR “infection/surgery”[MeSH Terms])))) AND (prosthetic joint infection[MeSH Terms] OR periprosthetic joint infection[MeSH Terms]).

We included patients who had undergone total hip, knee, or shoulder arthroplasty (THA, TKA, TSA). Index tests were PCR and the synovial fluid markers α-defensin (AD), interleukin 6 (IL-6), and leukocyte esterase (LE). Reference tests included joint fluid/serum analysis or tissue analysis (ESR/CRP level, cell count, culture, frozen section), which defined the MSIS criteria for PJI. Primary outcomes of interest were sensitivity and specificity, and secondary outcomes of interest included positive predictive value (PPV), negative predictive value (NPV), positive likelihood ratio (+LR), and negative likelihood ratio (–LR). Randomized controlled trials and controlled cohort studies in humans published within the past 10 years were included.

Results

Our full-text review yielded 15 papers that met our study inclusion criteria (Figure 1).

α-Defensin

One of the novel synovial biomarkers that has shown significant promise in diagnosing PJIs, even with difficult-to-detect organisms, is AD.

Figure 1.
Frangiamore and colleagues5 conducted a prospective study comparing patients with painful TSAs that required revision (n = 33). Patients were grouped based on objective clinical, laboratory, and histologic criteria of infection, which included preoperative clinical signs (swelling, sinus track, redness, drainage), elevated serum ESR or CRP, intraoperative gross findings (purulence, necrosis) and positive intraoperative frozen section. Synovial fluid aspiration was obtained preoperatively or intraoperatively. Of the 33 patients, 11 patients met the authors criteria for suspected PJI prior to final intraoperative culture results; 22 patients did not. Of the samples taken intraoperatively, Propionibacterium acnes was the most commonly isolated organism (9 cases), followed by coagulase-negative Staphylococcus (4 cases). AD demonstrated a sensitivity of 63%, specificity of 95%, +LR ratio of 12.1, and –LR ratio of 0.38. AD showed a strong association with growth of P acnes in the infected group (median signal-to-cutoff ratio, 4.45) compared with the noninfected group (median signal-to-cutoff ratio, 1.33) as well as strong associations with frozen section histology. Frangiamore and colleagues5 concluded that the use of AD in diagnosing PJIs with difficult-to-detect organisms was promising.

AD has shown even more impressive results as a biomarker for PJI in the hip and knee, where infection with low virulence organism is less common. In 2014, Deirmengian and colleagues6 conducted a prospective clinical study of 149 patients who underwent revision THA or TKA for aseptic loosening (n = 112) or PJI (n = 37) as defined by MSIS criteria. Aseptic loosening was diagnosed when there was no identifiable reason for pain, and MSIS criteria were not met. Synovial fluid aspirates were collected before or during surgery. AD correctly identified 143 of the 149 patients with confirmed infection with sensitivity of 97.3% (95% confidence interval [CI], 85.8%-99.6%) and specificity of 95.5% (95% CI, 89.9%-98.5%). Similarly, Bingham and colleagues7 conducted a retrospective clinical study of 61 assays done on 57 patients who underwent revision arthroplasty for PJI as defined by MSIS criteria. Synovial fluid aspirates were collected before or during surgery. AD correctly identified all 19 PJIs with sensitivity of 100% (95% CI, 79%-100%) and specificity of 95% (95% CI, 83%-99%). Sensitivity and specificity of the AD assay more accurately predicted infection than synovial cell count or serum ESR/CRP level did.

These results are supported by another prospective study by Deirmengian and colleagues8 differentiating aseptic failures and PJIs in THA or TKA. The sensitivity and specificity of AD in diagnosing PJI were 100% (95% CI, 85.05%-100%).

Table 1.
Synovial fluid was collected from 46 patients before and during surgery: 23 with PJI and 23 with aseptic failure as defined by MSIS criteria. All patients were tested for AD or LE. Of the 23 PJI cases, 18 were associated with a positive culture, with the most common organism being Staphylococcus epidermidis (n = 6). AD correctly diagnosed 100% of PJIs, whereas LE correctly diagnosed only 78%; the difference was statistically significant (P < 0.001).

In a prospective study of 102 patients who underwent revision THA or TKA secondary to aseptic loosening or PJI, Frangiamore and colleaguesalso demonstrated the value of AD as a diagnostic for PJI in primary and revision hip and knee arthroplasty.
Figure 2.
Based on MSIS criteria, 54 cases were classified as non-infected first-stage revision, 24 as infected first-stage revision, 35 as non-infected second-stage revision, and 3 as infected second-stage revision. For patients with first-stage revision THA or TKA, AD had sensitivity of 100% (95% CI, 86%-100%), specificity of 98% (95% CI, 90%-100%), PPV of 96% (95% CI, 80%-99%), and NPV of 100% (95% CI, 93%-100%). +LR was 54 (95% CI, 8-376), and –LR was 0. When combining all patients, AD outperformed serum ESR and CRP and synovial cell count as a biomarker for predicting PJI.

Table 1 and Figure 2 provide a concise review of the findings of each study.

Interleukin 6

Another synovial fluid biomarker that has shown promise in PJI diagnosis is IL-6. In 2015, Frangiamore and colleagues10 conducted a prospective clinical study of 32 patients who underwent revision TSA. Synovial fluid aspiration was obtained before or during surgery. MSIS criteria were used to establish the diagnosis of PJI. IL-6 had sensitivity of 87% and specificity of 90%, with +LR of 8.45 and –LR of 0.15 in predicting PJI. Synovial fluid IL-6 had strong associations with frozen section histology and growth of P acnes. Frangiamore and colleagues10 recommended an ideal IL-6 cutoff of 359.1 pg/mL and reported that, though not as accurate as AD, synovial fluid IL-6 levels can help predict positive cultures in patients who undergo revision TSA.

Lenski and Scherer11 conducted another retrospective clinical study of the diagnostic value of IL-6 in PJI.

Table 2.
Revision total joint arthroplasty (TJA) was performed for aseptic loosening (38 patients) or PJI (31 patients) based on criteria modeled after MSIS criteria. All joints were aspirated for synovial fluid IL-6, synovial fluid lactate dehydrogenase, synovial fluid glucose, synovial fluid lactate, synovial fluid WBCs, and serum CRP. IL-6 had sensitivity of 90.9%, specificity of 94.7%, +LR of 17.27, and –LR of 0.10. An optimal IL-6 cutoff value of 30,750 pg/mL was determined.

Randau and colleagues12 conducted a prospective clinical study of 120 patients who presented with painful THA or TKA and underwent revision for PJI, aseptic failure, or aseptic revision without signs of infection or loosening. Synovial fluid aspirate was collected before or during surgery.
Figure 3.
PJI was diagnosed with the modified MSIS criteria. IL-6 sensitivity and specificity depended on the cutoff value. A cutoff of >2100 pg/mL yielded sensitivity of 62.5% (95% CI, 43.69%-78.9%) and specificity of 85.71% (95% CI, 71.46%-94.57%), and a cutoff of >9000 pg/mL yielded sensitivity of 46.9% (95% CI, 29.09%-65.26%) and specificity of 97.62% (95% CI, 87.43%-99.94%). The authors concluded that synovial IL-6 is a more accurate marker than synovial WBC count.

Table 2 and Figure 3 provide a concise review of the findings of each study.

Leukocyte Esterase

LE strips are an inexpensive screening tool for PJI, according to some studies. In a prospective clinical study of 364 endoprosthetic joint (hip, knee, shoulder) interventions, Guenther and colleagues13 collected synovial fluid before surgery. Samples were tested with graded LE strips using PJI criteria set by the authors. Results were correlated with preoperative synovial fluid aspirations, serum CRP level, serum WBC count, and intraoperative histopathologic and microbiological findings. Whereas 293 (93.31%) of the 314 aseptic cases had negative test strip readings, 100% of the 50 infected cases were positive. LE had sensitivity of 100%, specificity of 96.5%, PPV of 82%, and NPV of 100%.

Wetters et al14 performed a prospective clinical study on 223 patients who underwent TKAs and THAs for suspected PJI based on having criteria defined by the authors of the study. Synovial fluid samples were collected either preoperatively or intraoperatively.

Table 3.
Using a synovial fluid WBC >3k WBC per microliter, the sensitivity, specificity, PPV, and NPV were 92.9%, 88.8%, 75%, and 97.2%, respectively. Using positive cultures or the presence of a draining sinus tract, the sensitivity, specificity, PPV, and NPV were 93.3%, 77%, 37.8%, and 98.7%, respectively. Of note, the most common organism found at the time of revision for infection was coagulase-negative Staphylococcus (6 out of 39).

Other authors have reported different findings that LE is an unreliable marker in PJI diagnosis. In one prospective clinical study of 85 patients who underwent primary or revision TSA, synovial fluid was collected during surgery.15 According to MSIS criteria, only 5 positive LE results predicted PJI among 21 primary and revision patients with positive cultures. Of the 7 revision patients who met the MSIS criteria for PJI, only 2 had a positive LE test. LE had sensitivity of 28.6%, specificity of 63.6%, PPV of 28.6%, and NPV of 87.5%. Six of the 7 revision patients grew P acnes. These results showed that LE was unreliable in detecting shoulder PJI.15

In another prospective clinical study, Tischler and colleagues16 enrolled 189 patients who underwent revision TKA or THA for aseptic failure or PJI as defined by the MSIS criteria. Synovial fluid was collected intraoperatively.
Figure 4.
Fifteen of the 52 patients with a MSIS defined PJI had positive cultures with the most common organism being coagulase-negative Staphylococcus (7). Two thresholds were used to consider a positive LE test. When using the first threshold that had a lower acceptance level for positivity, the sensitivity, specificity, PPV, and NPV were 79.2% (95% CI, 65.9%-89.2%), 80.8 (95% CI, 73.3%-87.1%), 61.8% (95% CI, 49.2%-73.3%), and 90.1% (95% CI, 84.3%-95.4%), respectively. When using the higher threshold, the sensitivity, specificity, PPV, and NPV were 66% (95% CI, 51.7%-78.5%), 97.1% (95% CI, 92.6%-99.2%), 89.7% (95% CI, 75.8%-97.1%), and 88% (95% CI, 81.7%-92.7%), respectively. Once again, these results were in line with LE not being a reliable marker in diagnosing PJI.

Table 3 and Figure 4 provide a concise review of the findings of each study.

 

 

Polymerase Chain Reaction

Studies have found that PCR analysis of synovial fluid is effective in detecting bacteria on the surface of implants removed during revision arthroplasties. Comparison of the 16S rRNA gene sequences of bacterial genomes showed a diverse range of bacterial species within biofilms on the surface of clinical and subclinical infections.17 These findings, along with those of other studies, suggest that PCR analysis of synovial fluid is useful in diagnosing PJI and identifying organisms and their sensitivities to antibiotics.

Gallo and colleagues18 performed a prospective clinical study on 115 patients who underwent revision TKAs or THAs. Synovial fluid was collected intraoperatively. PCR assays targeting the 16S rDNA were carried out on 101 patients. PJIs were classified based on criteria of the authors of this study, of which there were 42. The sensitivity, specificity, PPV, NPV, +LR, and -LR for PCR were 71.4% (95% CI, 61.5%-75.5%), 97% (95% CI, 91.7%-99.1%), 92.6% (95% CI, 79.8%-97.9%), 86.5% (95% CI, 81.8%-88.4%), 23.6 (95% CI, 5.9%-93.8%), and 0.29 (95% CI, 0.17%-0.49%), respectively. Of note the most common organism detected in 42 PJIs was coagulase-negative Staphylococcus.

