A 68-year-old Filipino man with a history of hypertension, type 2 diabetes, and osteoarthritis presented to the emergency department with a one-week history of increasing pain, swelling, erythema, and seepage of his right great toe. The patient denied paresthesias, fever, chills, night sweats, cough, dyspnea, or any change in his diet, medications (which included lisinopril, metformin, and acetaminophen as needed), or routine. Social history was negative for alcohol use and cigarette smoking.

He previously had similar symptoms in his right fourth toe that resulted in amputation. The patient was told at the time that he had a “bone infection” and amputation was necessary.

The patient was thin, alert, oriented, and in no acute distress. His vital signs and a cardiopulmonary exam were normal. The patient’s right great toe was tender to touch, with ulceration of the skin dorsally at the proximal nail fold. In addition, his toe was oozing a purulent, non-foul smelling discharge (FIGURE 1). Other pertinent findings included multiple enlarged joints on both hands with visible yellow-white subcutaneous nodules on the hands and dorsum of the forearm (FIGURE 2).

The patient’s white blood cell count was 10,800/mcL, C-reactive protein (CRP) was 18 mg/L, erythrocyte sedimentation rate (ESR) was 80 mm/hr, and uric acid was 12.5 mg/dL. His blood urea nitrogen was 52 mg/dL and creatinine was 2.5 mg/dL. A glycated hemoglobin test was 7.2%. A wound culture, aspirate from the dorsum of the toe, and x-ray were obtained.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Tophaceous gouty arthritis

The x-ray of the right great toe showed erosions of the metatarsophalangeal (MTP) joint (FIGURE 3). Given the patient’s age, underlying diabetes, skin ulceration, and elevation of CRP and ESR, the initial concern was for septic arthritis and osteomyelitis. However, the absence of leukocytosis and hyperglycemia argued against an infectious process.

The diagnosis of tophaceous gouty arthritis was confirmed by aspiration from the tophus, which demonstrated monosodium urate (MSU) crystals on polarized light microscopy. The patient presented with acute gout on the first right toe overlaying chronic tophaceous gout, complicated by renal failure.

Four phases. Gout progresses through 4 phases: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout (intervals between acute attacks), and chronic tophaceous gout.¹ Chronic tophaceous gout is characterized by tophi—collections of solid urate in connective tissues (from bone to bursa, tendons, ligaments, and entheses).² There are often multiple tophi and they may be calcified. An acute gouty attack is marked by a relatively sudden increase in pain and swelling, and may improve spontaneously over the course of 7 to 10 days.³

Gout is the most common form of inflammatory arthritis, with a prevalence in the United States of 3.9%.⁴The findings of several studies suggest that the prevalence and incidence of gout have risen in recent decades, which may be attributable to a growing aging population, the rise in obesity, increasing numbers of people who have other conditions such as heart disease, kidney disease, and/or diabetes, and the use of diuretics by individuals with cardiovascular disease.⁵

In a meta-analysis on gouty involvement of the first MTP joint, the occurrence of acute first MTP arthritis has been reported to be an independent predictor of MSU crystal presence in patients with gout.⁶ The presence of first MTP arthritis and the predilection for MSU deposition in the medial and dorsal aspects of the joint suggested an association, but no causation, between the 2 disease processes. The authors concluded that the distinction between osteoarthritis and gout as the cause of the joint damage is often difficult.

The diagnosis of gout may be made clinically based on established clinical criteria. The most commonly used are the 1977 American College of Rheumatology (ACR) criteria for the classification of acute arthritis of primary gout. (See “The 12 diagnostic criteria for gout.”⁷) However, in 2015, the ACR/European League Against Rheumatism (EULAR) published a new set of criteria that include the signs and symptoms of chronic gout, as well.⁸ (The ACR-EULAR Gout Classification Criteria Calculator may be accessed at http://goutclassificationcalculator.auckland.ac.nz/.)

Differential diagnosis includes trauma, septic and reactive arthritis

The differential diagnosis of acute gouty arthritis includes trauma, pseudogout (arthritis involving calcium pyrophosphate dehydrate), septic arthritis, reactive arthritis, post-streptococcal arthritis, and Lyme disease.

Trauma with a resulting acute or stress fracture can be determined by x-ray or magnetic resonance imaging (MRI).

Pseudogout requires aspiration of fluid and examination for calcium pyrophosphate crystals under polarizing microscopy.⁹

Septic arthritis may present in a similar manner to other causes of acute arthritis. Therefore, arthrocentesis is needed to identify the causative infectious agent.¹⁰ Septic arthritis was considered in our patient, given his age, history of diabetes mellitus, and finding of skin ulceration over the toe. However, our patient did not have systemic symptoms, and the joint aspiration did not show the presence of bacteria.

Reactive arthritis typically presents with inflammation of the ligaments and tendons at their sites of insertion into the bone, and can affect other areas of the body, such as the genitourinary and ocular systems.¹¹

Post-streptococcal arthritis (aka acute rheumatic fever [ARF]) and Lyme disease can also present with joint complaints. The arthritis in ARF is usually migratory and involves several joints. Fever, rash, and a history of group A streptococcal infection are also diagnostic features.¹² History of travel to an endemic area or seasonal exposure would further differentiate Lyme disease from other causes of arthritis.

Further inquiry during the patient’s hospitalization revealed that he ate a lot of seafood and organ meat.

Deciding on a course of treatment

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids.¹³ Various NSAIDs have been studied in the treatment of acute gout, but none showed absolute superiority over others. One option is naproxen 500 mg twice daily, but the choice of NSAID is mainly based on the adverse reaction profile and the physician’s preference.

Due to frequent gastrointestinal adverse effects and the concern for toxicity and drug interactions, colchicine and corticosteroids are not typically the first-line agents for acute gout treatment. Patients with frequent recurrent gouty attacks require urate-lowering therapies, such as allopurinol or probenecid. Other indications for urate-lowering therapies include evidence of tophaceous deposits in joints and soft tissues and gouty arthropathy.

Our patient’s renal failure was likely chronic, secondary to his untreated tophaceous gouty disease. Because his creatinine clearance was between 30 and 60 mL/min per 1.73 m², he was not treated with NSAIDs, but with colchicine 1.2 mg for his initial flare, followed with a single dose of 0.6 mg in one hour. The patient had dramatic improvement of his pain the following day.

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs, colchicine, and corticosteroids.

Patient education on chronic gout was also provided. We specifically discussed the patient’s dietary habits with him, advising him to minimize his intake of seafood, animal organs, and red meat products, which are high in purines. The patient was also told that he would need to start urate-lowering therapy to prevent recurrent gouty attacks and further complications from gout.

CORRESPONDENCE
Joseph Huang, MD, Fort Belvoir Community Hospital, Family Medicine Clinic, 1st Floor Eagle Pavilion, 9300 Dewitt Loop, Fort Belvoir, VA 22060; josephchunfu@gmail.com.

A 68-year-old Filipino man with a history of hypertension, type 2 diabetes, and osteoarthritis presented to the emergency department with a one-week history of increasing pain, swelling, erythema, and seepage of his right great toe. The patient denied paresthesias, fever, chills, night sweats, cough, dyspnea, or any change in his diet, medications (which included lisinopril, metformin, and acetaminophen as needed), or routine. Social history was negative for alcohol use and cigarette smoking.

He previously had similar symptoms in his right fourth toe that resulted in amputation. The patient was told at the time that he had a “bone infection” and amputation was necessary.

The patient was thin, alert, oriented, and in no acute distress. His vital signs and a cardiopulmonary exam were normal. The patient’s right great toe was tender to touch, with ulceration of the skin dorsally at the proximal nail fold. In addition, his toe was oozing a purulent, non-foul smelling discharge (FIGURE 1). Other pertinent findings included multiple enlarged joints on both hands with visible yellow-white subcutaneous nodules on the hands and dorsum of the forearm (FIGURE 2).

The patient’s white blood cell count was 10,800/mcL, C-reactive protein (CRP) was 18 mg/L, erythrocyte sedimentation rate (ESR) was 80 mm/hr, and uric acid was 12.5 mg/dL. His blood urea nitrogen was 52 mg/dL and creatinine was 2.5 mg/dL. A glycated hemoglobin test was 7.2%. A wound culture, aspirate from the dorsum of the toe, and x-ray were obtained.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Tophaceous gouty arthritis

The x-ray of the right great toe showed erosions of the metatarsophalangeal (MTP) joint (FIGURE 3). Given the patient’s age, underlying diabetes, skin ulceration, and elevation of CRP and ESR, the initial concern was for septic arthritis and osteomyelitis. However, the absence of leukocytosis and hyperglycemia argued against an infectious process.

The diagnosis of tophaceous gouty arthritis was confirmed by aspiration from the tophus, which demonstrated monosodium urate (MSU) crystals on polarized light microscopy. The patient presented with acute gout on the first right toe overlaying chronic tophaceous gout, complicated by renal failure.

Four phases. Gout progresses through 4 phases: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout (intervals between acute attacks), and chronic tophaceous gout.¹ Chronic tophaceous gout is characterized by tophi—collections of solid urate in connective tissues (from bone to bursa, tendons, ligaments, and entheses).² There are often multiple tophi and they may be calcified. An acute gouty attack is marked by a relatively sudden increase in pain and swelling, and may improve spontaneously over the course of 7 to 10 days.³

Gout is the most common form of inflammatory arthritis, with a prevalence in the United States of 3.9%.⁴The findings of several studies suggest that the prevalence and incidence of gout have risen in recent decades, which may be attributable to a growing aging population, the rise in obesity, increasing numbers of people who have other conditions such as heart disease, kidney disease, and/or diabetes, and the use of diuretics by individuals with cardiovascular disease.⁵

In a meta-analysis on gouty involvement of the first MTP joint, the occurrence of acute first MTP arthritis has been reported to be an independent predictor of MSU crystal presence in patients with gout.⁶ The presence of first MTP arthritis and the predilection for MSU deposition in the medial and dorsal aspects of the joint suggested an association, but no causation, between the 2 disease processes. The authors concluded that the distinction between osteoarthritis and gout as the cause of the joint damage is often difficult.

The diagnosis of gout may be made clinically based on established clinical criteria. The most commonly used are the 1977 American College of Rheumatology (ACR) criteria for the classification of acute arthritis of primary gout. (See “The 12 diagnostic criteria for gout.”⁷) However, in 2015, the ACR/European League Against Rheumatism (EULAR) published a new set of criteria that include the signs and symptoms of chronic gout, as well.⁸ (The ACR-EULAR Gout Classification Criteria Calculator may be accessed at http://goutclassificationcalculator.auckland.ac.nz/.)

Differential diagnosis includes trauma, septic and reactive arthritis

The differential diagnosis of acute gouty arthritis includes trauma, pseudogout (arthritis involving calcium pyrophosphate dehydrate), septic arthritis, reactive arthritis, post-streptococcal arthritis, and Lyme disease.