Marin and colleagues19 conducted a prospective study of 122 patients who underwent arthroplasty for suspected infection or aseptic loosening as defined by the authors’ clinicohistopathologic criteria. Synovial fluid and biopsy specimens were collected during surgery, and 40 patients met the infection criteria. The authors concluded that 16S PCR is more specific and has better PPV than culture does as one positive 16S PCR resulted in a specificity and PPV of PJI of 96.3% and 91.7%, respectively. However, they noted that culture was more sensitive in diagnosing PJI.

Jacovides and colleagues20 conducted a prospective study on 82 patients undergoing primary TKA, revision TKA, and revision THA.

Table 4.
The synovial fluid aspirate was collected intraoperatively. PJI was diagnosed based on study specific criteria, which was a combination of clinical suspicion and standard laboratory tests (ESR, CRP, cell count and tissue culture). Using the study’s criteria, PJI was diagnosed in 23 samples, and 57 samples were diagnosed as uninfected. When 1 or more species were present, the PCR-Electrospray Ionization Mass Spectrometry (PCR-ESI/MS) yielded a sensitivity, specificity, PPV, and NPV value of 95.7%, 12.3%, 30.6%, and 87.5%, respectively.

The low PCR sensitivities reported in the literature were explained in a review by Hartley and Harris.21 They wrote that BR 16S rDNA and sequencing of PJI samples inherently have low sensitivity because of the contamination that can occur from the PCR reagents themselves or from sample mishandling. Techniques that address contaminant (extraneous DNA) removal, such as ultraviolet irradiation and DNase treatment, reduce Taq DNA polymerase activity, which reduces PCR sensitivity.
Figure 5.
The simplest way to avoid the effects of “low-level contaminants” is to decrease the number of PCR cycles, which also reduces sensitivity. However, loss of contaminants has resulted in increased specificities in studies that have used BR 16S rDNA PCR. The authors also stated that, when PCR incorporates cloning and sequencing, mass spectroscopic detection, or species-specific PCR, sensitivity is higher with increased contamination.

Table 4 and Figure 5 provide a concise review of the findings of each study.

Discussion

Although there is no gold standard for the diagnosis of PJIs, several clinical and laboratory criteria guidelines are currently used to help clinicians diagnose infections of prosthetic joints. However, despite standardization of diagnostic criteria, PJI continue to be a diagnostic challenge.

Table 5.
Diagnosing PJI has been difficult for several reasons, including lack of highly sensitive and specific clinical findings and laboratory tests, as well as difficulty in culturing organisms, particularly fastidious organisms. More effective diagnostic tools are needed to avoid failing to accurately detect infections which lead to poor outcomes in patients who undergo TJA. Moreover, PJIs with low-virulence organisms are especially troublesome, as they can present with normal serum inflammatory markers and negative synovial fluid analysis and cultures from joint aspiration.22

AD is a highly sensitive and specific synovial fluid biomarker in detecting common PJIs.

Table 6.
AD has a higher sensitivity and specificity for detecting PJI, as compared to synovial fluid cell count, culture, ESR, and CRP.15,16,19 Moreover, it has been shown that as many as 38% to 88% of patients diagnosed with aseptic loosening have PJIs with low-grade organisms,23,24 such as Coagulase-negative S acnes and P acnes. Several studies reviewed in this article have demonstrated that AD can detect infections with these low virulence organisms. Our systematic review supports the claim that AD can potentially be used as a screening tool for PJI with common, as well as difficult-to-detect, organisms.
Figure 6.
Our findings also support the claim that novel synovial fluid biomarkers have the potential to become of significant diagnostic use and help improve the ability to diagnose PJIs when combined with current laboratory and clinical diagnostic criteria.

In summary, 5 AD studies5-9 had sensitivity ranging from 63% to 100% and specificity ranging from 95% to 100%; 3 IL-6 studies10-12 had sensitivity ranging from 46.8% to 90.9% and specificity ranging from 85.7% to 97.6%; 4 LE studies13-16 had sensitivity ranging from 28.6% to 100% and specificity ranging from 63.6% to 96.5%; and 3 PCR studies18-20 had sensitivity ranging from 67.1% to 95.7% and specificity ranging from 12.3% to 97.8%. Sensitivity and specificity were consistently higher for AD than for IL-6, LE, and PCR, though there was significant overlap, heterogeneity, and variation across all the included studies.
Figure 7.
Moreover, the outlier study with the lowest sensitivity for AD (63%) was in patients undergoing TSA, where P acnes infection is more common and has been reported to be more difficult to detect by standard diagnostic tools. Tables 5, 6 and Figures 6, 7 provide the data for each of these studies.

Although the overall incidence of PJI is low, infected revisions remain a substantial financial burden to hospitals, as annual costs of infected revisions is estimated to exceed $1.62 billion by 2020.25 The usefulness of novel biomarkers and PCR in diagnosing PJI can be found in their ability to diagnose infections and facilitate appropriate early treatment. Several of these tests are readily available commercially and have the potential to be cost-effective diagnostic tools. The price to perform an AD test from Synovasure TM (Zimmer Biomet) ranges from $93 to $143. LE also provides an economic option for diagnosing PJI, as LE strips are commercially available for the cost of about 25 cents. PCR has also become an economic option, as costs can average $15.50 per sample extraction or PCR assay and $42.50 per amplicon sequence as reported in a study by Vandercam and colleagues.26 Future studies are needed to determine a diagnostic algorithm which incorporates these novel synovial markers to improve diagnostic accuracy of PJI in the most cost effective manner.

The current literature supports that AD can potentially be used to screen for PJI. Our findings suggest novel synovial fluid biomarkers may become of significant diagnostic use when combined with current laboratory and clinical diagnostic criteria. We recommend use of AD in cases in which pain, stiffness, and poor TJA outcome cannot be explained by errors in surgical technique, and infection is suspected despite MSIS criteria not being met.

The studies reviewed in this manuscript were limited in that none presented level I evidence (12 had level II evidence, and 3 had level III evidence), and there was significant heterogeneity (some studies used their own diagnostic standard, and others used the MSIS criteria). Larger scale prospective studies comparing serum ESR/CRP level and synovial fluid analysis to novel synovial markers are needed.

Am J Orthop. 2017;46(4):190-198. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Novel synovial markers and PCR have the potential to improve the detection of PJIs.
  • 10Difficult-to-detect infections of prosthetic joints pose a diagnostic problem to surgeons and can lead to suboptimal outcomes.
  • AD is a highly sensitive and specific synovial fluid marker for detecting PJIs.
  • AD has shown promising results in detecting low virulence organisms.
  • Studies are needed to determine how to best incorporate novel synovial markers and PCR to current diagnostic criteria in order to improve diagnostic accuracy.

Approximately 7 million Americans are living with a hip or knee replacement.1 According to projections, primary hip arthroplasties will increase by 174% and knee arthroplasties by 673% by 2030. Revision arthroplasties are projected to increase by 137% for hips and 601% for knees during the same time period.2 Infection and aseptic loosening are the most common causes of implant failure.3 The literature shows that infection is the most common cause of failure within 2 years after surgery and that aseptic loosening is the most common cause for late revision.3

Recent studies suggest that prosthetic joint infection (PJI) may be underreported because of difficulty making a diagnosis and that cases of aseptic loosening may in fact be attributable to infections with low-virulence organisms.2,3 These findings have led to new efforts to develop uniform criteria for diagnosing PJIs. In 2011, the Musculoskeletal Infection Society (MSIS) offered a new definition for PJI diagnosis, based on clinical and laboratory criteria, to increase the accuracy of PJI diagnosis.4 The MSIS committee acknowledged that PJI may be present even if these criteria are not met, particularly in the case of low-virulence organisms, as patients may not present with clinical signs of infection and may have normal inflammatory markers and joint aspirates. Reports of PJI cases misdiagnosed as aseptic loosening suggest that current screening and diagnostic tools are not sensitive enough to detect all infections and that PJI is likely underdiagnosed.

According to MSIS criteria, the diagnosis of PJI can be made when there is a sinus tract communicating with the prosthesis, when a pathogen is isolated by culture from 2 or more separate tissue or fluid samples obtained from the affected prosthetic joint, or when 4 of 6 criteria are met. The 6 criteria are (1) elevated serum erythrocyte sedimentation rate (ESR) (>30 mm/hour) and elevated C-reactive protein (CRP) level (>10 mg/L); (2) elevated synovial white blood cell (WBC) count (1100-4000 cells/μL); (3) elevated synovial polymorphonuclear leukocytes (>64%); (4) purulence in affected joint; (5) isolation of a microorganism in a culture of periprosthetic tissue or fluid; and (6) more than 5 neutrophils per high-power field in 5 high-power fields observed.

In this review article, we discuss recently developed novel synovial biomarkers and polymerase chain reaction (PCR) technologies that may help increase the sensitivity and specificity of diagnostic guidelines for PJI.

Methods

Using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses), we performed a systematic review of specific synovial fluid markers and PCR used in PJI diagnosis. In May 2016, we searched the PubMed database for these criteria: ((((((PCR[Text Word]) OR IL-6[Text Word]) OR leukocyte esterase[Text Word]) OR alpha defensin[Text Word]) AND ((“infection/diagnosis”[MeSH Terms] OR “infection/surgery”[MeSH Terms])))) AND (prosthetic joint infection[MeSH Terms] OR periprosthetic joint infection[MeSH Terms]).

We included patients who had undergone total hip, knee, or shoulder arthroplasty (THA, TKA, TSA). Index tests were PCR and the synovial fluid markers α-defensin (AD), interleukin 6 (IL-6), and leukocyte esterase (LE). Reference tests included joint fluid/serum analysis or tissue analysis (ESR/CRP level, cell count, culture, frozen section), which defined the MSIS criteria for PJI. Primary outcomes of interest were sensitivity and specificity, and secondary outcomes of interest included positive predictive value (PPV), negative predictive value (NPV), positive likelihood ratio (+LR), and negative likelihood ratio (–LR). Randomized controlled trials and controlled cohort studies in humans published within the past 10 years were included.

Results

Our full-text review yielded 15 papers that met our study inclusion criteria (Figure 1).

α-Defensin

One of the novel synovial biomarkers that has shown significant promise in diagnosing PJIs, even with difficult-to-detect organisms, is AD.

Figure 1.
Frangiamore and colleagues5 conducted a prospective study comparing patients with painful TSAs that required revision (n = 33). Patients were grouped based on objective clinical, laboratory, and histologic criteria of infection, which included preoperative clinical signs (swelling, sinus track, redness, drainage), elevated serum ESR or CRP, intraoperative gross findings (purulence, necrosis) and positive intraoperative frozen section. Synovial fluid aspiration was obtained preoperatively or intraoperatively. Of the 33 patients, 11 patients met the authors criteria for suspected PJI prior to final intraoperative culture results; 22 patients did not. Of the samples taken intraoperatively, Propionibacterium acnes was the most commonly isolated organism (9 cases), followed by coagulase-negative Staphylococcus (4 cases). AD demonstrated a sensitivity of 63%, specificity of 95%, +LR ratio of 12.1, and –LR ratio of 0.38. AD showed a strong association with growth of P acnes in the infected group (median signal-to-cutoff ratio, 4.45) compared with the noninfected group (median signal-to-cutoff ratio, 1.33) as well as strong associations with frozen section histology. Frangiamore and colleagues5 concluded that the use of AD in diagnosing PJIs with difficult-to-detect organisms was promising.

AD has shown even more impressive results as a biomarker for PJI in the hip and knee, where infection with low virulence organism is less common. In 2014, Deirmengian and colleagues6 conducted a prospective clinical study of 149 patients who underwent revision THA or TKA for aseptic loosening (n = 112) or PJI (n = 37) as defined by MSIS criteria. Aseptic loosening was diagnosed when there was no identifiable reason for pain, and MSIS criteria were not met. Synovial fluid aspirates were collected before or during surgery. AD correctly identified 143 of the 149 patients with confirmed infection with sensitivity of 97.3% (95% confidence interval [CI], 85.8%-99.6%) and specificity of 95.5% (95% CI, 89.9%-98.5%). Similarly, Bingham and colleagues7 conducted a retrospective clinical study of 61 assays done on 57 patients who underwent revision arthroplasty for PJI as defined by MSIS criteria. Synovial fluid aspirates were collected before or during surgery. AD correctly identified all 19 PJIs with sensitivity of 100% (95% CI, 79%-100%) and specificity of 95% (95% CI, 83%-99%). Sensitivity and specificity of the AD assay more accurately predicted infection than synovial cell count or serum ESR/CRP level did.