Trauma with a resulting acute or stress fracture can be determined by x-ray or magnetic resonance imaging (MRI).

Pseudogout requires aspiration of fluid and examination for calcium pyrophosphate crystals under polarizing microscopy.⁹

Septic arthritis may present in a similar manner to other causes of acute arthritis. Therefore, arthrocentesis is needed to identify the causative infectious agent.¹⁰ Septic arthritis was considered in our patient, given his age, history of diabetes mellitus, and finding of skin ulceration over the toe. However, our patient did not have systemic symptoms, and the joint aspiration did not show the presence of bacteria.

Reactive arthritis typically presents with inflammation of the ligaments and tendons at their sites of insertion into the bone, and can affect other areas of the body, such as the genitourinary and ocular systems.¹¹

Post-streptococcal arthritis (aka acute rheumatic fever [ARF]) and Lyme disease can also present with joint complaints. The arthritis in ARF is usually migratory and involves several joints. Fever, rash, and a history of group A streptococcal infection are also diagnostic features.¹² History of travel to an endemic area or seasonal exposure would further differentiate Lyme disease from other causes of arthritis.

Further inquiry during the patient’s hospitalization revealed that he ate a lot of seafood and organ meat.

Deciding on a course of treatment

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids.¹³ Various NSAIDs have been studied in the treatment of acute gout, but none showed absolute superiority over others. One option is naproxen 500 mg twice daily, but the choice of NSAID is mainly based on the adverse reaction profile and the physician’s preference.

Due to frequent gastrointestinal adverse effects and the concern for toxicity and drug interactions, colchicine and corticosteroids are not typically the first-line agents for acute gout treatment. Patients with frequent recurrent gouty attacks require urate-lowering therapies, such as allopurinol or probenecid. Other indications for urate-lowering therapies include evidence of tophaceous deposits in joints and soft tissues and gouty arthropathy.

Our patient’s renal failure was likely chronic, secondary to his untreated tophaceous gouty disease. Because his creatinine clearance was between 30 and 60 mL/min per 1.73 m², he was not treated with NSAIDs, but with colchicine 1.2 mg for his initial flare, followed with a single dose of 0.6 mg in one hour. The patient had dramatic improvement of his pain the following day.

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs, colchicine, and corticosteroids.

Patient education on chronic gout was also provided. We specifically discussed the patient’s dietary habits with him, advising him to minimize his intake of seafood, animal organs, and red meat products, which are high in purines. The patient was also told that he would need to start urate-lowering therapy to prevent recurrent gouty attacks and further complications from gout.

CORRESPONDENCE
Joseph Huang, MD, Fort Belvoir Community Hospital, Family Medicine Clinic, 1st Floor Eagle Pavilion, 9300 Dewitt Loop, Fort Belvoir, VA 22060; josephchunfu@gmail.com.

A 68-year-old Filipino man with a history of hypertension, type 2 diabetes, and osteoarthritis presented to the emergency department with a one-week history of increasing pain, swelling, erythema, and seepage of his right great toe. The patient denied paresthesias, fever, chills, night sweats, cough, dyspnea, or any change in his diet, medications (which included lisinopril, metformin, and acetaminophen as needed), or routine. Social history was negative for alcohol use and cigarette smoking.

He previously had similar symptoms in his right fourth toe that resulted in amputation. The patient was told at the time that he had a “bone infection” and amputation was necessary.

The patient was thin, alert, oriented, and in no acute distress. His vital signs and a cardiopulmonary exam were normal. The patient’s right great toe was tender to touch, with ulceration of the skin dorsally at the proximal nail fold. In addition, his toe was oozing a purulent, non-foul smelling discharge (FIGURE 1). Other pertinent findings included multiple enlarged joints on both hands with visible yellow-white subcutaneous nodules on the hands and dorsum of the forearm (FIGURE 2).

The patient’s white blood cell count was 10,800/mcL, C-reactive protein (CRP) was 18 mg/L, erythrocyte sedimentation rate (ESR) was 80 mm/hr, and uric acid was 12.5 mg/dL. His blood urea nitrogen was 52 mg/dL and creatinine was 2.5 mg/dL. A glycated hemoglobin test was 7.2%. A wound culture, aspirate from the dorsum of the toe, and x-ray were obtained.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Tophaceous gouty arthritis

The x-ray of the right great toe showed erosions of the metatarsophalangeal (MTP) joint (FIGURE 3). Given the patient’s age, underlying diabetes, skin ulceration, and elevation of CRP and ESR, the initial concern was for septic arthritis and osteomyelitis. However, the absence of leukocytosis and hyperglycemia argued against an infectious process.

The diagnosis of tophaceous gouty arthritis was confirmed by aspiration from the tophus, which demonstrated monosodium urate (MSU) crystals on polarized light microscopy. The patient presented with acute gout on the first right toe overlaying chronic tophaceous gout, complicated by renal failure.

Four phases. Gout progresses through 4 phases: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout (intervals between acute attacks), and chronic tophaceous gout.¹ Chronic tophaceous gout is characterized by tophi—collections of solid urate in connective tissues (from bone to bursa, tendons, ligaments, and entheses).² There are often multiple tophi and they may be calcified. An acute gouty attack is marked by a relatively sudden increase in pain and swelling, and may improve spontaneously over the course of 7 to 10 days.³

Gout is the most common form of inflammatory arthritis, with a prevalence in the United States of 3.9%.⁴The findings of several studies suggest that the prevalence and incidence of gout have risen in recent decades, which may be attributable to a growing aging population, the rise in obesity, increasing numbers of people who have other conditions such as heart disease, kidney disease, and/or diabetes, and the use of diuretics by individuals with cardiovascular disease.⁵

In a meta-analysis on gouty involvement of the first MTP joint, the occurrence of acute first MTP arthritis has been reported to be an independent predictor of MSU crystal presence in patients with gout.⁶ The presence of first MTP arthritis and the predilection for MSU deposition in the medial and dorsal aspects of the joint suggested an association, but no causation, between the 2 disease processes. The authors concluded that the distinction between osteoarthritis and gout as the cause of the joint damage is often difficult.

The diagnosis of gout may be made clinically based on established clinical criteria. The most commonly used are the 1977 American College of Rheumatology (ACR) criteria for the classification of acute arthritis of primary gout. (See “The 12 diagnostic criteria for gout.”⁷) However, in 2015, the ACR/European League Against Rheumatism (EULAR) published a new set of criteria that include the signs and symptoms of chronic gout, as well.⁸ (The ACR-EULAR Gout Classification Criteria Calculator may be accessed at http://goutclassificationcalculator.auckland.ac.nz/.)

Differential diagnosis includes trauma, septic and reactive arthritis

The differential diagnosis of acute gouty arthritis includes trauma, pseudogout (arthritis involving calcium pyrophosphate dehydrate), septic arthritis, reactive arthritis, post-streptococcal arthritis, and Lyme disease.

Trauma with a resulting acute or stress fracture can be determined by x-ray or magnetic resonance imaging (MRI).

Pseudogout requires aspiration of fluid and examination for calcium pyrophosphate crystals under polarizing microscopy.⁹

Septic arthritis may present in a similar manner to other causes of acute arthritis. Therefore, arthrocentesis is needed to identify the causative infectious agent.¹⁰ Septic arthritis was considered in our patient, given his age, history of diabetes mellitus, and finding of skin ulceration over the toe. However, our patient did not have systemic symptoms, and the joint aspiration did not show the presence of bacteria.

Reactive arthritis typically presents with inflammation of the ligaments and tendons at their sites of insertion into the bone, and can affect other areas of the body, such as the genitourinary and ocular systems.¹¹

Post-streptococcal arthritis (aka acute rheumatic fever [ARF]) and Lyme disease can also present with joint complaints. The arthritis in ARF is usually migratory and involves several joints. Fever, rash, and a history of group A streptococcal infection are also diagnostic features.¹² History of travel to an endemic area or seasonal exposure would further differentiate Lyme disease from other causes of arthritis.

Further inquiry during the patient’s hospitalization revealed that he ate a lot of seafood and organ meat.

Deciding on a course of treatment

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids.¹³ Various NSAIDs have been studied in the treatment of acute gout, but none showed absolute superiority over others. One option is naproxen 500 mg twice daily, but the choice of NSAID is mainly based on the adverse reaction profile and the physician’s preference.

Due to frequent gastrointestinal adverse effects and the concern for toxicity and drug interactions, colchicine and corticosteroids are not typically the first-line agents for acute gout treatment. Patients with frequent recurrent gouty attacks require urate-lowering therapies, such as allopurinol or probenecid. Other indications for urate-lowering therapies include evidence of tophaceous deposits in joints and soft tissues and gouty arthropathy.

Our patient’s renal failure was likely chronic, secondary to his untreated tophaceous gouty disease. Because his creatinine clearance was between 30 and 60 mL/min per 1.73 m², he was not treated with NSAIDs, but with colchicine 1.2 mg for his initial flare, followed with a single dose of 0.6 mg in one hour. The patient had dramatic improvement of his pain the following day.

Initial treatment choices for acute gout include nonsteroidal anti-inflammatory drugs, colchicine, and corticosteroids.

Patient education on chronic gout was also provided. We specifically discussed the patient’s dietary habits with him, advising him to minimize his intake of seafood, animal organs, and red meat products, which are high in purines. The patient was also told that he would need to start urate-lowering therapy to prevent recurrent gouty attacks and further complications from gout.

CORRESPONDENCE
Joseph Huang, MD, Fort Belvoir Community Hospital, Family Medicine Clinic, 1st Floor Eagle Pavilion, 9300 Dewitt Loop, Fort Belvoir, VA 22060; josephchunfu@gmail.com.

Evidence summary

A 2013 Cochrane review of 17 RCTs with 2596 patients compared corticosteroids with placebo for treating bronchiolitis in children younger than 2 years.¹ The studies used dexamethasone, prednisolone, prednisone, and budesonide delivered by oral, inhaled, intravenous (IV), or intramuscular (IM) routes, ranging between a one-day dose to a 5-day taper. Doses ranged from 0.5 to 2 mg/kg/d for oral and parenteral routes and 0.2 to 1 mg for inhalation. Outcomes were rate of admissions at Days 1 and 7 from outpatient trials and length of stay among inpatients.

Investigators found no significant difference in admission rates at Day 1 and Day 7 between children treated with corticosteroids compared with placebo (Day 1: 8 trials, 1762 patients; relative risk [RR]=0.92; 95% confidence interval [CI], 0.78-1.1; Day 7: 5 trials, 1530 patients; RR=0.86; 95% CI, 0.70-1.1). Length of hospital stay didn’t differ between children treated with corticosteroids and children who received placebo (8 trials, 633 patients; mean difference= −0.18 days; 95% CI, −0.39 to 0.04).

Corticosteroid + epinephrine can lower hospital admissions

A 2009 multicenter, double-blind RCT with 800 patients (infants 6 weeks to 12 months of age with a first episode of bronchiolitis) that was included in the 2013 Cochrane review also compared the combination of epinephrine and corticosteroid with placebo and either agent alone.²

Infants were assigned to 4 groups: oral dexamethasone alone (1 mg/kg in the emergency room [ER] on Day 1, followed by 0.6 mg/kg daily for 5 days); nebulized epinephrine alone (2 treatments of 3 mL epinephrine 1:1000 solution); combined dexamethasone and epinephrine; and placebo. The primary outcome was hospital admission as long as 7 days after being seen in the ER.

Rates of admission were similar for the dexamethasone and placebo groups (25.6% vs 26.4%, respectively; RR=0.96; 95% CI, 0.69-1.3). The epinephrine group’s rate of admission was 23.7% (RR=0.88; CI, 0.63–1.23). Only the dexamethasone-epinephrine group had a lower rate of admission compared with placebo (17% vs 26%; RR=0.65; 95% CI, 0.45-0.95). The number needed to treat with dexamethasone-epinephrine to prevent one hospital admission was 11.

Review prompts revised recommendations

Based on the Cochrane review, the American Academy of Pediatrics (AAP) revised its evidence-based clinical practice guideline in 2014 to recommend that clinicians not administer systemic corticosteroids to infants with a diagnosis of bronchiolitis in any setting (evidence quality B, strong recommendation, based on results of multiple RCTs).³ The AAP advocates additional large trials to clarify whether combination therapy (corticosteroids plus agents with α or β agonist activity) is effective.

Evidence summary

A 2013 Cochrane review of 17 RCTs with 2596 patients compared corticosteroids with placebo for treating bronchiolitis in children younger than 2 years.¹ The studies used dexamethasone, prednisolone, prednisone, and budesonide delivered by oral, inhaled, intravenous (IV), or intramuscular (IM) routes, ranging between a one-day dose to a 5-day taper. Doses ranged from 0.5 to 2 mg/kg/d for oral and parenteral routes and 0.2 to 1 mg for inhalation. Outcomes were rate of admissions at Days 1 and 7 from outpatient trials and length of stay among inpatients.

Investigators found no significant difference in admission rates at Day 1 and Day 7 between children treated with corticosteroids compared with placebo (Day 1: 8 trials, 1762 patients; relative risk [RR]=0.92; 95% confidence interval [CI], 0.78-1.1; Day 7: 5 trials, 1530 patients; RR=0.86; 95% CI, 0.70-1.1). Length of hospital stay didn’t differ between children treated with corticosteroids and children who received placebo (8 trials, 633 patients; mean difference= −0.18 days; 95% CI, −0.39 to 0.04).

Corticosteroid + epinephrine can lower hospital admissions

A 2009 multicenter, double-blind RCT with 800 patients (infants 6 weeks to 12 months of age with a first episode of bronchiolitis) that was included in the 2013 Cochrane review also compared the combination of epinephrine and corticosteroid with placebo and either agent alone.²

Infants were assigned to 4 groups: oral dexamethasone alone (1 mg/kg in the emergency room [ER] on Day 1, followed by 0.6 mg/kg daily for 5 days); nebulized epinephrine alone (2 treatments of 3 mL epinephrine 1:1000 solution); combined dexamethasone and epinephrine; and placebo. The primary outcome was hospital admission as long as 7 days after being seen in the ER.

Rates of admission were similar for the dexamethasone and placebo groups (25.6% vs 26.4%, respectively; RR=0.96; 95% CI, 0.69-1.3). The epinephrine group’s rate of admission was 23.7% (RR=0.88; CI, 0.63–1.23). Only the dexamethasone-epinephrine group had a lower rate of admission compared with placebo (17% vs 26%; RR=0.65; 95% CI, 0.45-0.95). The number needed to treat with dexamethasone-epinephrine to prevent one hospital admission was 11.

Review prompts revised recommendations

Based on the Cochrane review, the American Academy of Pediatrics (AAP) revised its evidence-based clinical practice guideline in 2014 to recommend that clinicians not administer systemic corticosteroids to infants with a diagnosis of bronchiolitis in any setting (evidence quality B, strong recommendation, based on results of multiple RCTs).³ The AAP advocates additional large trials to clarify whether combination therapy (corticosteroids plus agents with α or β agonist activity) is effective.

Evidence summary

A 2013 Cochrane review of 17 RCTs with 2596 patients compared corticosteroids with placebo for treating bronchiolitis in children younger than 2 years.¹ The studies used dexamethasone, prednisolone, prednisone, and budesonide delivered by oral, inhaled, intravenous (IV), or intramuscular (IM) routes, ranging between a one-day dose to a 5-day taper. Doses ranged from 0.5 to 2 mg/kg/d for oral and parenteral routes and 0.2 to 1 mg for inhalation. Outcomes were rate of admissions at Days 1 and 7 from outpatient trials and length of stay among inpatients.

Investigators found no significant difference in admission rates at Day 1 and Day 7 between children treated with corticosteroids compared with placebo (Day 1: 8 trials, 1762 patients; relative risk [RR]=0.92; 95% confidence interval [CI], 0.78-1.1; Day 7: 5 trials, 1530 patients; RR=0.86; 95% CI, 0.70-1.1). Length of hospital stay didn’t differ between children treated with corticosteroids and children who received placebo (8 trials, 633 patients; mean difference= −0.18 days; 95% CI, −0.39 to 0.04).

Corticosteroid + epinephrine can lower hospital admissions

A 2009 multicenter, double-blind RCT with 800 patients (infants 6 weeks to 12 months of age with a first episode of bronchiolitis) that was included in the 2013 Cochrane review also compared the combination of epinephrine and corticosteroid with placebo and either agent alone.²

Infants were assigned to 4 groups: oral dexamethasone alone (1 mg/kg in the emergency room [ER] on Day 1, followed by 0.6 mg/kg daily for 5 days); nebulized epinephrine alone (2 treatments of 3 mL epinephrine 1:1000 solution); combined dexamethasone and epinephrine; and placebo. The primary outcome was hospital admission as long as 7 days after being seen in the ER.

Rates of admission were similar for the dexamethasone and placebo groups (25.6% vs 26.4%, respectively; RR=0.96; 95% CI, 0.69-1.3). The epinephrine group’s rate of admission was 23.7% (RR=0.88; CI, 0.63–1.23). Only the dexamethasone-epinephrine group had a lower rate of admission compared with placebo (17% vs 26%; RR=0.65; 95% CI, 0.45-0.95). The number needed to treat with dexamethasone-epinephrine to prevent one hospital admission was 11.

Review prompts revised recommendations

Based on the Cochrane review, the American Academy of Pediatrics (AAP) revised its evidence-based clinical practice guideline in 2014 to recommend that clinicians not administer systemic corticosteroids to infants with a diagnosis of bronchiolitis in any setting (evidence quality B, strong recommendation, based on results of multiple RCTs).³ The AAP advocates additional large trials to clarify whether combination therapy (corticosteroids plus agents with α or β agonist activity) is effective.

Immunotherapy using sublingual tablets containing house dust mite allergen extended the interval until patients developed a moderate asthma exacerbation in a manufacturer-sponsored clinical trial reported online April 26 in JAMA.

However, patients’ scores on both the Asthma Control Questionnaire and the Asthma Quality of Life Questionnaire showed no difference between active treatment and placebo. And 25%-27% of the study participants dropped out of the study, usually citing asthma exacerbations, adverse events, or “withdrawal of consent.” Further studies are needed to assess long-term efficacy and safety, said Dr. J. Christian Virchow of the department of pulmonology/intensive care medicine, University of Rostock (Germany), and his associates.

©Eraxion/Thinkstock

The trial, involving 834 adults with asthma related to house dust mite allergy that was not well controlled by inhaled corticosteroids and short-acting beta-agonists, was performed at 109 sites in 13 European countries during a 2-year period. These participants were randomly assigned to receive add-on daily sublingual tablets containing low-dose dust-mite extract (275 patients), high-dose extract (282 patients), or placebo (277 patients) for 7-12 months. During the final 6 months of the intervention, corticosteroids were reduced by half for 3 months and then withdrawn for 3 months.

The primary efficacy outcome (time to the first asthma exacerbation) was extended by both doses of active drug, compared with placebo, with hazard ratios of 0.69 for the lower dose and 0.66 for the higher dose, the investigators said (JAMA. 2016 Apr 26;315[16]:1715-25).

Adverse events were significantly more frequent with active treatment, affecting 39% of patients receiving the lower dose and 46% of those receiving the higher dose of active immunotherapy, compared with only 17% of patients receiving placebo. However, this study was not adequately powered to compare adverse events across groups, Dr. Virchow and his associates noted.

The most frequently reported adverse events were oral pruritus, mouth edema, and throat irritation, which developed within a median of 1-2 minutes of taking the first dose on day 1 and persisted for a median of 4-23 days. There were 32 serious adverse events, including erosive esophagitis, hepatocellular injury, arthralgia, laryngeal edema, and asthma.

This trial was limited in that treatment duration was much shorter than that for a standard course of immunotherapy, which is often 3 years. This prevents drawing conclusions regarding the sustained effect of the treatment. “Furthermore, because the ultimate aim of allergen immunotherapy is disease modification beyond the duration of treatment, a follow-up after the end of treatment would have been relevant,” the investigators said.

This study was sponsored by the Danish pharmaceutical company ALK. Dr. Virchow reported ties to 31 industry sources; his associates also reported ties to numerous industry sources.

Immunotherapy using sublingual tablets containing house dust mite allergen extended the interval until patients developed a moderate asthma exacerbation in a manufacturer-sponsored clinical trial reported online April 26 in JAMA.

However, patients’ scores on both the Asthma Control Questionnaire and the Asthma Quality of Life Questionnaire showed no difference between active treatment and placebo. And 25%-27% of the study participants dropped out of the study, usually citing asthma exacerbations, adverse events, or “withdrawal of consent.” Further studies are needed to assess long-term efficacy and safety, said Dr. J. Christian Virchow of the department of pulmonology/intensive care medicine, University of Rostock (Germany), and his associates.

©Eraxion/Thinkstock

The trial, involving 834 adults with asthma related to house dust mite allergy that was not well controlled by inhaled corticosteroids and short-acting beta-agonists, was performed at 109 sites in 13 European countries during a 2-year period. These participants were randomly assigned to receive add-on daily sublingual tablets containing low-dose dust-mite extract (275 patients), high-dose extract (282 patients), or placebo (277 patients) for 7-12 months. During the final 6 months of the intervention, corticosteroids were reduced by half for 3 months and then withdrawn for 3 months.

The primary efficacy outcome (time to the first asthma exacerbation) was extended by both doses of active drug, compared with placebo, with hazard ratios of 0.69 for the lower dose and 0.66 for the higher dose, the investigators said (JAMA. 2016 Apr 26;315[16]:1715-25).