These results are supported by another prospective study by Deirmengian and colleagues8 differentiating aseptic failures and PJIs in THA or TKA. The sensitivity and specificity of AD in diagnosing PJI were 100% (95% CI, 85.05%-100%).

Table 1.
Synovial fluid was collected from 46 patients before and during surgery: 23 with PJI and 23 with aseptic failure as defined by MSIS criteria. All patients were tested for AD or LE. Of the 23 PJI cases, 18 were associated with a positive culture, with the most common organism being Staphylococcus epidermidis (n = 6). AD correctly diagnosed 100% of PJIs, whereas LE correctly diagnosed only 78%; the difference was statistically significant (P < 0.001).

In a prospective study of 102 patients who underwent revision THA or TKA secondary to aseptic loosening or PJI, Frangiamore and colleaguesalso demonstrated the value of AD as a diagnostic for PJI in primary and revision hip and knee arthroplasty.
Figure 2.
Based on MSIS criteria, 54 cases were classified as non-infected first-stage revision, 24 as infected first-stage revision, 35 as non-infected second-stage revision, and 3 as infected second-stage revision. For patients with first-stage revision THA or TKA, AD had sensitivity of 100% (95% CI, 86%-100%), specificity of 98% (95% CI, 90%-100%), PPV of 96% (95% CI, 80%-99%), and NPV of 100% (95% CI, 93%-100%). +LR was 54 (95% CI, 8-376), and –LR was 0. When combining all patients, AD outperformed serum ESR and CRP and synovial cell count as a biomarker for predicting PJI.

Table 1 and Figure 2 provide a concise review of the findings of each study.

Interleukin 6

Another synovial fluid biomarker that has shown promise in PJI diagnosis is IL-6. In 2015, Frangiamore and colleagues10 conducted a prospective clinical study of 32 patients who underwent revision TSA. Synovial fluid aspiration was obtained before or during surgery. MSIS criteria were used to establish the diagnosis of PJI. IL-6 had sensitivity of 87% and specificity of 90%, with +LR of 8.45 and –LR of 0.15 in predicting PJI. Synovial fluid IL-6 had strong associations with frozen section histology and growth of P acnes. Frangiamore and colleagues10 recommended an ideal IL-6 cutoff of 359.1 pg/mL and reported that, though not as accurate as AD, synovial fluid IL-6 levels can help predict positive cultures in patients who undergo revision TSA.

Lenski and Scherer11 conducted another retrospective clinical study of the diagnostic value of IL-6 in PJI.

Table 2.
Revision total joint arthroplasty (TJA) was performed for aseptic loosening (38 patients) or PJI (31 patients) based on criteria modeled after MSIS criteria. All joints were aspirated for synovial fluid IL-6, synovial fluid lactate dehydrogenase, synovial fluid glucose, synovial fluid lactate, synovial fluid WBCs, and serum CRP. IL-6 had sensitivity of 90.9%, specificity of 94.7%, +LR of 17.27, and –LR of 0.10. An optimal IL-6 cutoff value of 30,750 pg/mL was determined.

Randau and colleagues12 conducted a prospective clinical study of 120 patients who presented with painful THA or TKA and underwent revision for PJI, aseptic failure, or aseptic revision without signs of infection or loosening. Synovial fluid aspirate was collected before or during surgery.
Figure 3.
PJI was diagnosed with the modified MSIS criteria. IL-6 sensitivity and specificity depended on the cutoff value. A cutoff of >2100 pg/mL yielded sensitivity of 62.5% (95% CI, 43.69%-78.9%) and specificity of 85.71% (95% CI, 71.46%-94.57%), and a cutoff of >9000 pg/mL yielded sensitivity of 46.9% (95% CI, 29.09%-65.26%) and specificity of 97.62% (95% CI, 87.43%-99.94%). The authors concluded that synovial IL-6 is a more accurate marker than synovial WBC count.

Table 2 and Figure 3 provide a concise review of the findings of each study.

Leukocyte Esterase

LE strips are an inexpensive screening tool for PJI, according to some studies. In a prospective clinical study of 364 endoprosthetic joint (hip, knee, shoulder) interventions, Guenther and colleagues13 collected synovial fluid before surgery. Samples were tested with graded LE strips using PJI criteria set by the authors. Results were correlated with preoperative synovial fluid aspirations, serum CRP level, serum WBC count, and intraoperative histopathologic and microbiological findings. Whereas 293 (93.31%) of the 314 aseptic cases had negative test strip readings, 100% of the 50 infected cases were positive. LE had sensitivity of 100%, specificity of 96.5%, PPV of 82%, and NPV of 100%.

Wetters et al14 performed a prospective clinical study on 223 patients who underwent TKAs and THAs for suspected PJI based on having criteria defined by the authors of the study. Synovial fluid samples were collected either preoperatively or intraoperatively.

Table 3.
Using a synovial fluid WBC >3k WBC per microliter, the sensitivity, specificity, PPV, and NPV were 92.9%, 88.8%, 75%, and 97.2%, respectively. Using positive cultures or the presence of a draining sinus tract, the sensitivity, specificity, PPV, and NPV were 93.3%, 77%, 37.8%, and 98.7%, respectively. Of note, the most common organism found at the time of revision for infection was coagulase-negative Staphylococcus (6 out of 39).

Other authors have reported different findings that LE is an unreliable marker in PJI diagnosis. In one prospective clinical study of 85 patients who underwent primary or revision TSA, synovial fluid was collected during surgery.15 According to MSIS criteria, only 5 positive LE results predicted PJI among 21 primary and revision patients with positive cultures. Of the 7 revision patients who met the MSIS criteria for PJI, only 2 had a positive LE test. LE had sensitivity of 28.6%, specificity of 63.6%, PPV of 28.6%, and NPV of 87.5%. Six of the 7 revision patients grew P acnes. These results showed that LE was unreliable in detecting shoulder PJI.15

In another prospective clinical study, Tischler and colleagues16 enrolled 189 patients who underwent revision TKA or THA for aseptic failure or PJI as defined by the MSIS criteria. Synovial fluid was collected intraoperatively.
Figure 4.
Fifteen of the 52 patients with a MSIS defined PJI had positive cultures with the most common organism being coagulase-negative Staphylococcus (7). Two thresholds were used to consider a positive LE test. When using the first threshold that had a lower acceptance level for positivity, the sensitivity, specificity, PPV, and NPV were 79.2% (95% CI, 65.9%-89.2%), 80.8 (95% CI, 73.3%-87.1%), 61.8% (95% CI, 49.2%-73.3%), and 90.1% (95% CI, 84.3%-95.4%), respectively. When using the higher threshold, the sensitivity, specificity, PPV, and NPV were 66% (95% CI, 51.7%-78.5%), 97.1% (95% CI, 92.6%-99.2%), 89.7% (95% CI, 75.8%-97.1%), and 88% (95% CI, 81.7%-92.7%), respectively. Once again, these results were in line with LE not being a reliable marker in diagnosing PJI.

Table 3 and Figure 4 provide a concise review of the findings of each study.

 

 

Polymerase Chain Reaction

Studies have found that PCR analysis of synovial fluid is effective in detecting bacteria on the surface of implants removed during revision arthroplasties. Comparison of the 16S rRNA gene sequences of bacterial genomes showed a diverse range of bacterial species within biofilms on the surface of clinical and subclinical infections.17 These findings, along with those of other studies, suggest that PCR analysis of synovial fluid is useful in diagnosing PJI and identifying organisms and their sensitivities to antibiotics.

Gallo and colleagues18 performed a prospective clinical study on 115 patients who underwent revision TKAs or THAs. Synovial fluid was collected intraoperatively. PCR assays targeting the 16S rDNA were carried out on 101 patients. PJIs were classified based on criteria of the authors of this study, of which there were 42. The sensitivity, specificity, PPV, NPV, +LR, and -LR for PCR were 71.4% (95% CI, 61.5%-75.5%), 97% (95% CI, 91.7%-99.1%), 92.6% (95% CI, 79.8%-97.9%), 86.5% (95% CI, 81.8%-88.4%), 23.6 (95% CI, 5.9%-93.8%), and 0.29 (95% CI, 0.17%-0.49%), respectively. Of note the most common organism detected in 42 PJIs was coagulase-negative Staphylococcus.

Marin and colleagues19 conducted a prospective study of 122 patients who underwent arthroplasty for suspected infection or aseptic loosening as defined by the authors’ clinicohistopathologic criteria. Synovial fluid and biopsy specimens were collected during surgery, and 40 patients met the infection criteria. The authors concluded that 16S PCR is more specific and has better PPV than culture does as one positive 16S PCR resulted in a specificity and PPV of PJI of 96.3% and 91.7%, respectively. However, they noted that culture was more sensitive in diagnosing PJI.

Jacovides and colleagues20 conducted a prospective study on 82 patients undergoing primary TKA, revision TKA, and revision THA.

Table 4.
The synovial fluid aspirate was collected intraoperatively. PJI was diagnosed based on study specific criteria, which was a combination of clinical suspicion and standard laboratory tests (ESR, CRP, cell count and tissue culture). Using the study’s criteria, PJI was diagnosed in 23 samples, and 57 samples were diagnosed as uninfected. When 1 or more species were present, the PCR-Electrospray Ionization Mass Spectrometry (PCR-ESI/MS) yielded a sensitivity, specificity, PPV, and NPV value of 95.7%, 12.3%, 30.6%, and 87.5%, respectively.

The low PCR sensitivities reported in the literature were explained in a review by Hartley and Harris.21 They wrote that BR 16S rDNA and sequencing of PJI samples inherently have low sensitivity because of the contamination that can occur from the PCR reagents themselves or from sample mishandling. Techniques that address contaminant (extraneous DNA) removal, such as ultraviolet irradiation and DNase treatment, reduce Taq DNA polymerase activity, which reduces PCR sensitivity.
Figure 5.
The simplest way to avoid the effects of “low-level contaminants” is to decrease the number of PCR cycles, which also reduces sensitivity. However, loss of contaminants has resulted in increased specificities in studies that have used BR 16S rDNA PCR. The authors also stated that, when PCR incorporates cloning and sequencing, mass spectroscopic detection, or species-specific PCR, sensitivity is higher with increased contamination.

Table 4 and Figure 5 provide a concise review of the findings of each study.

Discussion

Although there is no gold standard for the diagnosis of PJIs, several clinical and laboratory criteria guidelines are currently used to help clinicians diagnose infections of prosthetic joints. However, despite standardization of diagnostic criteria, PJI continue to be a diagnostic challenge.

Table 5.
Diagnosing PJI has been difficult for several reasons, including lack of highly sensitive and specific clinical findings and laboratory tests, as well as difficulty in culturing organisms, particularly fastidious organisms. More effective diagnostic tools are needed to avoid failing to accurately detect infections which lead to poor outcomes in patients who undergo TJA. Moreover, PJIs with low-virulence organisms are especially troublesome, as they can present with normal serum inflammatory markers and negative synovial fluid analysis and cultures from joint aspiration.22

AD is a highly sensitive and specific synovial fluid biomarker in detecting common PJIs.

Table 6.
AD has a higher sensitivity and specificity for detecting PJI, as compared to synovial fluid cell count, culture, ESR, and CRP.15,16,19 Moreover, it has been shown that as many as 38% to 88% of patients diagnosed with aseptic loosening have PJIs with low-grade organisms,23,24 such as Coagulase-negative S acnes and P acnes. Several studies reviewed in this article have demonstrated that AD can detect infections with these low virulence organisms. Our systematic review supports the claim that AD can potentially be used as a screening tool for PJI with common, as well as difficult-to-detect, organisms.
Figure 6.
Our findings also support the claim that novel synovial fluid biomarkers have the potential to become of significant diagnostic use and help improve the ability to diagnose PJIs when combined with current laboratory and clinical diagnostic criteria.

In summary, 5 AD studies5-9 had sensitivity ranging from 63% to 100% and specificity ranging from 95% to 100%; 3 IL-6 studies10-12 had sensitivity ranging from 46.8% to 90.9% and specificity ranging from 85.7% to 97.6%; 4 LE studies13-16 had sensitivity ranging from 28.6% to 100% and specificity ranging from 63.6% to 96.5%; and 3 PCR studies18-20 had sensitivity ranging from 67.1% to 95.7% and specificity ranging from 12.3% to 97.8%. Sensitivity and specificity were consistently higher for AD than for IL-6, LE, and PCR, though there was significant overlap, heterogeneity, and variation across all the included studies.
Figure 7.
Moreover, the outlier study with the lowest sensitivity for AD (63%) was in patients undergoing TSA, where P acnes infection is more common and has been reported to be more difficult to detect by standard diagnostic tools. Tables 5, 6 and Figures 6, 7 provide the data for each of these studies.

Although the overall incidence of PJI is low, infected revisions remain a substantial financial burden to hospitals, as annual costs of infected revisions is estimated to exceed $1.62 billion by 2020.25 The usefulness of novel biomarkers and PCR in diagnosing PJI can be found in their ability to diagnose infections and facilitate appropriate early treatment. Several of these tests are readily available commercially and have the potential to be cost-effective diagnostic tools. The price to perform an AD test from Synovasure TM (Zimmer Biomet) ranges from $93 to $143. LE also provides an economic option for diagnosing PJI, as LE strips are commercially available for the cost of about 25 cents. PCR has also become an economic option, as costs can average $15.50 per sample extraction or PCR assay and $42.50 per amplicon sequence as reported in a study by Vandercam and colleagues.26 Future studies are needed to determine a diagnostic algorithm which incorporates these novel synovial markers to improve diagnostic accuracy of PJI in the most cost effective manner.

The current literature supports that AD can potentially be used to screen for PJI. Our findings suggest novel synovial fluid biomarkers may become of significant diagnostic use when combined with current laboratory and clinical diagnostic criteria. We recommend use of AD in cases in which pain, stiffness, and poor TJA outcome cannot be explained by errors in surgical technique, and infection is suspected despite MSIS criteria not being met.

The studies reviewed in this manuscript were limited in that none presented level I evidence (12 had level II evidence, and 3 had level III evidence), and there was significant heterogeneity (some studies used their own diagnostic standard, and others used the MSIS criteria). Larger scale prospective studies comparing serum ESR/CRP level and synovial fluid analysis to novel synovial markers are needed.

Am J Orthop. 2017;46(4):190-198. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Maradit Kremers H, Larson DR, Crowson CS, et al. Prevalence of total hip and knee replacement in the United States. J Bone Joint Surg Am. 2015;97(17):1386-1397.

2. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785.

3. Sharkey PF, Lichstein PM, Shen C, Tokarski AT, Parvizi J. Why are total knee arthroplasties failing today—has anything changed after 10 years? J Arthroplasty. 2014;29(9):1774-1778.

4. Butler-Wu SM, Burns EM, Pottinger PS, et al. Optimization of periprosthetic culture for diagnosis of Propionibacterium acnes prosthetic joint infection. J Clin Microbiol. 2011;49(7):2490-2495.

5. Frangiamore SJ, Saleh A, Grosso MJ, et al. α-Defensin as a predictor of periprosthetic shoulder infection. J Shoulder Elbow Surg. 2015;24(7):1021-1027.

6. Deirmengian C, Kardos K, Kilmartin P, Cameron A, Schiller K, Parvizi J. Combined measurement of synovial fluid α-defensin and C-reactive protein levels: highly accurate for diagnosing periprosthetic joint infection. J Bone Joint Surg Am. 2014;96(17):1439-1445.

7. Bingham J, Clarke H, Spangehl M, Schwartz A, Beauchamp C, Goldberg B. The alpha defensin-1 biomarker assay can be used to evaluate the potentially infected total joint arthroplasty. Clin Orthop Relat Res. 2014;472(12):4006-4009.

8. Deirmengian C, Kardos K, Kilmartin P, et al. The alpha-defensin test for periprosthetic joint infection outperforms the leukocyte esterase test strip. Clin Orthop Relat Res. 2015;473(1):198-203.

9. Frangiamore SJ, Gajewski ND, Saleh A, Farias-Kovac M, Barsoum WK, Higuera CA. α-Defensin accuracy to diagnose periprosthetic joint infection—best available test? J Arthroplasty. 2016;31(2):456-460.

10. Frangiamore SJ, Saleh A, Kovac MF, et al. Synovial fluid interleukin-6 as a predictor of periprosthetic shoulder infection. J Bone Joint Surg Am. 2015;97(1):63-70.

11. Lenski M, Scherer MA. Synovial IL-6 as inflammatory marker in periprosthetic joint infections. J Arthroplasty. 2014;29(6):1105-1109.

12. Randau TM, Friedrich MJ, Wimmer MD, et al. Interleukin-6 in serum and in synovial fluid enhances the differentiation between periprosthetic joint infection and aseptic loosening. PLoS One. 2014;9(2):e89045.

13. Guenther D, Kokenge T, Jacobs O, et al. Excluding infections in arthroplasty using leucocyte esterase test. Int Orthop. 2014;38(11):2385-2390.

14. Wetters NG, Berend KR, Lombardi AV, Morris MJ, Tucker TL, Della Valle CJ. Leukocyte esterase reagent strips for the rapid diagnosis of periprosthetic joint infection. J Arthroplasty. 2012;27(8 suppl):8-11.

15. Nelson GN, Paxton ES, Narzikul A, Williams G, Lazarus MD, Abboud JA. Leukocyte esterase in the diagnosis of shoulder periprosthetic joint infection. J Shoulder Elbow Surg. 2015;24(9):1421-1426.

16. Tischler EH, Cavanaugh PK, Parvizi J. Leukocyte esterase strip test: matched for Musculoskeletal Infection Society criteria. J Bone Joint Surg Am. 2014;96(22):1917-1920.

17. Dempsey KE, Riggio MP, Lennon A, et al. Identification of bacteria on the surface of clinically infected and non-infected prosthetic hip joints removed during revision arthroplasties by 16S rRNA gene sequencing and by microbiological culture. Arthritis Res Ther. 2007;9(3):R46.

18. Gallo J, Kolar M, Dendis M, et al. Culture and PCR analysis of joint fluid in the diagnosis of prosthetic joint infection. New Microbiol. 2008;31(1):97-104.

19. Marin M, Garcia-Lechuz JM, Alonso P, et al. Role of universal 16S rRNA gene PCR and sequencing in diagnosis of prosthetic joint infection. J Clin Microbiol. 2012;50(3):583-589.

20. Jacovides CL, Kreft R, Adeli B, Hozack B, Ehrlich GD, Parvizi J. Successful identification of pathogens by polymerase chain reaction (PCR)-based electron spray ionization time-of-flight mass spectrometry (ESI-TOF-MS) in culture-negative periprosthetic joint infection. J Bone Joint Surg Am. 2012;94(24):2247-2254.

21. Hartley JC, Harris KA. Molecular techniques for diagnosing prosthetic joint infections. J Antimicrob Chemother. 2014;69(suppl 1):i21-i24.

22. Zappe B, Graf S, Ochsner PE, Zimmerli W, Sendi P. Propionibacterium spp. in prosthetic joint infections: a diagnostic challenge. Arch Orthop Trauma Surg. 2008;128(10):1039-1046.

23. Rasouli MR, Harandi AA, Adeli B, Purtill JJ, Parvizi J. Revision total knee arthroplasty: infection should be ruled out in all cases. J Arthroplasty. 2012;27(6):1239-1243.e1-e2.

24. Hunt RW, Bond MJ, Pater GD. Psychological responses to cancer: a case for cancer support groups. Community Health Stud. 1990;14(1):35-38.

25. Kurtz SM, Lau E, Schmier J, Ong KL, Zhao K, Parvizi J. Infection burden for hip and knee arthroplasty in the United States. J Arthroplasty. 2008;23(7):984-991.

26. Vandercam B, Jeumont S, Cornu O, et al. Amplification-based DNA analysis in the diagnosis of prosthetic joint infection. J Mol Diagn. 2008;10(6):537-543.

References

1. Maradit Kremers H, Larson DR, Crowson CS, et al. Prevalence of total hip and knee replacement in the United States. J Bone Joint Surg Am. 2015;97(17):1386-1397.

2. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785.

3. Sharkey PF, Lichstein PM, Shen C, Tokarski AT, Parvizi J. Why are total knee arthroplasties failing today—has anything changed after 10 years? J Arthroplasty. 2014;29(9):1774-1778.

4. Butler-Wu SM, Burns EM, Pottinger PS, et al. Optimization of periprosthetic culture for diagnosis of Propionibacterium acnes prosthetic joint infection. J Clin Microbiol. 2011;49(7):2490-2495.

5. Frangiamore SJ, Saleh A, Grosso MJ, et al. α-Defensin as a predictor of periprosthetic shoulder infection. J Shoulder Elbow Surg. 2015;24(7):1021-1027.

6. Deirmengian C, Kardos K, Kilmartin P, Cameron A, Schiller K, Parvizi J. Combined measurement of synovial fluid α-defensin and C-reactive protein levels: highly accurate for diagnosing periprosthetic joint infection. J Bone Joint Surg Am. 2014;96(17):1439-1445.

7. Bingham J, Clarke H, Spangehl M, Schwartz A, Beauchamp C, Goldberg B. The alpha defensin-1 biomarker assay can be used to evaluate the potentially infected total joint arthroplasty. Clin Orthop Relat Res. 2014;472(12):4006-4009.

8. Deirmengian C, Kardos K, Kilmartin P, et al. The alpha-defensin test for periprosthetic joint infection outperforms the leukocyte esterase test strip. Clin Orthop Relat Res. 2015;473(1):198-203.

9. Frangiamore SJ, Gajewski ND, Saleh A, Farias-Kovac M, Barsoum WK, Higuera CA. α-Defensin accuracy to diagnose periprosthetic joint infection—best available test? J Arthroplasty. 2016;31(2):456-460.

10. Frangiamore SJ, Saleh A, Kovac MF, et al. Synovial fluid interleukin-6 as a predictor of periprosthetic shoulder infection. J Bone Joint Surg Am. 2015;97(1):63-70.

11. Lenski M, Scherer MA. Synovial IL-6 as inflammatory marker in periprosthetic joint infections. J Arthroplasty. 2014;29(6):1105-1109.

12. Randau TM, Friedrich MJ, Wimmer MD, et al. Interleukin-6 in serum and in synovial fluid enhances the differentiation between periprosthetic joint infection and aseptic loosening. PLoS One. 2014;9(2):e89045.

13. Guenther D, Kokenge T, Jacobs O, et al. Excluding infections in arthroplasty using leucocyte esterase test. Int Orthop. 2014;38(11):2385-2390.

14. Wetters NG, Berend KR, Lombardi AV, Morris MJ, Tucker TL, Della Valle CJ. Leukocyte esterase reagent strips for the rapid diagnosis of periprosthetic joint infection. J Arthroplasty. 2012;27(8 suppl):8-11.

15. Nelson GN, Paxton ES, Narzikul A, Williams G, Lazarus MD, Abboud JA. Leukocyte esterase in the diagnosis of shoulder periprosthetic joint infection. J Shoulder Elbow Surg. 2015;24(9):1421-1426.