Adverse events were significantly more frequent with active treatment, affecting 39% of patients receiving the lower dose and 46% of those receiving the higher dose of active immunotherapy, compared with only 17% of patients receiving placebo. However, this study was not adequately powered to compare adverse events across groups, Dr. Virchow and his associates noted.

The most frequently reported adverse events were oral pruritus, mouth edema, and throat irritation, which developed within a median of 1-2 minutes of taking the first dose on day 1 and persisted for a median of 4-23 days. There were 32 serious adverse events, including erosive esophagitis, hepatocellular injury, arthralgia, laryngeal edema, and asthma.

This trial was limited in that treatment duration was much shorter than that for a standard course of immunotherapy, which is often 3 years. This prevents drawing conclusions regarding the sustained effect of the treatment. “Furthermore, because the ultimate aim of allergen immunotherapy is disease modification beyond the duration of treatment, a follow-up after the end of treatment would have been relevant,” the investigators said.

This study was sponsored by the Danish pharmaceutical company ALK. Dr. Virchow reported ties to 31 industry sources; his associates also reported ties to numerous industry sources.

Immunotherapy using sublingual tablets containing house dust mite allergen extended the interval until patients developed a moderate asthma exacerbation in a manufacturer-sponsored clinical trial reported online April 26 in JAMA.

However, patients’ scores on both the Asthma Control Questionnaire and the Asthma Quality of Life Questionnaire showed no difference between active treatment and placebo. And 25%-27% of the study participants dropped out of the study, usually citing asthma exacerbations, adverse events, or “withdrawal of consent.” Further studies are needed to assess long-term efficacy and safety, said Dr. J. Christian Virchow of the department of pulmonology/intensive care medicine, University of Rostock (Germany), and his associates.

©Eraxion/Thinkstock

The trial, involving 834 adults with asthma related to house dust mite allergy that was not well controlled by inhaled corticosteroids and short-acting beta-agonists, was performed at 109 sites in 13 European countries during a 2-year period. These participants were randomly assigned to receive add-on daily sublingual tablets containing low-dose dust-mite extract (275 patients), high-dose extract (282 patients), or placebo (277 patients) for 7-12 months. During the final 6 months of the intervention, corticosteroids were reduced by half for 3 months and then withdrawn for 3 months.

The primary efficacy outcome (time to the first asthma exacerbation) was extended by both doses of active drug, compared with placebo, with hazard ratios of 0.69 for the lower dose and 0.66 for the higher dose, the investigators said (JAMA. 2016 Apr 26;315[16]:1715-25).

Adverse events were significantly more frequent with active treatment, affecting 39% of patients receiving the lower dose and 46% of those receiving the higher dose of active immunotherapy, compared with only 17% of patients receiving placebo. However, this study was not adequately powered to compare adverse events across groups, Dr. Virchow and his associates noted.

The most frequently reported adverse events were oral pruritus, mouth edema, and throat irritation, which developed within a median of 1-2 minutes of taking the first dose on day 1 and persisted for a median of 4-23 days. There were 32 serious adverse events, including erosive esophagitis, hepatocellular injury, arthralgia, laryngeal edema, and asthma.

This trial was limited in that treatment duration was much shorter than that for a standard course of immunotherapy, which is often 3 years. This prevents drawing conclusions regarding the sustained effect of the treatment. “Furthermore, because the ultimate aim of allergen immunotherapy is disease modification beyond the duration of treatment, a follow-up after the end of treatment would have been relevant,” the investigators said.

This study was sponsored by the Danish pharmaceutical company ALK. Dr. Virchow reported ties to 31 industry sources; his associates also reported ties to numerous industry sources.

DePuy Synthes Mitek Sports Medicine
(https://www.depuysynthes.com/hcp/mitek-sports-medicine)

Gryphon® Suture Anchor with Proknot™ Technology

Paul Favorito, MD, Wellington Orthopaedic and Sports Medicine, Cincinnati, OH

The Gryphon^® suture anchor with Proknot™ technology is a doubled No. 1 Permacord^® high-strength orthopedic suture with a proprietary pre-tied sliding knot. The suture construct is loaded onto a 3.0-mm Gryphonsuture anchor (Peek or Biocryl Rapide^® biocomposite material) and has clinical indications for labral repair of the shoulder and hip. In a laboratory setting, Pro­knot technology has been tested against other high-tensile sutures and commonly tied arthroscopic knots.¹ Proknot technology demonstrated higher ultimate strength, significantly less knot volume, and better reproducibility among surgeons.

Surgical pearl: I use the Gryphon Proknot suture anchor for all shoulder Bankart and superior labral anterior to posterior (SLAP) repairs. I have colleagues who also use this anchor for hip arthroscopy.

Once opened on the back table, the surgical assistant may ink the free limb of suture for easy arthroscopic identification. The anchor is placed and, in the case of hard bone frequently encountered in younger patients, a 2.5-mm drill bit may be substituted for the usual 2.4-mm. One important goal of any labral repair is to position knots away from the articular surface. The free suture limb is passed through the labrum, retrieved, and delivered through the open, pre-tied knot on the suture card.

Once the knot is released and dressed, the knot pusher is placed over the suture and the knot is advanced and preliminarily tensioned medial to the articular surface. The suture limbs are separated and one limb of the suture is removed from the knot pusher. As few as 1, or up to 3, half hitches may be placed to secure the knot, taking care to direct it away from the joint surface. The result is a strong but well-positioned knot with minimal mass securing the soft tissue.

DePuy Synthes Mitek Sports Medicine
(https://www.depuysynthes.com/hcp/mitek-sports-medicine)

Gryphon® Suture Anchor with Proknot™ Technology

Paul Favorito, MD, Wellington Orthopaedic and Sports Medicine, Cincinnati, OH

The Gryphon^® suture anchor with Proknot™ technology is a doubled No. 1 Permacord^® high-strength orthopedic suture with a proprietary pre-tied sliding knot. The suture construct is loaded onto a 3.0-mm Gryphonsuture anchor (Peek or Biocryl Rapide^® biocomposite material) and has clinical indications for labral repair of the shoulder and hip. In a laboratory setting, Pro­knot technology has been tested against other high-tensile sutures and commonly tied arthroscopic knots.¹ Proknot technology demonstrated higher ultimate strength, significantly less knot volume, and better reproducibility among surgeons.

Surgical pearl: I use the Gryphon Proknot suture anchor for all shoulder Bankart and superior labral anterior to posterior (SLAP) repairs. I have colleagues who also use this anchor for hip arthroscopy.

Once opened on the back table, the surgical assistant may ink the free limb of suture for easy arthroscopic identification. The anchor is placed and, in the case of hard bone frequently encountered in younger patients, a 2.5-mm drill bit may be substituted for the usual 2.4-mm. One important goal of any labral repair is to position knots away from the articular surface. The free suture limb is passed through the labrum, retrieved, and delivered through the open, pre-tied knot on the suture card.

Once the knot is released and dressed, the knot pusher is placed over the suture and the knot is advanced and preliminarily tensioned medial to the articular surface. The suture limbs are separated and one limb of the suture is removed from the knot pusher. As few as 1, or up to 3, half hitches may be placed to secure the knot, taking care to direct it away from the joint surface. The result is a strong but well-positioned knot with minimal mass securing the soft tissue.

DePuy Synthes Mitek Sports Medicine
(https://www.depuysynthes.com/hcp/mitek-sports-medicine)

Gryphon® Suture Anchor with Proknot™ Technology

Paul Favorito, MD, Wellington Orthopaedic and Sports Medicine, Cincinnati, OH

The Gryphon^® suture anchor with Proknot™ technology is a doubled No. 1 Permacord^® high-strength orthopedic suture with a proprietary pre-tied sliding knot. The suture construct is loaded onto a 3.0-mm Gryphonsuture anchor (Peek or Biocryl Rapide^® biocomposite material) and has clinical indications for labral repair of the shoulder and hip. In a laboratory setting, Pro­knot technology has been tested against other high-tensile sutures and commonly tied arthroscopic knots.¹ Proknot technology demonstrated higher ultimate strength, significantly less knot volume, and better reproducibility among surgeons.

Surgical pearl: I use the Gryphon Proknot suture anchor for all shoulder Bankart and superior labral anterior to posterior (SLAP) repairs. I have colleagues who also use this anchor for hip arthroscopy.

Once opened on the back table, the surgical assistant may ink the free limb of suture for easy arthroscopic identification. The anchor is placed and, in the case of hard bone frequently encountered in younger patients, a 2.5-mm drill bit may be substituted for the usual 2.4-mm. One important goal of any labral repair is to position knots away from the articular surface. The free suture limb is passed through the labrum, retrieved, and delivered through the open, pre-tied knot on the suture card.

Once the knot is released and dressed, the knot pusher is placed over the suture and the knot is advanced and preliminarily tensioned medial to the articular surface. The suture limbs are separated and one limb of the suture is removed from the knot pusher. As few as 1, or up to 3, half hitches may be placed to secure the knot, taking care to direct it away from the joint surface. The result is a strong but well-positioned knot with minimal mass securing the soft tissue.

ORLANDO, FL—Using arthroscopic superior capsule reconstruction (ASCR) to treat patients with massive rotator cuff tears can improve shoulder strength and function, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers used ASCR to treat 100 patients (average age: 66) who had irreparable rotator cuff tears that failed during previous treatment. Physical exams, x-rays, and magnetic resonance imaging were performed before surgery, at 3, 6 and 12 months following surgery, and on a yearly basis thereafter. Rates of return to work or sport were analyzed in 34 patients who were employed and 26 patients who were recreational athletes before the rotator cuff tear.

Overall, 92% of patients significantly improved their strength and shoulder function. In all, 32 patients returned fully to their previous work and 2 patients returned with reduced hours and workloads. All 26 patients who played sports prior to injury fully returned to their activities.

ORLANDO, FL—Using arthroscopic superior capsule reconstruction (ASCR) to treat patients with massive rotator cuff tears can improve shoulder strength and function, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers used ASCR to treat 100 patients (average age: 66) who had irreparable rotator cuff tears that failed during previous treatment. Physical exams, x-rays, and magnetic resonance imaging were performed before surgery, at 3, 6 and 12 months following surgery, and on a yearly basis thereafter. Rates of return to work or sport were analyzed in 34 patients who were employed and 26 patients who were recreational athletes before the rotator cuff tear.

Overall, 92% of patients significantly improved their strength and shoulder function. In all, 32 patients returned fully to their previous work and 2 patients returned with reduced hours and workloads. All 26 patients who played sports prior to injury fully returned to their activities.

ORLANDO, FL—Using arthroscopic superior capsule reconstruction (ASCR) to treat patients with massive rotator cuff tears can improve shoulder strength and function, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers used ASCR to treat 100 patients (average age: 66) who had irreparable rotator cuff tears that failed during previous treatment. Physical exams, x-rays, and magnetic resonance imaging were performed before surgery, at 3, 6 and 12 months following surgery, and on a yearly basis thereafter. Rates of return to work or sport were analyzed in 34 patients who were employed and 26 patients who were recreational athletes before the rotator cuff tear.