16. Tischler EH, Cavanaugh PK, Parvizi J. Leukocyte esterase strip test: matched for Musculoskeletal Infection Society criteria. J Bone Joint Surg Am. 2014;96(22):1917-1920.

17. Dempsey KE, Riggio MP, Lennon A, et al. Identification of bacteria on the surface of clinically infected and non-infected prosthetic hip joints removed during revision arthroplasties by 16S rRNA gene sequencing and by microbiological culture. Arthritis Res Ther. 2007;9(3):R46.

18. Gallo J, Kolar M, Dendis M, et al. Culture and PCR analysis of joint fluid in the diagnosis of prosthetic joint infection. New Microbiol. 2008;31(1):97-104.

19. Marin M, Garcia-Lechuz JM, Alonso P, et al. Role of universal 16S rRNA gene PCR and sequencing in diagnosis of prosthetic joint infection. J Clin Microbiol. 2012;50(3):583-589.

20. Jacovides CL, Kreft R, Adeli B, Hozack B, Ehrlich GD, Parvizi J. Successful identification of pathogens by polymerase chain reaction (PCR)-based electron spray ionization time-of-flight mass spectrometry (ESI-TOF-MS) in culture-negative periprosthetic joint infection. J Bone Joint Surg Am. 2012;94(24):2247-2254.

21. Hartley JC, Harris KA. Molecular techniques for diagnosing prosthetic joint infections. J Antimicrob Chemother. 2014;69(suppl 1):i21-i24.

22. Zappe B, Graf S, Ochsner PE, Zimmerli W, Sendi P. Propionibacterium spp. in prosthetic joint infections: a diagnostic challenge. Arch Orthop Trauma Surg. 2008;128(10):1039-1046.

23. Rasouli MR, Harandi AA, Adeli B, Purtill JJ, Parvizi J. Revision total knee arthroplasty: infection should be ruled out in all cases. J Arthroplasty. 2012;27(6):1239-1243.e1-e2.

24. Hunt RW, Bond MJ, Pater GD. Psychological responses to cancer: a case for cancer support groups. Community Health Stud. 1990;14(1):35-38.

25. Kurtz SM, Lau E, Schmier J, Ong KL, Zhao K, Parvizi J. Infection burden for hip and knee arthroplasty in the United States. J Arthroplasty. 2008;23(7):984-991.

26. Vandercam B, Jeumont S, Cornu O, et al. Amplification-based DNA analysis in the diagnosis of prosthetic joint infection. J Mol Diagn. 2008;10(6):537-543.

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Traumatic Anterior Shoulder Instability: The US Military Experience

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Traumatic Anterior Shoulder Instability: The US Military Experience

Take-Home Points

  • Arthroscopic stabilization performed early results in better outcomes in patients with Bankart lesions.
  • A subcritical level of bone loss of 13.5% has been shown to have a significant effect on outcomes, in addition to the established “critical amount”.
  • Bone loss is a bipolar issue. Both sides must be considered in order to properly address shoulder instability.
  • Off-track measurement has been shown to be even more positively predictive of outcomes than glenoid bone loss assessment.
  • There are several bone loss management options including, the most common coracoid transfer, as well as distal tibial allograft and distal clavicular autograft.

Given its relatively young age, high activity level, and centralized medical care system, the US military population is ideal for studying traumatic anterior shoulder instability. There is a long history of military surgeons who have made significant contributions that have advanced our understanding of this pathology and its treatment and results. In this article, we describe the scope, treatment, and results of this pathology in the US military population.

Incidence and Pathology

At the United States Military Academy (USMA), Owens and colleagues1 studied the incidence of shoulder instability, including dislocation and subluxation, and found anterior instability events were far more common than in civilian populations. The incidence of shoulder instability was 0.08 per 1000 person-years in the general US population vs 1.69 per 1000 person-years in US military personnel. The factors associated with increased risk of shoulder instability injury in the military population were male sex, white race, junior enlisted rank, and age under 30 years. Owens and colleagues2 noted that subluxation accounted for almost 85% of the total anterior instability events. Owens and colleagues3 found the pathology in subluxation events was similar to that in full dislocations, with a soft-tissue anterior Bankart lesion and a Hill-Sachs lesion detected on magnetic resonance imaging in more than 90% of patients. In another study at the USMA, DeBerardino and colleagues4 noted that 97% of arthroscopically assessed shoulders in first-time dislocators involved complete detachment of the capsuloligamentous complex from the anterior glenoid rim and neck—a so-called Bankart lesion. Thus, in a military population, anterior instability resulting from subluxation or dislocation is a common finding that is often represented by a soft-tissue Bankart lesion and a Hill-Sachs defect.

Natural History of Traumatic Anterior Shoulder Instability in the Military

Several studies have evaluated the outcomes of nonoperative and operative treatment of shoulder instability. Although most have found better outcomes with operative intervention, Aronen and Regan5 reported good results (25% recurrence at nearly 3-year follow-up) with nonoperative treatment and adherence to a strict rehabilitation program. Most other comparative studies in this population have published contrary results. Wheeler and colleagues6 studied the natural history of anterior shoulder dislocations in a USMA cadet cohort and found recurrent instability after shoulder dislocation in 92% of cadets who had nonoperative treatment. Similarly, DeBerardino and colleagues4 found that, in the USMA, 90% of first-time traumatic anterior shoulder dislocations managed nonoperatively experienced recurrent instability. In a series of Army soldiers with shoulder instability, Bottoni and colleagues7 reported that 75% of nonoperatively managed patients had recurrent instability, and, of these, 67% progressed to surgical intervention. Nonoperative treatment for a first-time dislocation is still reasonable if a cadet or soldier needs to quickly return to functional duties. Athletes who develop shoulder instability during their playing season have been studied in a military population as well. In a multicenter study of service academy athletes with anterior instability, Dickens and colleagues8 found that, with conservative management and accelerated rehabilitation of in-season shoulder instability, 73% of athletes returned to sport by a mean of 5 days. However, the durability of this treatment should be questioned, as 64% later experienced recurrence.

Arthroscopic Stabilization of Acute Anterior Shoulder Dislocations

In an early series of cases of traumatic anterior shoulder instability in USMA cadets, Wheeler and colleagues6 found that, at 14 months, 78% of arthroscopically stabilized cases and 92% of nonoperatively treated cases were successful. Then, in the 1990s, DeBerardino and colleagues4 studied a series of young, active patients in the USMA and noted significantly better results with arthroscopic treatment, vs nonoperative treatment, at 2- to 5-year follow-up. Of the arthroscopically treated shoulders, 88% remained stable during the study and returned to preinjury activity levels, and 12% experienced recurrent instability (risk factors included 2+ sulcus sign, poor capsular labral tissue, and history of bilateral shoulder instability). In a long-term follow-up (mean, 11.7 years; range, 9.1-13.9 years) of the same cohort, Owens and colleagues9 found that 14% of patients available for follow-up had undergone revision stabilization surgery, and, of these, 21% reported experiencing subluxation events. The authors concluded that, in first-time dislocators in this active military population, acute arthroscopic Bankart repair resulted in excellent return to athletics and subjective function, and had acceptable recurrence and reoperation rates. Bottoni and colleagues,7 in a prospective, randomized evaluation of arthroscopic stabilization of acute, traumatic, first-time shoulder dislocations in the Army, noted an 89% success rate for arthroscopic treatment at an average follow-up of 36 months, with no recurrent instability. DeBerardino and colleagues10 compared West Point patients treated nonoperatively with those arthroscopically treated with staples, transglenoid sutures, or bioabsorbable anchors. Recurrence rates were 85% for nonoperative treatment, 22% for staples, 14% for transglenoid sutures, and 10% for bioabsorbable anchors.

Arthroscopic Versus Open Stabilization of Anterior Shoulder Instability

In a prospective, randomized clinical trial comparing open and arthroscopic shoulder stabilization for recurrent anterior instability in active-duty Army personnel, Bottoni and colleagues11 found comparable clinical outcomes. Stabilization surgery failed clinically in only 3 cases, 2 open and 1 arthroscopic. The authors concluded that arthroscopic stabilization can be safely performed for recurrent shoulder instability and that arthroscopic outcomes are similar to open outcomes. In a series of anterior shoulder subluxations in young athletes with Bankart lesions, Owens and colleagues12 found that open and arthroscopic stabilization performed early resulted in better outcomes, regardless of technique used. Recurrent subluxation occurred at a mean of 17 months in 3 of the 10 patients in the open group and 3 of the 9 patients in the arthroscopic group, for an overall recurrence rate of 31%. The authors concluded that, in this patient population with Bankart lesions caused by anterior subluxation events, surgery should be performed early.

Bone Lesions

Burkhart and De Beer13 first noted that bone loss has emerged as one of the most important considerations in the setting of shoulder instability in active patients. Other authors have found this to be true in military populations.14,15

The diagnosis of bone loss may include historical findings, such as increased number and ease of dislocations, as well as dislocation in lower positions of abduction. Physical examination findings may include apprehension in the midrange of motion. Advanced imaging, such as magnetic resonance arthrography, has since been validated as equivalent to 3-dimensional computed tomography (3-D CT) in determining glenoid bone loss.16 In 2007, Mologne and colleagues15 studied the amount of glenoid bone loss and the presence of fragmented bone or attritional bone loss and its effect on outcomes. They evaluated 21 patients who had arthroscopic treatment for anterior instability with anteroinferior glenoid bone loss between 20% and 30%. Average follow-up was 34 months. All patients received 3 or 4 anterior anchors. No patient with a bone fragment incorporated into the repair experienced recurrence or subluxation, whereas 30% of patients with attritional bone loss had recurrent instability.15

 

 

Classifying Bone Loss and Recognizing Its Effects

Burkhart and De Beer13 helped define the role and significance of bone loss in the setting of shoulder instability. They defined significant bone loss as an engaging Hill-Sachs lesion of the humerus in an abducted and externally rotated position or an “inverted pear” lesion of the glenoid. Overall analysis revealed recurrence in 4% of cases without significant bone loss and 65% of cases with significant bone loss. In a subanalysis of contact-sport athletes in the setting of bone loss, the failure rate increased to 89%, from 6.5%. Aiding in the quantitative assessment of glenoid bone loss, Itoi and colleagues17 showed that 21% glenoid bone loss resulted in instability that would not be corrected by a soft-tissue procedure alone. Bone loss of 20% to 25% has since been considered a “critical amount,” above which an arthroscopic Bankart has been questioned. More recently, several authors have shown that even less bone loss can have a significant effect on outcomes. Shaha and colleagues18 established that a subcritical level of bone loss (13.5%) on the anteroinferior glenoid resulted in clinical failure (as determined with the Western Ontario Shoulder Instability Index) even in cases in which frank recurrence or subluxation was avoided. It is thought that, in recurrent instability, glenoid bone loss incident rate is as high as 90%, and the corresponding percentage of patients with Hill-Sachs lesions is almost 100%.19,20 Thus, it is increasingly understood that bone loss is a bipolar issue and that both sides must be considered in order to properly address shoulder instability in this setting. In 2007, Yamamoto and colleagues21 introduced the glenoid track, a method for predicting whether a Hill-Sachs lesion will engage. Di Giacomo and colleagues22 refined the track concept to quantitatively determine which lesions will engage in the setting of both glenoid and humeral bone loss. Metzger and colleagues,23 confirming the track concept arthroscopically, found that manipulation with anesthesia and arthroscopic visualization was well predicted by preoperative track measurements, and thus these measurements can be a good guide for surgical management (Figures 1A, 1B).