Overall, 92% of patients significantly improved their strength and shoulder function. In all, 32 patients returned fully to their previous work and 2 patients returned with reduced hours and workloads. All 26 patients who played sports prior to injury fully returned to their activities.

The musculoskeletal (MSK) ultrasound evaluation of the shoulder provides a cost- and time-efficient imaging modality with similar diagnostic power as magnetic resonance imaging (MRI).^1,2 Its portable point-of-care applications can be used in the office, in the operating room, and in sideline athletic event coverage, as we discussed in Part 1 of this series.³

MSK ultrasound may seem difficult and daunting, and many articles have quoted steep learning curves.^4,5 However, in our experience in teaching many ultrasound courses, this modality can be learned quite quickly with the proper instruction. Physicians are already familiar with anatomy and usually have had some exposure to MRI.⁴ Taking courses in MSK ultrasound or simply learning the basic concepts of ultrasound and then learning the machine controls is usually a good start.^5-8 Practice scanning normal individuals, comparing the images from an MRI to learn how to reproduce the same planes and images. This will allow the user to become familiar with normal anatomy and how to see the images on the ultrasound screen.^5-8 Vollman and colleagues⁹ showed that in trainees, combining MRI images with sonograms enhances the ability to correctly identify MSK ultrasound anatomy from 40.9% to 72.5%, when compared with learning from ultrasound images alone.

There are currently no certifications necessary to perform ultrasound scans or bill for them; however, some insurance carriers may require demonstrating relevant, documented training for reimbursement.³ Various organizations are trying to develop certifications and regulations for ultrasound to standardize the use of this modality. In the United States, the American Institute of Ultrasound in Medicine (AIUM) and the American Registry for Diagnostic Medical Sonography (ARDMS) provide guidelines and particular MSK ultrasound certifications.^10,11

Basic Ultrasound Principles

The ultrasound machine creates electrical impulses that are turned into sound waves by piezoelectric crystals at the probe’s footprint. These sound waves bounce off tissues and return to the probe, where they are converted electronically to an image on the monitor. Depending on the echogenicity of the scanned tissue, the ultrasound beam will either reflect or be absorbed at different rates. This variance is transmitted on the monitor as a grayscale image. When ultrasound waves are highly reflective, like in bone or fat, they are characterized as hyperechoic. The opposite occurs when ultrasound waves are absorbed like in the fluid of a cystic cavity or joint effusion, and the image appears black. This is described as anechoic.¹² Intermediate tissues such as tendons that are less reflective are seen as hypoechoic and appear gray. When a tissue has a similar echogenicity to its surrounding tissues, it is called isoechoic.¹²

The transducer is the scanning component of the ultrasound machine. Transducers come in 2 shapes: linear and curvilinear. The linear probe creates a straight image that is equal to the size of the transducer footprint. The curvilinear probe creates a wider, wedge-shaped panoramic image.

Linear probes are of higher frequency and generate higher resolution images of shallower structures, while curvilinear probes have greater depth penetration but generate lower resolution images. A high frequency of 10 to 15 MHz is preferred for anatomy between 2 cm to 4 cm depth.¹³ Midrange frequency of 5 to 10 MHz is preferred at 5 cm to 6 cm depth, and low-frequency 2 to 5 MHz probes are preferred for anatomical structures >6 cm depth.¹³

Anisotropy is the property of being directionally dependent, as opposed to isotropy, which implies identical properties in all directions. This anisotropic effect is dependent on the angle of the insonating beam. The maximum return echo occurs when the ultrasound beam is perpendicular to the tendon. Decreasing the insonating angle on a normal tendon will cause it to change from brightly hyperechoic (the actual echo from tightly bound tendon fibers) to darkly hypoechoic. If the angle is then increased, the tendon will again appear hyperechoic. If the artifact causes a normal tendon to appear hypoechoic, it may falsely lead to a diagnosis of tendinosis or tear.

Posterior acoustic shadowing is present when a hyperechoic structure reflects the ultrasound beam so much that it creates a dark shadow underneath it.^12,14 This phenomenon is possible since the ultrasound beam cannot penetrate the hyperechoic structure and reflects off its inferior tissues. Reverberation is when the beam is repeated back and forth between 2 parallel highly reflective surfaces. The initial reflection will be displayed correctly, while the subsequent ultrasound waves will be delayed and appear at a farther distance from the transducer.^12,14

The point where the beam is at its narrowest point generates the section of the image that is best visualized.¹⁵ This is called the focal zone, and it can be adjusted to highlight the desired area of evaluation. Gain controls adjust the amount of black, gray, and white on the monitor and can be adjusted to focus the desired image.¹³ Depth settings are fundamental in finding the desired targets. It is recommended to start with a higher depth setting to get an overview and progressively decrease the depth to key in on the desired anatomy.¹³ Color Doppler can be used to view movement within structures and to identify vessels, synovitis, and neovascularization in tendinopathy.¹³

Ultrasound of the Shoulder

Patients should be seated, if possible, on a rotating seat. The examiner’s shoulder should be higher than the patient’s shoulder.¹⁶ The user holds the ultrasound probe between the thumb and index fingers while resting the hypothenar eminence on the patient to serve as a fulcrum and steadying force. The examination should take 5 to 15 minutes, depending on the examiner’s expertise and the amount of anatomy being scanned.

Examining the body requires knowledge of anatomy. The examination and accuracy are determined by the technician using the probe. The probe can be angled any direction and be placed obliquely on the subject. The advantage here is that anatomy in the human body is not always planar. Muscles and tissues can run obliquely or even perpendicular to each other. When evaluating anatomy, the examiner should keep in mind what structure he or she is looking for; where it should be found; what landmarks can be used to easily locate it; what orientation it has; and what the normal anatomy should look like.

Muscle appears as a lattice with larger areas of hypoechoic muscle tissue and hyperechoic fascial perimysium layers traversing through it.¹⁷ The actual muscle tissue appears hypoechoic from the fluid or blood found within. Scarring, fibrosis, calcification, or chronic injury will change the tissue to appear denser or hyperechoic.¹⁷ Acute injury will appear hypoechoic from the inflammatory response and influx of blood. Tendon appears dense and hyperechoic with striations within the tissue, sometimes referred to as a horse’s tail.¹⁷ When torn, there will be a disassociation of the tissue with a hypoechoic region between the 2 ends. The attachment to the bone and muscle tissue should appear uniform. Hyperechoic areas within the tendon may be from calcification. Ligament appears similar to tendon but is more isoechoic and connects bone to bone. Evaluation of the entire length and the attachments to the bone are critical to evaluate for disease.

Bone appears bright hyperechoic, smooth, and flat, while hyaline cartilage is hypoechoic, smooth, and runs superiorly in a parallel pattern to its respective inferior cortical bone.¹⁷

Fibrocartilage is hyperechoic and typically triangularly shaped, such as in the glenohumeral labrum. Nerves appear fascicular and hypoechoic surrounded by hyperechoic epineurium.¹⁴

The epidermis and dermis are the most superficial structure on top of the screen, and are also hyperechoic.¹⁷

The Diagnostic Shoulder Examination

The proximal long head of the biceps tendon (LHBT) is the easiest structure in the shoulder to identify because of the anatomic structure, the bicipital groove. By keeping the arm relaxed, perpendicular to the ground, and in neutral rotation, the probe can be placed perpendicular to the arm over the proximal shoulder (Figure 1A).^16-20 By finding the groove, the biceps tendon will usually be found resting within the groove (Figure 1B). This is the short axis view and is equivalent to an MRI in the axial plane.

The long axis view of the proximal biceps tendon is found by keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The user should be sure to visualize the entire tendon on the screen. If only part of the tendon is seen along only part of the screen, then the probe is oblique to the tendon. In this case, the probe area showing the tendon must be stabilized as the center or set point. The other part of the probe will then pivot until all of the tendon is seen on the screen. The MRI equivalent to the long axis of the proximal biceps tendon is the sagittal view.

Ultrasound is a dynamic evaluation. Moving the probe or moving the patient will change what and how something is imaged. The proximal biceps tendon is a good example of this concept. The bicipital groove is very deep proximally and flattens out as it travels distally to the mid-humerus. The examiner should continually adjust his or her hand/probe/patient position as well as depth/gain and other console functions to adapt to the dynamics of the scan. While keeping the bicep tendon in a short axis view, the tendon can be dynamically evaluated for subluxation by internally and externally rotating the arm.

To find the subscapularis, the arm remains in a neutral position with the hand supinated and the probe is held parallel with the ground. After finding the bicipital groove, the subscapularis tendon insertion is just medial to the groove (Figure 1B). By externally rotating the arm, the subscapularis tendon/muscle will come into a long axis view.^16-20 The MRI equivalent to the long axis view of the subscapularis is the axial view. Dynamic testing can be done by internally and externally rotating the arm to evaluate for impingement of the subscapularis tendon as it slides underneath the coracoid process. To view the subscapularis tendon in short axis, the tendon is kept in the center of the screen/probe, and the probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The MRI equivalent is the sagittal view.

Some have recommended using the modified Crass or Middleton position to evaluate the supraspinatus, where the hand is in the “back pocket”.¹⁹ However, many patients with shoulder pain have trouble with this position. By resting the ipsilateral hand on the ipsilateral hip and then dropping the elbow, the supraspinatus insertion can still be brought out from under the acromion. This does bring the insertion anterior out of the scapular plane, so an adjustment is required in probe positioning to properly see the supraspinatus short and long axis. To find the long axis, the probe is placed parallel to a plane that spans the contralateral shoulder and ipsilateral hip (Figure 2A). The fibers of the supraspinatus should be inserting directly lateral to the humeral head without any intervening space (Figure 2B). If any space exists, a partial articular supraspinatus tendon avulsion (PASTA) lesion is present, and its thickness can be directly measured. Moving more posterior will show the flattening of the tuberosity and the fibers of the infraspinatus moving away from the humeral head—the bare spot. The MRI equivalent is the coronal view.

To view the supraspinatus tendon in short axis, maintain the arm in the same position, keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The probe should now be in a parallel plane between the ipsilateral shoulder and the contralateral hip. The biceps tendon in cross-section will be found anteriorly, and the articular cartilage will appear as a black layer over the bone. Dynamic testing includes placing the probe in a coronal plane between the acromion and greater tuberosity. When the patient abducts the arm while in internal rotation, the supraspinatus tendon will slide underneath the coracoacromial arch showing potential external impingement.¹⁵ The MRI equivalent is the sagittal plane.