Figure 1.
At Tripler Army Medical Center, Shaha and colleagues14 clinically validated the concept in a series of arthroscopic stabilization cases. They found that the recurrence rate was 8% for “on-track” patients’ and 75% for “off-track” patients treated with the same intervention. In addition, positive predictive value was 75% for the off-track measurement and 44% for the glenoid bone loss assessment alone. The authors recommended the preoperative off-track measurement over the glenoid bone loss assessment.
Figure 2.
In an analysis of computer modeling of 3-D CT of patients who underwent Bankart repair, Arciero and colleagues24 found that bipolar bone defects (glenoid bone loss combined with humeral head Hill-Sachs lesion) had an additive and combined negative effect on soft-tissue Bankart repair. In particular, soft-tissue Bankart repair could be compromised by a 2-mm glenoid defect combined with a medium-size Hill-Sachs lesion or, conversely, by a 4-mm glenoid defect combined with a small Hill-Sachs lesion (Figures 2A, 2B).

Strategies for Addressing Bone Loss in Anterior Shoulder Instability

Several approaches for managing bone loss in shoulder instability have been described—the most common being coracoid transfer (Latarjet procedure). Waterman and colleagues25 recently studied the effects of coracoid transfer, distal tibial allograft, and iliac crest augmentation on anterior shoulder instability in US military patients treated between 2006 and 2012. Of 64 patients who underwent a bone block procedure, 16 (25%) had a complication during short-term follow-up. Complications included neurologic injury, pain, infection, hardware failure, and recurrent instability.

Figure 3.
After undergoing 1 of the 3 procedures, 33% of patients had persistent pain, and 23% had recurrent instability. In an older, long-term study of Naval Academy midshipmen, patients who underwent a modified Bristow procedure between 1975 and 1979 demonstrated 70% good to excellent results at an average follow-up of 26.4 years.26
Figure 4.
The recurrent instability rate was 15%, with 9% of the cohort dislocating again and 6% of the cohort experiencing recurrent subluxation. Direct bone grafting to the glenoid has also been described. Provencher and colleagues27 introduced use of distal tibial allograft in addressing bony deficiency, and clinical results were promising (Figures 3A-3C). Tokish and colleagues28 introduced use of distal clavicular autograft in addressing these deficiencies but did not report clinical outcomes (Figures 4A-4C).

Conclusion

Traumatic anterior shoulder instability is a common pathology that continues to significantly challenge the readiness of the US military. Military surgeon-researchers have a long history of investigating approaches to the treatment of this pathology—applying good science to a large controlled population, using a single medical record, and demonstrating a commitment to return service members to the ready defense of the nation.

Am J Orthop. 2017;46(4):184-189. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Owens BD, Dawson L, Burks R, Cameron KL. Incidence of shoulder dislocation in the United States military: demographic considerations from a high-risk population. J Bone Joint Surg Am. 2009;91(4):791-796.

2. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.

3. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611.

4. DeBerardino TM, Arciero RA, Taylor DC, Uhorchak JM. Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes. Two- to five-year follow-up. Am J Sports Med. 2001;29(5):586-592.

5. Aronen JG, Regan K. Decreasing the incidence of recurrence of first time anterior shoulder dislocations with rehabilitation. Am J Sports Med. 1984;12(4):283-291.

6. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217.

7. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med. 2002;30(4):576-580.

8. Dickens JF, Owens BD, Cameron KL, et al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850.

9. Owens BD, DeBerardino TM, Nelson BJ, et al. Long-term follow-up of acute arthroscopic Bankart repair for initial anterior shoulder dislocations in young athletes. Am J Sports Med. 2009;37(4):669-673.

10. DeBerardino TM, Arciero RA, Taylor DC. Arthroscopic stabilization of acute initial anterior shoulder dislocation: the West Point experience. J South Orthop Assoc. 1996;5(4):263-271.

11. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737.

12. Owens BD, Cameron KL, Peck KY, et al. Arthroscopic versus open stabilization for anterior shoulder subluxations. Orthop J Sports Med. 2015;3(1):2325967115571084.

13. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.14. Shaha JS, Cook JB, Rowles DJ, Bottoni CR, Shaha SH, Tokish JM. Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98(22):1918-1923.

15. Mologne TS, Provencher MT, Menzel KA, Vachon TA, Dewing CB. Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am J Sports Med. 2007;35(8):1276-1283.

16. Markenstein JE, Jaspars KC, van der Hulst VP, Willems WJ. The quantification of glenoid bone loss in anterior shoulder instability; MR-arthro compared to 3D-CT. Skeletal Radiol. 2014;43(4):475-483.

17. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46.

18. Shaha JS, Cook JB, Song DJ, et al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725.

19. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

20. Provencher MT, Frank RM, Leclere LE, et al. The Hill-Sachs lesion: diagnosis, classification, and management. J Am Acad Orthop Surg. 2012;20(4):242-252.

21. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649-656.

22. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98.

23. Metzger PD, Barlow B, Leonardelli D, Peace W, Solomon DJ, Provencher MT. Clinical application of the “glenoid track” concept for defining humeral head engagement in anterior shoulder instability: a preliminary report. Orthop J Sports Med. 2013;1(2):2325967113496213.

24. Arciero RA, Parrino A, Bernhardson AS, et al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1429.

25. Waterman BR, Chandler PJ, Teague E, Provencher MT, Tokish JM, Pallis MP. Short-term outcomes of glenoid bone block augmentation for complex anterior shoulder instability in a high-risk population. Arthroscopy. 2016;32(9):1784-1790.

26. Schroder DT, Provencher MT, Mologne TS, Muldoon MP, Cox JS. The modified Bristow procedure for anterior shoulder instability: 26-year outcomes in Naval Academy midshipmen. Am J Sports Med. 2006;34(5):778-786.

27. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

28. Tokish JM, Fitzpatrick K, Cook JB, Mallon WJ. Arthroscopic distal clavicular autograft for treating shoulder instability with glenoid bone loss. Arthrosc Tech. 2014;3(4):e475-e481.

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Take-Home Points

  • Arthroscopic stabilization performed early results in better outcomes in patients with Bankart lesions.
  • A subcritical level of bone loss of 13.5% has been shown to have a significant effect on outcomes, in addition to the established “critical amount”.
  • Bone loss is a bipolar issue. Both sides must be considered in order to properly address shoulder instability.
  • Off-track measurement has been shown to be even more positively predictive of outcomes than glenoid bone loss assessment.
  • There are several bone loss management options including, the most common coracoid transfer, as well as distal tibial allograft and distal clavicular autograft.

Given its relatively young age, high activity level, and centralized medical care system, the US military population is ideal for studying traumatic anterior shoulder instability. There is a long history of military surgeons who have made significant contributions that have advanced our understanding of this pathology and its treatment and results. In this article, we describe the scope, treatment, and results of this pathology in the US military population.

Incidence and Pathology

At the United States Military Academy (USMA), Owens and colleagues1 studied the incidence of shoulder instability, including dislocation and subluxation, and found anterior instability events were far more common than in civilian populations. The incidence of shoulder instability was 0.08 per 1000 person-years in the general US population vs 1.69 per 1000 person-years in US military personnel. The factors associated with increased risk of shoulder instability injury in the military population were male sex, white race, junior enlisted rank, and age under 30 years. Owens and colleagues2 noted that subluxation accounted for almost 85% of the total anterior instability events. Owens and colleagues3 found the pathology in subluxation events was similar to that in full dislocations, with a soft-tissue anterior Bankart lesion and a Hill-Sachs lesion detected on magnetic resonance imaging in more than 90% of patients. In another study at the USMA, DeBerardino and colleagues4 noted that 97% of arthroscopically assessed shoulders in first-time dislocators involved complete detachment of the capsuloligamentous complex from the anterior glenoid rim and neck—a so-called Bankart lesion. Thus, in a military population, anterior instability resulting from subluxation or dislocation is a common finding that is often represented by a soft-tissue Bankart lesion and a Hill-Sachs defect.

Natural History of Traumatic Anterior Shoulder Instability in the Military

Several studies have evaluated the outcomes of nonoperative and operative treatment of shoulder instability. Although most have found better outcomes with operative intervention, Aronen and Regan5 reported good results (25% recurrence at nearly 3-year follow-up) with nonoperative treatment and adherence to a strict rehabilitation program. Most other comparative studies in this population have published contrary results. Wheeler and colleagues6 studied the natural history of anterior shoulder dislocations in a USMA cadet cohort and found recurrent instability after shoulder dislocation in 92% of cadets who had nonoperative treatment. Similarly, DeBerardino and colleagues4 found that, in the USMA, 90% of first-time traumatic anterior shoulder dislocations managed nonoperatively experienced recurrent instability. In a series of Army soldiers with shoulder instability, Bottoni and colleagues7 reported that 75% of nonoperatively managed patients had recurrent instability, and, of these, 67% progressed to surgical intervention. Nonoperative treatment for a first-time dislocation is still reasonable if a cadet or soldier needs to quickly return to functional duties. Athletes who develop shoulder instability during their playing season have been studied in a military population as well. In a multicenter study of service academy athletes with anterior instability, Dickens and colleagues8 found that, with conservative management and accelerated rehabilitation of in-season shoulder instability, 73% of athletes returned to sport by a mean of 5 days. However, the durability of this treatment should be questioned, as 64% later experienced recurrence.

Arthroscopic Stabilization of Acute Anterior Shoulder Dislocations

In an early series of cases of traumatic anterior shoulder instability in USMA cadets, Wheeler and colleagues6 found that, at 14 months, 78% of arthroscopically stabilized cases and 92% of nonoperatively treated cases were successful. Then, in the 1990s, DeBerardino and colleagues4 studied a series of young, active patients in the USMA and noted significantly better results with arthroscopic treatment, vs nonoperative treatment, at 2- to 5-year follow-up. Of the arthroscopically treated shoulders, 88% remained stable during the study and returned to preinjury activity levels, and 12% experienced recurrent instability (risk factors included 2+ sulcus sign, poor capsular labral tissue, and history of bilateral shoulder instability). In a long-term follow-up (mean, 11.7 years; range, 9.1-13.9 years) of the same cohort, Owens and colleagues9 found that 14% of patients available for follow-up had undergone revision stabilization surgery, and, of these, 21% reported experiencing subluxation events. The authors concluded that, in first-time dislocators in this active military population, acute arthroscopic Bankart repair resulted in excellent return to athletics and subjective function, and had acceptable recurrence and reoperation rates. Bottoni and colleagues,7 in a prospective, randomized evaluation of arthroscopic stabilization of acute, traumatic, first-time shoulder dislocations in the Army, noted an 89% success rate for arthroscopic treatment at an average follow-up of 36 months, with no recurrent instability. DeBerardino and colleagues10 compared West Point patients treated nonoperatively with those arthroscopically treated with staples, transglenoid sutures, or bioabsorbable anchors. Recurrence rates were 85% for nonoperative treatment, 22% for staples, 14% for transglenoid sutures, and 10% for bioabsorbable anchors.

Arthroscopic Versus Open Stabilization of Anterior Shoulder Instability

In a prospective, randomized clinical trial comparing open and arthroscopic shoulder stabilization for recurrent anterior instability in active-duty Army personnel, Bottoni and colleagues11 found comparable clinical outcomes. Stabilization surgery failed clinically in only 3 cases, 2 open and 1 arthroscopic. The authors concluded that arthroscopic stabilization can be safely performed for recurrent shoulder instability and that arthroscopic outcomes are similar to open outcomes. In a series of anterior shoulder subluxations in young athletes with Bankart lesions, Owens and colleagues12 found that open and arthroscopic stabilization performed early resulted in better outcomes, regardless of technique used. Recurrent subluxation occurred at a mean of 17 months in 3 of the 10 patients in the open group and 3 of the 9 patients in the arthroscopic group, for an overall recurrence rate of 31%. The authors concluded that, in this patient population with Bankart lesions caused by anterior subluxation events, surgery should be performed early.

Bone Lesions

Burkhart and De Beer13 first noted that bone loss has emerged as one of the most important considerations in the setting of shoulder instability in active patients. Other authors have found this to be true in military populations.14,15

The diagnosis of bone loss may include historical findings, such as increased number and ease of dislocations, as well as dislocation in lower positions of abduction. Physical examination findings may include apprehension in the midrange of motion. Advanced imaging, such as magnetic resonance arthrography, has since been validated as equivalent to 3-dimensional computed tomography (3-D CT) in determining glenoid bone loss.16 In 2007, Mologne and colleagues15 studied the amount of glenoid bone loss and the presence of fragmented bone or attritional bone loss and its effect on outcomes. They evaluated 21 patients who had arthroscopic treatment for anterior instability with anteroinferior glenoid bone loss between 20% and 30%. Average follow-up was 34 months. All patients received 3 or 4 anterior anchors. No patient with a bone fragment incorporated into the repair experienced recurrence or subluxation, whereas 30% of patients with attritional bone loss had recurrent instability.15

 

 

Classifying Bone Loss and Recognizing Its Effects

Burkhart and De Beer13 helped define the role and significance of bone loss in the setting of shoulder instability. They defined significant bone loss as an engaging Hill-Sachs lesion of the humerus in an abducted and externally rotated position or an “inverted pear” lesion of the glenoid. Overall analysis revealed recurrence in 4% of cases without significant bone loss and 65% of cases with significant bone loss. In a subanalysis of contact-sport athletes in the setting of bone loss, the failure rate increased to 89%, from 6.5%. Aiding in the quantitative assessment of glenoid bone loss, Itoi and colleagues17 showed that 21% glenoid bone loss resulted in instability that would not be corrected by a soft-tissue procedure alone. Bone loss of 20% to 25% has since been considered a “critical amount,” above which an arthroscopic Bankart has been questioned. More recently, several authors have shown that even less bone loss can have a significant effect on outcomes. Shaha and colleagues18 established that a subcritical level of bone loss (13.5%) on the anteroinferior glenoid resulted in clinical failure (as determined with the Western Ontario Shoulder Instability Index) even in cases in which frank recurrence or subluxation was avoided. It is thought that, in recurrent instability, glenoid bone loss incident rate is as high as 90%, and the corresponding percentage of patients with Hill-Sachs lesions is almost 100%.19,20 Thus, it is increasingly understood that bone loss is a bipolar issue and that both sides must be considered in order to properly address shoulder instability in this setting. In 2007, Yamamoto and colleagues21 introduced the glenoid track, a method for predicting whether a Hill-Sachs lesion will engage. Di Giacomo and colleagues22 refined the track concept to quantitatively determine which lesions will engage in the setting of both glenoid and humeral bone loss. Metzger and colleagues,23 confirming the track concept arthroscopically, found that manipulation with anesthesia and arthroscopic visualization was well predicted by preoperative track measurements, and thus these measurements can be a good guide for surgical management (Figures 1A, 1B).

Figure 1.
At Tripler Army Medical Center, Shaha and colleagues14 clinically validated the concept in a series of arthroscopic stabilization cases. They found that the recurrence rate was 8% for “on-track” patients’ and 75% for “off-track” patients treated with the same intervention. In addition, positive predictive value was 75% for the off-track measurement and 44% for the glenoid bone loss assessment alone. The authors recommended the preoperative off-track measurement over the glenoid bone loss assessment.
Figure 2.
In an analysis of computer modeling of 3-D CT of patients who underwent Bankart repair, Arciero and colleagues24 found that bipolar bone defects (glenoid bone loss combined with humeral head Hill-Sachs lesion) had an additive and combined negative effect on soft-tissue Bankart repair. In particular, soft-tissue Bankart repair could be compromised by a 2-mm glenoid defect combined with a medium-size Hill-Sachs lesion or, conversely, by a 4-mm glenoid defect combined with a small Hill-Sachs lesion (Figures 2A, 2B).

Strategies for Addressing Bone Loss in Anterior Shoulder Instability

Several approaches for managing bone loss in shoulder instability have been described—the most common being coracoid transfer (Latarjet procedure). Waterman and colleagues25 recently studied the effects of coracoid transfer, distal tibial allograft, and iliac crest augmentation on anterior shoulder instability in US military patients treated between 2006 and 2012. Of 64 patients who underwent a bone block procedure, 16 (25%) had a complication during short-term follow-up. Complications included neurologic injury, pain, infection, hardware failure, and recurrent instability.

Figure 3.
After undergoing 1 of the 3 procedures, 33% of patients had persistent pain, and 23% had recurrent instability. In an older, long-term study of Naval Academy midshipmen, patients who underwent a modified Bristow procedure between 1975 and 1979 demonstrated 70% good to excellent results at an average follow-up of 26.4 years.26
Figure 4.
The recurrent instability rate was 15%, with 9% of the cohort dislocating again and 6% of the cohort experiencing recurrent subluxation. Direct bone grafting to the glenoid has also been described. Provencher and colleagues27 introduced use of distal tibial allograft in addressing bony deficiency, and clinical results were promising (Figures 3A-3C). Tokish and colleagues28 introduced use of distal clavicular autograft in addressing these deficiencies but did not report clinical outcomes (Figures 4A-4C).

Conclusion

Traumatic anterior shoulder instability is a common pathology that continues to significantly challenge the readiness of the US military. Military surgeon-researchers have a long history of investigating approaches to the treatment of this pathology—applying good science to a large controlled population, using a single medical record, and demonstrating a commitment to return service members to the ready defense of the nation.

Am J Orthop. 2017;46(4):184-189. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Arthroscopic stabilization performed early results in better outcomes in patients with Bankart lesions.
  • A subcritical level of bone loss of 13.5% has been shown to have a significant effect on outcomes, in addition to the established “critical amount”.
  • Bone loss is a bipolar issue. Both sides must be considered in order to properly address shoulder instability.
  • Off-track measurement has been shown to be even more positively predictive of outcomes than glenoid bone loss assessment.
  • There are several bone loss management options including, the most common coracoid transfer, as well as distal tibial allograft and distal clavicular autograft.

Given its relatively young age, high activity level, and centralized medical care system, the US military population is ideal for studying traumatic anterior shoulder instability. There is a long history of military surgeons who have made significant contributions that have advanced our understanding of this pathology and its treatment and results. In this article, we describe the scope, treatment, and results of this pathology in the US military population.

Incidence and Pathology

At the United States Military Academy (USMA), Owens and colleagues1 studied the incidence of shoulder instability, including dislocation and subluxation, and found anterior instability events were far more common than in civilian populations. The incidence of shoulder instability was 0.08 per 1000 person-years in the general US population vs 1.69 per 1000 person-years in US military personnel. The factors associated with increased risk of shoulder instability injury in the military population were male sex, white race, junior enlisted rank, and age under 30 years. Owens and colleagues2 noted that subluxation accounted for almost 85% of the total anterior instability events. Owens and colleagues3 found the pathology in subluxation events was similar to that in full dislocations, with a soft-tissue anterior Bankart lesion and a Hill-Sachs lesion detected on magnetic resonance imaging in more than 90% of patients. In another study at the USMA, DeBerardino and colleagues4 noted that 97% of arthroscopically assessed shoulders in first-time dislocators involved complete detachment of the capsuloligamentous complex from the anterior glenoid rim and neck—a so-called Bankart lesion. Thus, in a military population, anterior instability resulting from subluxation or dislocation is a common finding that is often represented by a soft-tissue Bankart lesion and a Hill-Sachs defect.

Natural History of Traumatic Anterior Shoulder Instability in the Military

Several studies have evaluated the outcomes of nonoperative and operative treatment of shoulder instability. Although most have found better outcomes with operative intervention, Aronen and Regan5 reported good results (25% recurrence at nearly 3-year follow-up) with nonoperative treatment and adherence to a strict rehabilitation program. Most other comparative studies in this population have published contrary results. Wheeler and colleagues6 studied the natural history of anterior shoulder dislocations in a USMA cadet cohort and found recurrent instability after shoulder dislocation in 92% of cadets who had nonoperative treatment. Similarly, DeBerardino and colleagues4 found that, in the USMA, 90% of first-time traumatic anterior shoulder dislocations managed nonoperatively experienced recurrent instability. In a series of Army soldiers with shoulder instability, Bottoni and colleagues7 reported that 75% of nonoperatively managed patients had recurrent instability, and, of these, 67% progressed to surgical intervention. Nonoperative treatment for a first-time dislocation is still reasonable if a cadet or soldier needs to quickly return to functional duties. Athletes who develop shoulder instability during their playing season have been studied in a military population as well. In a multicenter study of service academy athletes with anterior instability, Dickens and colleagues8 found that, with conservative management and accelerated rehabilitation of in-season shoulder instability, 73% of athletes returned to sport by a mean of 5 days. However, the durability of this treatment should be questioned, as 64% later experienced recurrence.

Arthroscopic Stabilization of Acute Anterior Shoulder Dislocations

In an early series of cases of traumatic anterior shoulder instability in USMA cadets, Wheeler and colleagues6 found that, at 14 months, 78% of arthroscopically stabilized cases and 92% of nonoperatively treated cases were successful. Then, in the 1990s, DeBerardino and colleagues4 studied a series of young, active patients in the USMA and noted significantly better results with arthroscopic treatment, vs nonoperative treatment, at 2- to 5-year follow-up. Of the arthroscopically treated shoulders, 88% remained stable during the study and returned to preinjury activity levels, and 12% experienced recurrent instability (risk factors included 2+ sulcus sign, poor capsular labral tissue, and history of bilateral shoulder instability). In a long-term follow-up (mean, 11.7 years; range, 9.1-13.9 years) of the same cohort, Owens and colleagues9 found that 14% of patients available for follow-up had undergone revision stabilization surgery, and, of these, 21% reported experiencing subluxation events. The authors concluded that, in first-time dislocators in this active military population, acute arthroscopic Bankart repair resulted in excellent return to athletics and subjective function, and had acceptable recurrence and reoperation rates. Bottoni and colleagues,7 in a prospective, randomized evaluation of arthroscopic stabilization of acute, traumatic, first-time shoulder dislocations in the Army, noted an 89% success rate for arthroscopic treatment at an average follow-up of 36 months, with no recurrent instability. DeBerardino and colleagues10 compared West Point patients treated nonoperatively with those arthroscopically treated with staples, transglenoid sutures, or bioabsorbable anchors. Recurrence rates were 85% for nonoperative treatment, 22% for staples, 14% for transglenoid sutures, and 10% for bioabsorbable anchors.

Arthroscopic Versus Open Stabilization of Anterior Shoulder Instability

In a prospective, randomized clinical trial comparing open and arthroscopic shoulder stabilization for recurrent anterior instability in active-duty Army personnel, Bottoni and colleagues11 found comparable clinical outcomes. Stabilization surgery failed clinically in only 3 cases, 2 open and 1 arthroscopic. The authors concluded that arthroscopic stabilization can be safely performed for recurrent shoulder instability and that arthroscopic outcomes are similar to open outcomes. In a series of anterior shoulder subluxations in young athletes with Bankart lesions, Owens and colleagues12 found that open and arthroscopic stabilization performed early resulted in better outcomes, regardless of technique used. Recurrent subluxation occurred at a mean of 17 months in 3 of the 10 patients in the open group and 3 of the 9 patients in the arthroscopic group, for an overall recurrence rate of 31%. The authors concluded that, in this patient population with Bankart lesions caused by anterior subluxation events, surgery should be performed early.