The glenohumeral joint is best viewed posteriorly, limiting how much of the intra-articular portion of the joint can be imaged. The arm remains in a neutral position; palpate for the posterior acromion and place the probe just inferior to it, wedging up against it (Figure 3A). The glenohumeral joint will be seen by keeping the probe parallel to the ground (Figure 3B). The MRI equivalent is the axial plane. If a joint effusion exists, it can be seen in the posterior recess.¹⁵ A hyperechoic triangular region in between the humeral head and the glenoid will represent the glenoid labrum (Figure 3B). By internally and externally rotating the arm, the joint and labrum complex can be dynamically examined. From the labrum, scanning superior and medial can sometimes show the spinoglenoid notch where a paralabral cyst might be seen.¹⁵

Using the glenohumeral joint as a reference, the infraspinatus muscle is easily visualized. Maintaining the arm in neutral position with the probe over the glenohumeral joint, the infraspinatus will become apparent as it lays in long axis view superficially between the posterior deltoid and glenohumeral joint (Figure 3B).^16-20 The teres minor lies just inferiorly. The MRI equivalent is the axial plane. To view the infraspinatus and teres minor in short axis, the probe is then rotated 90° on its center axis. The infraspinatus (superiorly) and teres minor (inferiorly) muscles will be visible in short axis within the infraspinatus fossa.¹⁵ The MRI equivalent is the sagittal view.

The acromioclavicular joint is superficial and easy to image. The arm remains in a neutral position, and we can palpate the joint for easy localization. The probe is placed anteriorly in a coronal plane over the acromion and clavicle. By scanning anteriorly and posteriorly, a joint effusion referred to as a Geyser sign might be seen. The MRI equivalent is the coronal view.

Available Certifications

The AIUM certification is a voluntary peer reviewed process that acknowledges that a practice is meeting national standards and aids in improving their respective MSK ultrasound protocols. They also provide guidelines on demonstrating training and competence on performing and/or interpreting diagnostic MSK examinations (Table).¹⁰ The ARDMS certification provides an actual individual certification referred to as “Registered” in MSK ultrasound.¹¹ The physician must perform 150 diagnostic MSK ultrasound evaluations within 36 months of applying and pass a 200-question examination that is offered twice per year.¹¹ None of these certifications are mandated by the American Medical Association (AMA) or American Osteopathic Association (AOA).

Maintenance and Continuing Medical Education (CME)

The AIUM recommends that a minimum of 50 diagnostic MSK ultrasound evaluations be performed per year for skill maintenance.¹⁰ Furthermore, 10 hours of AMA PRA Category 1 Credits™ or American Osteopathic Association Category 1-A Credits specific to MSK ultrasound must be completed by physicians performing and/or interpreting these examinations every 3 years.¹⁰ ARDMS recommends a minimum of 30 MSK ultrasound-specific CMEs in preparation for their “Registered” MSK evaluation.¹

Conclusion

MSK ultrasound is a dynamic, real-time imaging modality that can improve cost efficiency and patient care. Its portability allows for its use anywhere. Learning the skill may seem daunting, but with the proper courses and education, the technology can be easily learned. By correlating a known modality like MRI, the user will easily begin to read ultrasound images. No current certification is needed to use or bill for ultrasound, but various institutions are developing criteria and testing. Two organizations, AIUM and ARDMS, provide guidelines and certifications to demonstrate competency, which may become necessary in the very near future.

The musculoskeletal (MSK) ultrasound evaluation of the shoulder provides a cost- and time-efficient imaging modality with similar diagnostic power as magnetic resonance imaging (MRI).^1,2 Its portable point-of-care applications can be used in the office, in the operating room, and in sideline athletic event coverage, as we discussed in Part 1 of this series.³

MSK ultrasound may seem difficult and daunting, and many articles have quoted steep learning curves.^4,5 However, in our experience in teaching many ultrasound courses, this modality can be learned quite quickly with the proper instruction. Physicians are already familiar with anatomy and usually have had some exposure to MRI.⁴ Taking courses in MSK ultrasound or simply learning the basic concepts of ultrasound and then learning the machine controls is usually a good start.^5-8 Practice scanning normal individuals, comparing the images from an MRI to learn how to reproduce the same planes and images. This will allow the user to become familiar with normal anatomy and how to see the images on the ultrasound screen.^5-8 Vollman and colleagues⁹ showed that in trainees, combining MRI images with sonograms enhances the ability to correctly identify MSK ultrasound anatomy from 40.9% to 72.5%, when compared with learning from ultrasound images alone.

There are currently no certifications necessary to perform ultrasound scans or bill for them; however, some insurance carriers may require demonstrating relevant, documented training for reimbursement.³ Various organizations are trying to develop certifications and regulations for ultrasound to standardize the use of this modality. In the United States, the American Institute of Ultrasound in Medicine (AIUM) and the American Registry for Diagnostic Medical Sonography (ARDMS) provide guidelines and particular MSK ultrasound certifications.^10,11

Basic Ultrasound Principles

The ultrasound machine creates electrical impulses that are turned into sound waves by piezoelectric crystals at the probe’s footprint. These sound waves bounce off tissues and return to the probe, where they are converted electronically to an image on the monitor. Depending on the echogenicity of the scanned tissue, the ultrasound beam will either reflect or be absorbed at different rates. This variance is transmitted on the monitor as a grayscale image. When ultrasound waves are highly reflective, like in bone or fat, they are characterized as hyperechoic. The opposite occurs when ultrasound waves are absorbed like in the fluid of a cystic cavity or joint effusion, and the image appears black. This is described as anechoic.¹² Intermediate tissues such as tendons that are less reflective are seen as hypoechoic and appear gray. When a tissue has a similar echogenicity to its surrounding tissues, it is called isoechoic.¹²

The transducer is the scanning component of the ultrasound machine. Transducers come in 2 shapes: linear and curvilinear. The linear probe creates a straight image that is equal to the size of the transducer footprint. The curvilinear probe creates a wider, wedge-shaped panoramic image.

Linear probes are of higher frequency and generate higher resolution images of shallower structures, while curvilinear probes have greater depth penetration but generate lower resolution images. A high frequency of 10 to 15 MHz is preferred for anatomy between 2 cm to 4 cm depth.¹³ Midrange frequency of 5 to 10 MHz is preferred at 5 cm to 6 cm depth, and low-frequency 2 to 5 MHz probes are preferred for anatomical structures >6 cm depth.¹³

Anisotropy is the property of being directionally dependent, as opposed to isotropy, which implies identical properties in all directions. This anisotropic effect is dependent on the angle of the insonating beam. The maximum return echo occurs when the ultrasound beam is perpendicular to the tendon. Decreasing the insonating angle on a normal tendon will cause it to change from brightly hyperechoic (the actual echo from tightly bound tendon fibers) to darkly hypoechoic. If the angle is then increased, the tendon will again appear hyperechoic. If the artifact causes a normal tendon to appear hypoechoic, it may falsely lead to a diagnosis of tendinosis or tear.

Posterior acoustic shadowing is present when a hyperechoic structure reflects the ultrasound beam so much that it creates a dark shadow underneath it.^12,14 This phenomenon is possible since the ultrasound beam cannot penetrate the hyperechoic structure and reflects off its inferior tissues. Reverberation is when the beam is repeated back and forth between 2 parallel highly reflective surfaces. The initial reflection will be displayed correctly, while the subsequent ultrasound waves will be delayed and appear at a farther distance from the transducer.^12,14

The point where the beam is at its narrowest point generates the section of the image that is best visualized.¹⁵ This is called the focal zone, and it can be adjusted to highlight the desired area of evaluation. Gain controls adjust the amount of black, gray, and white on the monitor and can be adjusted to focus the desired image.¹³ Depth settings are fundamental in finding the desired targets. It is recommended to start with a higher depth setting to get an overview and progressively decrease the depth to key in on the desired anatomy.¹³ Color Doppler can be used to view movement within structures and to identify vessels, synovitis, and neovascularization in tendinopathy.¹³

Ultrasound of the Shoulder

Patients should be seated, if possible, on a rotating seat. The examiner’s shoulder should be higher than the patient’s shoulder.¹⁶ The user holds the ultrasound probe between the thumb and index fingers while resting the hypothenar eminence on the patient to serve as a fulcrum and steadying force. The examination should take 5 to 15 minutes, depending on the examiner’s expertise and the amount of anatomy being scanned.

Examining the body requires knowledge of anatomy. The examination and accuracy are determined by the technician using the probe. The probe can be angled any direction and be placed obliquely on the subject. The advantage here is that anatomy in the human body is not always planar. Muscles and tissues can run obliquely or even perpendicular to each other. When evaluating anatomy, the examiner should keep in mind what structure he or she is looking for; where it should be found; what landmarks can be used to easily locate it; what orientation it has; and what the normal anatomy should look like.

Muscle appears as a lattice with larger areas of hypoechoic muscle tissue and hyperechoic fascial perimysium layers traversing through it.¹⁷ The actual muscle tissue appears hypoechoic from the fluid or blood found within. Scarring, fibrosis, calcification, or chronic injury will change the tissue to appear denser or hyperechoic.¹⁷ Acute injury will appear hypoechoic from the inflammatory response and influx of blood. Tendon appears dense and hyperechoic with striations within the tissue, sometimes referred to as a horse’s tail.¹⁷ When torn, there will be a disassociation of the tissue with a hypoechoic region between the 2 ends. The attachment to the bone and muscle tissue should appear uniform. Hyperechoic areas within the tendon may be from calcification. Ligament appears similar to tendon but is more isoechoic and connects bone to bone. Evaluation of the entire length and the attachments to the bone are critical to evaluate for disease.

Bone appears bright hyperechoic, smooth, and flat, while hyaline cartilage is hypoechoic, smooth, and runs superiorly in a parallel pattern to its respective inferior cortical bone.¹⁷

Fibrocartilage is hyperechoic and typically triangularly shaped, such as in the glenohumeral labrum. Nerves appear fascicular and hypoechoic surrounded by hyperechoic epineurium.¹⁴

The epidermis and dermis are the most superficial structure on top of the screen, and are also hyperechoic.¹⁷

The Diagnostic Shoulder Examination

The proximal long head of the biceps tendon (LHBT) is the easiest structure in the shoulder to identify because of the anatomic structure, the bicipital groove. By keeping the arm relaxed, perpendicular to the ground, and in neutral rotation, the probe can be placed perpendicular to the arm over the proximal shoulder (Figure 1A).^16-20 By finding the groove, the biceps tendon will usually be found resting within the groove (Figure 1B). This is the short axis view and is equivalent to an MRI in the axial plane.

The long axis view of the proximal biceps tendon is found by keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The user should be sure to visualize the entire tendon on the screen. If only part of the tendon is seen along only part of the screen, then the probe is oblique to the tendon. In this case, the probe area showing the tendon must be stabilized as the center or set point. The other part of the probe will then pivot until all of the tendon is seen on the screen. The MRI equivalent to the long axis of the proximal biceps tendon is the sagittal view.

Ultrasound is a dynamic evaluation. Moving the probe or moving the patient will change what and how something is imaged. The proximal biceps tendon is a good example of this concept. The bicipital groove is very deep proximally and flattens out as it travels distally to the mid-humerus. The examiner should continually adjust his or her hand/probe/patient position as well as depth/gain and other console functions to adapt to the dynamics of the scan. While keeping the bicep tendon in a short axis view, the tendon can be dynamically evaluated for subluxation by internally and externally rotating the arm.

To find the subscapularis, the arm remains in a neutral position with the hand supinated and the probe is held parallel with the ground. After finding the bicipital groove, the subscapularis tendon insertion is just medial to the groove (Figure 1B). By externally rotating the arm, the subscapularis tendon/muscle will come into a long axis view.^16-20 The MRI equivalent to the long axis view of the subscapularis is the axial view. Dynamic testing can be done by internally and externally rotating the arm to evaluate for impingement of the subscapularis tendon as it slides underneath the coracoid process. To view the subscapularis tendon in short axis, the tendon is kept in the center of the screen/probe, and the probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The MRI equivalent is the sagittal view.

Some have recommended using the modified Crass or Middleton position to evaluate the supraspinatus, where the hand is in the “back pocket”.¹⁹ However, many patients with shoulder pain have trouble with this position. By resting the ipsilateral hand on the ipsilateral hip and then dropping the elbow, the supraspinatus insertion can still be brought out from under the acromion. This does bring the insertion anterior out of the scapular plane, so an adjustment is required in probe positioning to properly see the supraspinatus short and long axis. To find the long axis, the probe is placed parallel to a plane that spans the contralateral shoulder and ipsilateral hip (Figure 2A). The fibers of the supraspinatus should be inserting directly lateral to the humeral head without any intervening space (Figure 2B). If any space exists, a partial articular supraspinatus tendon avulsion (PASTA) lesion is present, and its thickness can be directly measured. Moving more posterior will show the flattening of the tuberosity and the fibers of the infraspinatus moving away from the humeral head—the bare spot. The MRI equivalent is the coronal view.

To view the supraspinatus tendon in short axis, maintain the arm in the same position, keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The probe should now be in a parallel plane between the ipsilateral shoulder and the contralateral hip. The biceps tendon in cross-section will be found anteriorly, and the articular cartilage will appear as a black layer over the bone. Dynamic testing includes placing the probe in a coronal plane between the acromion and greater tuberosity. When the patient abducts the arm while in internal rotation, the supraspinatus tendon will slide underneath the coracoacromial arch showing potential external impingement.¹⁵ The MRI equivalent is the sagittal plane.

The glenohumeral joint is best viewed posteriorly, limiting how much of the intra-articular portion of the joint can be imaged. The arm remains in a neutral position; palpate for the posterior acromion and place the probe just inferior to it, wedging up against it (Figure 3A). The glenohumeral joint will be seen by keeping the probe parallel to the ground (Figure 3B). The MRI equivalent is the axial plane. If a joint effusion exists, it can be seen in the posterior recess.¹⁵ A hyperechoic triangular region in between the humeral head and the glenoid will represent the glenoid labrum (Figure 3B). By internally and externally rotating the arm, the joint and labrum complex can be dynamically examined. From the labrum, scanning superior and medial can sometimes show the spinoglenoid notch where a paralabral cyst might be seen.¹⁵

Using the glenohumeral joint as a reference, the infraspinatus muscle is easily visualized. Maintaining the arm in neutral position with the probe over the glenohumeral joint, the infraspinatus will become apparent as it lays in long axis view superficially between the posterior deltoid and glenohumeral joint (Figure 3B).^16-20 The teres minor lies just inferiorly. The MRI equivalent is the axial plane. To view the infraspinatus and teres minor in short axis, the probe is then rotated 90° on its center axis. The infraspinatus (superiorly) and teres minor (inferiorly) muscles will be visible in short axis within the infraspinatus fossa.¹⁵ The MRI equivalent is the sagittal view.

The acromioclavicular joint is superficial and easy to image. The arm remains in a neutral position, and we can palpate the joint for easy localization. The probe is placed anteriorly in a coronal plane over the acromion and clavicle. By scanning anteriorly and posteriorly, a joint effusion referred to as a Geyser sign might be seen. The MRI equivalent is the coronal view.

Available Certifications

The AIUM certification is a voluntary peer reviewed process that acknowledges that a practice is meeting national standards and aids in improving their respective MSK ultrasound protocols. They also provide guidelines on demonstrating training and competence on performing and/or interpreting diagnostic MSK examinations (Table).¹⁰ The ARDMS certification provides an actual individual certification referred to as “Registered” in MSK ultrasound.¹¹ The physician must perform 150 diagnostic MSK ultrasound evaluations within 36 months of applying and pass a 200-question examination that is offered twice per year.¹¹ None of these certifications are mandated by the American Medical Association (AMA) or American Osteopathic Association (AOA).

Maintenance and Continuing Medical Education (CME)

The AIUM recommends that a minimum of 50 diagnostic MSK ultrasound evaluations be performed per year for skill maintenance.¹⁰ Furthermore, 10 hours of AMA PRA Category 1 Credits™ or American Osteopathic Association Category 1-A Credits specific to MSK ultrasound must be completed by physicians performing and/or interpreting these examinations every 3 years.¹⁰ ARDMS recommends a minimum of 30 MSK ultrasound-specific CMEs in preparation for their “Registered” MSK evaluation.¹

Conclusion

MSK ultrasound is a dynamic, real-time imaging modality that can improve cost efficiency and patient care. Its portability allows for its use anywhere. Learning the skill may seem daunting, but with the proper courses and education, the technology can be easily learned. By correlating a known modality like MRI, the user will easily begin to read ultrasound images. No current certification is needed to use or bill for ultrasound, but various institutions are developing criteria and testing. Two organizations, AIUM and ARDMS, provide guidelines and certifications to demonstrate competency, which may become necessary in the very near future.

The musculoskeletal (MSK) ultrasound evaluation of the shoulder provides a cost- and time-efficient imaging modality with similar diagnostic power as magnetic resonance imaging (MRI).^1,2 Its portable point-of-care applications can be used in the office, in the operating room, and in sideline athletic event coverage, as we discussed in Part 1 of this series.³

MSK ultrasound may seem difficult and daunting, and many articles have quoted steep learning curves.^4,5 However, in our experience in teaching many ultrasound courses, this modality can be learned quite quickly with the proper instruction. Physicians are already familiar with anatomy and usually have had some exposure to MRI.⁴ Taking courses in MSK ultrasound or simply learning the basic concepts of ultrasound and then learning the machine controls is usually a good start.^5-8 Practice scanning normal individuals, comparing the images from an MRI to learn how to reproduce the same planes and images. This will allow the user to become familiar with normal anatomy and how to see the images on the ultrasound screen.^5-8 Vollman and colleagues⁹ showed that in trainees, combining MRI images with sonograms enhances the ability to correctly identify MSK ultrasound anatomy from 40.9% to 72.5%, when compared with learning from ultrasound images alone.

There are currently no certifications necessary to perform ultrasound scans or bill for them; however, some insurance carriers may require demonstrating relevant, documented training for reimbursement.³ Various organizations are trying to develop certifications and regulations for ultrasound to standardize the use of this modality. In the United States, the American Institute of Ultrasound in Medicine (AIUM) and the American Registry for Diagnostic Medical Sonography (ARDMS) provide guidelines and particular MSK ultrasound certifications.^10,11

Basic Ultrasound Principles

The ultrasound machine creates electrical impulses that are turned into sound waves by piezoelectric crystals at the probe’s footprint. These sound waves bounce off tissues and return to the probe, where they are converted electronically to an image on the monitor. Depending on the echogenicity of the scanned tissue, the ultrasound beam will either reflect or be absorbed at different rates. This variance is transmitted on the monitor as a grayscale image. When ultrasound waves are highly reflective, like in bone or fat, they are characterized as hyperechoic. The opposite occurs when ultrasound waves are absorbed like in the fluid of a cystic cavity or joint effusion, and the image appears black. This is described as anechoic.¹² Intermediate tissues such as tendons that are less reflective are seen as hypoechoic and appear gray. When a tissue has a similar echogenicity to its surrounding tissues, it is called isoechoic.¹²

The transducer is the scanning component of the ultrasound machine. Transducers come in 2 shapes: linear and curvilinear. The linear probe creates a straight image that is equal to the size of the transducer footprint. The curvilinear probe creates a wider, wedge-shaped panoramic image.

Linear probes are of higher frequency and generate higher resolution images of shallower structures, while curvilinear probes have greater depth penetration but generate lower resolution images. A high frequency of 10 to 15 MHz is preferred for anatomy between 2 cm to 4 cm depth.¹³ Midrange frequency of 5 to 10 MHz is preferred at 5 cm to 6 cm depth, and low-frequency 2 to 5 MHz probes are preferred for anatomical structures >6 cm depth.¹³

Anisotropy is the property of being directionally dependent, as opposed to isotropy, which implies identical properties in all directions. This anisotropic effect is dependent on the angle of the insonating beam. The maximum return echo occurs when the ultrasound beam is perpendicular to the tendon. Decreasing the insonating angle on a normal tendon will cause it to change from brightly hyperechoic (the actual echo from tightly bound tendon fibers) to darkly hypoechoic. If the angle is then increased, the tendon will again appear hyperechoic. If the artifact causes a normal tendon to appear hypoechoic, it may falsely lead to a diagnosis of tendinosis or tear.

Posterior acoustic shadowing is present when a hyperechoic structure reflects the ultrasound beam so much that it creates a dark shadow underneath it.^12,14 This phenomenon is possible since the ultrasound beam cannot penetrate the hyperechoic structure and reflects off its inferior tissues. Reverberation is when the beam is repeated back and forth between 2 parallel highly reflective surfaces. The initial reflection will be displayed correctly, while the subsequent ultrasound waves will be delayed and appear at a farther distance from the transducer.^12,14

The point where the beam is at its narrowest point generates the section of the image that is best visualized.¹⁵ This is called the focal zone, and it can be adjusted to highlight the desired area of evaluation. Gain controls adjust the amount of black, gray, and white on the monitor and can be adjusted to focus the desired image.¹³ Depth settings are fundamental in finding the desired targets. It is recommended to start with a higher depth setting to get an overview and progressively decrease the depth to key in on the desired anatomy.¹³ Color Doppler can be used to view movement within structures and to identify vessels, synovitis, and neovascularization in tendinopathy.¹³

Ultrasound of the Shoulder

Patients should be seated, if possible, on a rotating seat. The examiner’s shoulder should be higher than the patient’s shoulder.¹⁶ The user holds the ultrasound probe between the thumb and index fingers while resting the hypothenar eminence on the patient to serve as a fulcrum and steadying force. The examination should take 5 to 15 minutes, depending on the examiner’s expertise and the amount of anatomy being scanned.