Bone Lesions

Burkhart and De Beer13 first noted that bone loss has emerged as one of the most important considerations in the setting of shoulder instability in active patients. Other authors have found this to be true in military populations.14,15

The diagnosis of bone loss may include historical findings, such as increased number and ease of dislocations, as well as dislocation in lower positions of abduction. Physical examination findings may include apprehension in the midrange of motion. Advanced imaging, such as magnetic resonance arthrography, has since been validated as equivalent to 3-dimensional computed tomography (3-D CT) in determining glenoid bone loss.16 In 2007, Mologne and colleagues15 studied the amount of glenoid bone loss and the presence of fragmented bone or attritional bone loss and its effect on outcomes. They evaluated 21 patients who had arthroscopic treatment for anterior instability with anteroinferior glenoid bone loss between 20% and 30%. Average follow-up was 34 months. All patients received 3 or 4 anterior anchors. No patient with a bone fragment incorporated into the repair experienced recurrence or subluxation, whereas 30% of patients with attritional bone loss had recurrent instability.15

 

 

Classifying Bone Loss and Recognizing Its Effects

Burkhart and De Beer13 helped define the role and significance of bone loss in the setting of shoulder instability. They defined significant bone loss as an engaging Hill-Sachs lesion of the humerus in an abducted and externally rotated position or an “inverted pear” lesion of the glenoid. Overall analysis revealed recurrence in 4% of cases without significant bone loss and 65% of cases with significant bone loss. In a subanalysis of contact-sport athletes in the setting of bone loss, the failure rate increased to 89%, from 6.5%. Aiding in the quantitative assessment of glenoid bone loss, Itoi and colleagues17 showed that 21% glenoid bone loss resulted in instability that would not be corrected by a soft-tissue procedure alone. Bone loss of 20% to 25% has since been considered a “critical amount,” above which an arthroscopic Bankart has been questioned. More recently, several authors have shown that even less bone loss can have a significant effect on outcomes. Shaha and colleagues18 established that a subcritical level of bone loss (13.5%) on the anteroinferior glenoid resulted in clinical failure (as determined with the Western Ontario Shoulder Instability Index) even in cases in which frank recurrence or subluxation was avoided. It is thought that, in recurrent instability, glenoid bone loss incident rate is as high as 90%, and the corresponding percentage of patients with Hill-Sachs lesions is almost 100%.19,20 Thus, it is increasingly understood that bone loss is a bipolar issue and that both sides must be considered in order to properly address shoulder instability in this setting. In 2007, Yamamoto and colleagues21 introduced the glenoid track, a method for predicting whether a Hill-Sachs lesion will engage. Di Giacomo and colleagues22 refined the track concept to quantitatively determine which lesions will engage in the setting of both glenoid and humeral bone loss. Metzger and colleagues,23 confirming the track concept arthroscopically, found that manipulation with anesthesia and arthroscopic visualization was well predicted by preoperative track measurements, and thus these measurements can be a good guide for surgical management (Figures 1A, 1B).

Figure 1.
At Tripler Army Medical Center, Shaha and colleagues14 clinically validated the concept in a series of arthroscopic stabilization cases. They found that the recurrence rate was 8% for “on-track” patients’ and 75% for “off-track” patients treated with the same intervention. In addition, positive predictive value was 75% for the off-track measurement and 44% for the glenoid bone loss assessment alone. The authors recommended the preoperative off-track measurement over the glenoid bone loss assessment.
Figure 2.
In an analysis of computer modeling of 3-D CT of patients who underwent Bankart repair, Arciero and colleagues24 found that bipolar bone defects (glenoid bone loss combined with humeral head Hill-Sachs lesion) had an additive and combined negative effect on soft-tissue Bankart repair. In particular, soft-tissue Bankart repair could be compromised by a 2-mm glenoid defect combined with a medium-size Hill-Sachs lesion or, conversely, by a 4-mm glenoid defect combined with a small Hill-Sachs lesion (Figures 2A, 2B).

Strategies for Addressing Bone Loss in Anterior Shoulder Instability

Several approaches for managing bone loss in shoulder instability have been described—the most common being coracoid transfer (Latarjet procedure). Waterman and colleagues25 recently studied the effects of coracoid transfer, distal tibial allograft, and iliac crest augmentation on anterior shoulder instability in US military patients treated between 2006 and 2012. Of 64 patients who underwent a bone block procedure, 16 (25%) had a complication during short-term follow-up. Complications included neurologic injury, pain, infection, hardware failure, and recurrent instability.

Figure 3.
After undergoing 1 of the 3 procedures, 33% of patients had persistent pain, and 23% had recurrent instability. In an older, long-term study of Naval Academy midshipmen, patients who underwent a modified Bristow procedure between 1975 and 1979 demonstrated 70% good to excellent results at an average follow-up of 26.4 years.26
Figure 4.
The recurrent instability rate was 15%, with 9% of the cohort dislocating again and 6% of the cohort experiencing recurrent subluxation. Direct bone grafting to the glenoid has also been described. Provencher and colleagues27 introduced use of distal tibial allograft in addressing bony deficiency, and clinical results were promising (Figures 3A-3C). Tokish and colleagues28 introduced use of distal clavicular autograft in addressing these deficiencies but did not report clinical outcomes (Figures 4A-4C).

Conclusion

Traumatic anterior shoulder instability is a common pathology that continues to significantly challenge the readiness of the US military. Military surgeon-researchers have a long history of investigating approaches to the treatment of this pathology—applying good science to a large controlled population, using a single medical record, and demonstrating a commitment to return service members to the ready defense of the nation.

Am J Orthop. 2017;46(4):184-189. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Owens BD, Dawson L, Burks R, Cameron KL. Incidence of shoulder dislocation in the United States military: demographic considerations from a high-risk population. J Bone Joint Surg Am. 2009;91(4):791-796.

2. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.

3. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611.

4. DeBerardino TM, Arciero RA, Taylor DC, Uhorchak JM. Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes. Two- to five-year follow-up. Am J Sports Med. 2001;29(5):586-592.

5. Aronen JG, Regan K. Decreasing the incidence of recurrence of first time anterior shoulder dislocations with rehabilitation. Am J Sports Med. 1984;12(4):283-291.

6. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217.

7. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med. 2002;30(4):576-580.

8. Dickens JF, Owens BD, Cameron KL, et al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850.

9. Owens BD, DeBerardino TM, Nelson BJ, et al. Long-term follow-up of acute arthroscopic Bankart repair for initial anterior shoulder dislocations in young athletes. Am J Sports Med. 2009;37(4):669-673.

10. DeBerardino TM, Arciero RA, Taylor DC. Arthroscopic stabilization of acute initial anterior shoulder dislocation: the West Point experience. J South Orthop Assoc. 1996;5(4):263-271.

11. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737.

12. Owens BD, Cameron KL, Peck KY, et al. Arthroscopic versus open stabilization for anterior shoulder subluxations. Orthop J Sports Med. 2015;3(1):2325967115571084.

13. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.14. Shaha JS, Cook JB, Rowles DJ, Bottoni CR, Shaha SH, Tokish JM. Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98(22):1918-1923.

15. Mologne TS, Provencher MT, Menzel KA, Vachon TA, Dewing CB. Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am J Sports Med. 2007;35(8):1276-1283.

16. Markenstein JE, Jaspars KC, van der Hulst VP, Willems WJ. The quantification of glenoid bone loss in anterior shoulder instability; MR-arthro compared to 3D-CT. Skeletal Radiol. 2014;43(4):475-483.

17. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46.

18. Shaha JS, Cook JB, Song DJ, et al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725.

19. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

20. Provencher MT, Frank RM, Leclere LE, et al. The Hill-Sachs lesion: diagnosis, classification, and management. J Am Acad Orthop Surg. 2012;20(4):242-252.

21. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649-656.

22. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98.

23. Metzger PD, Barlow B, Leonardelli D, Peace W, Solomon DJ, Provencher MT. Clinical application of the “glenoid track” concept for defining humeral head engagement in anterior shoulder instability: a preliminary report. Orthop J Sports Med. 2013;1(2):2325967113496213.

24. Arciero RA, Parrino A, Bernhardson AS, et al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1429.

25. Waterman BR, Chandler PJ, Teague E, Provencher MT, Tokish JM, Pallis MP. Short-term outcomes of glenoid bone block augmentation for complex anterior shoulder instability in a high-risk population. Arthroscopy. 2016;32(9):1784-1790.

26. Schroder DT, Provencher MT, Mologne TS, Muldoon MP, Cox JS. The modified Bristow procedure for anterior shoulder instability: 26-year outcomes in Naval Academy midshipmen. Am J Sports Med. 2006;34(5):778-786.

27. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

28. Tokish JM, Fitzpatrick K, Cook JB, Mallon WJ. Arthroscopic distal clavicular autograft for treating shoulder instability with glenoid bone loss. Arthrosc Tech. 2014;3(4):e475-e481.

References

1. Owens BD, Dawson L, Burks R, Cameron KL. Incidence of shoulder dislocation in the United States military: demographic considerations from a high-risk population. J Bone Joint Surg Am. 2009;91(4):791-796.

2. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.

3. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611.

4. DeBerardino TM, Arciero RA, Taylor DC, Uhorchak JM. Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes. Two- to five-year follow-up. Am J Sports Med. 2001;29(5):586-592.

5. Aronen JG, Regan K. Decreasing the incidence of recurrence of first time anterior shoulder dislocations with rehabilitation. Am J Sports Med. 1984;12(4):283-291.

6. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217.

7. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med. 2002;30(4):576-580.

8. Dickens JF, Owens BD, Cameron KL, et al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850.

9. Owens BD, DeBerardino TM, Nelson BJ, et al. Long-term follow-up of acute arthroscopic Bankart repair for initial anterior shoulder dislocations in young athletes. Am J Sports Med. 2009;37(4):669-673.

10. DeBerardino TM, Arciero RA, Taylor DC. Arthroscopic stabilization of acute initial anterior shoulder dislocation: the West Point experience. J South Orthop Assoc. 1996;5(4):263-271.

11. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737.

12. Owens BD, Cameron KL, Peck KY, et al. Arthroscopic versus open stabilization for anterior shoulder subluxations. Orthop J Sports Med. 2015;3(1):2325967115571084.

13. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.14. Shaha JS, Cook JB, Rowles DJ, Bottoni CR, Shaha SH, Tokish JM. Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98(22):1918-1923.

15. Mologne TS, Provencher MT, Menzel KA, Vachon TA, Dewing CB. Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am J Sports Med. 2007;35(8):1276-1283.

16. Markenstein JE, Jaspars KC, van der Hulst VP, Willems WJ. The quantification of glenoid bone loss in anterior shoulder instability; MR-arthro compared to 3D-CT. Skeletal Radiol. 2014;43(4):475-483.

17. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46.

18. Shaha JS, Cook JB, Song DJ, et al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725.

19. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

20. Provencher MT, Frank RM, Leclere LE, et al. The Hill-Sachs lesion: diagnosis, classification, and management. J Am Acad Orthop Surg. 2012;20(4):242-252.

21. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649-656.

22. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98.

23. Metzger PD, Barlow B, Leonardelli D, Peace W, Solomon DJ, Provencher MT. Clinical application of the “glenoid track” concept for defining humeral head engagement in anterior shoulder instability: a preliminary report. Orthop J Sports Med. 2013;1(2):2325967113496213.

24. Arciero RA, Parrino A, Bernhardson AS, et al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1429.

25. Waterman BR, Chandler PJ, Teague E, Provencher MT, Tokish JM, Pallis MP. Short-term outcomes of glenoid bone block augmentation for complex anterior shoulder instability in a high-risk population. Arthroscopy. 2016;32(9):1784-1790.

26. Schroder DT, Provencher MT, Mologne TS, Muldoon MP, Cox JS. The modified Bristow procedure for anterior shoulder instability: 26-year outcomes in Naval Academy midshipmen. Am J Sports Med. 2006;34(5):778-786.

27. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

28. Tokish JM, Fitzpatrick K, Cook JB, Mallon WJ. Arthroscopic distal clavicular autograft for treating shoulder instability with glenoid bone loss. Arthrosc Tech. 2014;3(4):e475-e481.

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The American Journal of Orthopedics - 46(4)
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