Examining the body requires knowledge of anatomy. The examination and accuracy are determined by the technician using the probe. The probe can be angled any direction and be placed obliquely on the subject. The advantage here is that anatomy in the human body is not always planar. Muscles and tissues can run obliquely or even perpendicular to each other. When evaluating anatomy, the examiner should keep in mind what structure he or she is looking for; where it should be found; what landmarks can be used to easily locate it; what orientation it has; and what the normal anatomy should look like.

Muscle appears as a lattice with larger areas of hypoechoic muscle tissue and hyperechoic fascial perimysium layers traversing through it.¹⁷ The actual muscle tissue appears hypoechoic from the fluid or blood found within. Scarring, fibrosis, calcification, or chronic injury will change the tissue to appear denser or hyperechoic.¹⁷ Acute injury will appear hypoechoic from the inflammatory response and influx of blood. Tendon appears dense and hyperechoic with striations within the tissue, sometimes referred to as a horse’s tail.¹⁷ When torn, there will be a disassociation of the tissue with a hypoechoic region between the 2 ends. The attachment to the bone and muscle tissue should appear uniform. Hyperechoic areas within the tendon may be from calcification. Ligament appears similar to tendon but is more isoechoic and connects bone to bone. Evaluation of the entire length and the attachments to the bone are critical to evaluate for disease.

Bone appears bright hyperechoic, smooth, and flat, while hyaline cartilage is hypoechoic, smooth, and runs superiorly in a parallel pattern to its respective inferior cortical bone.¹⁷

Fibrocartilage is hyperechoic and typically triangularly shaped, such as in the glenohumeral labrum. Nerves appear fascicular and hypoechoic surrounded by hyperechoic epineurium.¹⁴

The epidermis and dermis are the most superficial structure on top of the screen, and are also hyperechoic.¹⁷

The Diagnostic Shoulder Examination

The proximal long head of the biceps tendon (LHBT) is the easiest structure in the shoulder to identify because of the anatomic structure, the bicipital groove. By keeping the arm relaxed, perpendicular to the ground, and in neutral rotation, the probe can be placed perpendicular to the arm over the proximal shoulder (Figure 1A).^16-20 By finding the groove, the biceps tendon will usually be found resting within the groove (Figure 1B). This is the short axis view and is equivalent to an MRI in the axial plane.

The long axis view of the proximal biceps tendon is found by keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The user should be sure to visualize the entire tendon on the screen. If only part of the tendon is seen along only part of the screen, then the probe is oblique to the tendon. In this case, the probe area showing the tendon must be stabilized as the center or set point. The other part of the probe will then pivot until all of the tendon is seen on the screen. The MRI equivalent to the long axis of the proximal biceps tendon is the sagittal view.

Ultrasound is a dynamic evaluation. Moving the probe or moving the patient will change what and how something is imaged. The proximal biceps tendon is a good example of this concept. The bicipital groove is very deep proximally and flattens out as it travels distally to the mid-humerus. The examiner should continually adjust his or her hand/probe/patient position as well as depth/gain and other console functions to adapt to the dynamics of the scan. While keeping the bicep tendon in a short axis view, the tendon can be dynamically evaluated for subluxation by internally and externally rotating the arm.

To find the subscapularis, the arm remains in a neutral position with the hand supinated and the probe is held parallel with the ground. After finding the bicipital groove, the subscapularis tendon insertion is just medial to the groove (Figure 1B). By externally rotating the arm, the subscapularis tendon/muscle will come into a long axis view.^16-20 The MRI equivalent to the long axis view of the subscapularis is the axial view. Dynamic testing can be done by internally and externally rotating the arm to evaluate for impingement of the subscapularis tendon as it slides underneath the coracoid process. To view the subscapularis tendon in short axis, the tendon is kept in the center of the screen/probe, and the probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The MRI equivalent is the sagittal view.

Some have recommended using the modified Crass or Middleton position to evaluate the supraspinatus, where the hand is in the “back pocket”.¹⁹ However, many patients with shoulder pain have trouble with this position. By resting the ipsilateral hand on the ipsilateral hip and then dropping the elbow, the supraspinatus insertion can still be brought out from under the acromion. This does bring the insertion anterior out of the scapular plane, so an adjustment is required in probe positioning to properly see the supraspinatus short and long axis. To find the long axis, the probe is placed parallel to a plane that spans the contralateral shoulder and ipsilateral hip (Figure 2A). The fibers of the supraspinatus should be inserting directly lateral to the humeral head without any intervening space (Figure 2B). If any space exists, a partial articular supraspinatus tendon avulsion (PASTA) lesion is present, and its thickness can be directly measured. Moving more posterior will show the flattening of the tuberosity and the fibers of the infraspinatus moving away from the humeral head—the bare spot. The MRI equivalent is the coronal view.

To view the supraspinatus tendon in short axis, maintain the arm in the same position, keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The probe should now be in a parallel plane between the ipsilateral shoulder and the contralateral hip. The biceps tendon in cross-section will be found anteriorly, and the articular cartilage will appear as a black layer over the bone. Dynamic testing includes placing the probe in a coronal plane between the acromion and greater tuberosity. When the patient abducts the arm while in internal rotation, the supraspinatus tendon will slide underneath the coracoacromial arch showing potential external impingement.¹⁵ The MRI equivalent is the sagittal plane.

The glenohumeral joint is best viewed posteriorly, limiting how much of the intra-articular portion of the joint can be imaged. The arm remains in a neutral position; palpate for the posterior acromion and place the probe just inferior to it, wedging up against it (Figure 3A). The glenohumeral joint will be seen by keeping the probe parallel to the ground (Figure 3B). The MRI equivalent is the axial plane. If a joint effusion exists, it can be seen in the posterior recess.¹⁵ A hyperechoic triangular region in between the humeral head and the glenoid will represent the glenoid labrum (Figure 3B). By internally and externally rotating the arm, the joint and labrum complex can be dynamically examined. From the labrum, scanning superior and medial can sometimes show the spinoglenoid notch where a paralabral cyst might be seen.¹⁵

Using the glenohumeral joint as a reference, the infraspinatus muscle is easily visualized. Maintaining the arm in neutral position with the probe over the glenohumeral joint, the infraspinatus will become apparent as it lays in long axis view superficially between the posterior deltoid and glenohumeral joint (Figure 3B).^16-20 The teres minor lies just inferiorly. The MRI equivalent is the axial plane. To view the infraspinatus and teres minor in short axis, the probe is then rotated 90° on its center axis. The infraspinatus (superiorly) and teres minor (inferiorly) muscles will be visible in short axis within the infraspinatus fossa.¹⁵ The MRI equivalent is the sagittal view.

The acromioclavicular joint is superficial and easy to image. The arm remains in a neutral position, and we can palpate the joint for easy localization. The probe is placed anteriorly in a coronal plane over the acromion and clavicle. By scanning anteriorly and posteriorly, a joint effusion referred to as a Geyser sign might be seen. The MRI equivalent is the coronal view.

Available Certifications

The AIUM certification is a voluntary peer reviewed process that acknowledges that a practice is meeting national standards and aids in improving their respective MSK ultrasound protocols. They also provide guidelines on demonstrating training and competence on performing and/or interpreting diagnostic MSK examinations (Table).¹⁰ The ARDMS certification provides an actual individual certification referred to as “Registered” in MSK ultrasound.¹¹ The physician must perform 150 diagnostic MSK ultrasound evaluations within 36 months of applying and pass a 200-question examination that is offered twice per year.¹¹ None of these certifications are mandated by the American Medical Association (AMA) or American Osteopathic Association (AOA).

Maintenance and Continuing Medical Education (CME)

The AIUM recommends that a minimum of 50 diagnostic MSK ultrasound evaluations be performed per year for skill maintenance.¹⁰ Furthermore, 10 hours of AMA PRA Category 1 Credits™ or American Osteopathic Association Category 1-A Credits specific to MSK ultrasound must be completed by physicians performing and/or interpreting these examinations every 3 years.¹⁰ ARDMS recommends a minimum of 30 MSK ultrasound-specific CMEs in preparation for their “Registered” MSK evaluation.¹

Conclusion

MSK ultrasound is a dynamic, real-time imaging modality that can improve cost efficiency and patient care. Its portability allows for its use anywhere. Learning the skill may seem daunting, but with the proper courses and education, the technology can be easily learned. By correlating a known modality like MRI, the user will easily begin to read ultrasound images. No current certification is needed to use or bill for ultrasound, but various institutions are developing criteria and testing. Two organizations, AIUM and ARDMS, provide guidelines and certifications to demonstrate competency, which may become necessary in the very near future.

ORLANDO, FL—Preseason prevention programs can improve deficits in young baseball pitchers, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers evaluated 143 pitchers, of which 88 participated in additional preseason training and 76 continued with normal training. The median age of the pitchers was 15.7 years.

The prevention program, which was supervised by an athletic trainer and required a commitment of 15 minutes 4 times a week, included resistance training with dumbbell weights, elastic tubing, and a focused flexibility program. Pitchers who participated in the prevention program had reduced internal rotation and horizontal adduction deficits. Pitchers who had previous injuries and participated in the preseason training program were 4 times less likely to suffer an injury than those in the general arm care program.

ORLANDO, FL—Preseason prevention programs can improve deficits in young baseball pitchers, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers evaluated 143 pitchers, of which 88 participated in additional preseason training and 76 continued with normal training. The median age of the pitchers was 15.7 years.

The prevention program, which was supervised by an athletic trainer and required a commitment of 15 minutes 4 times a week, included resistance training with dumbbell weights, elastic tubing, and a focused flexibility program. Pitchers who participated in the prevention program had reduced internal rotation and horizontal adduction deficits. Pitchers who had previous injuries and participated in the preseason training program were 4 times less likely to suffer an injury than those in the general arm care program.

ORLANDO, FL—Preseason prevention programs can improve deficits in young baseball pitchers, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers evaluated 143 pitchers, of which 88 participated in additional preseason training and 76 continued with normal training. The median age of the pitchers was 15.7 years.

The prevention program, which was supervised by an athletic trainer and required a commitment of 15 minutes 4 times a week, included resistance training with dumbbell weights, elastic tubing, and a focused flexibility program. Pitchers who participated in the prevention program had reduced internal rotation and horizontal adduction deficits. Pitchers who had previous injuries and participated in the preseason training program were 4 times less likely to suffer an injury than those in the general arm care program.

ORLANDO, FL—Using soft tissue allografts for anterior cruciate ligament (ACL) reconstructions may increase the risks for a revision reconstruction postoperatively, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers analyzed data from the Kaiser Permanente ACLR Registry. Of the cases analyzed, 4,557 involved bone-patellar tendon-bone (BPTB) autografts, 3,751 soft tissue allograft, and 5,707 hamstring allograft.

After a 3-year follow-up, the overall revision rates were 2.5% for BPTB autographs, 3.5% for hamstring autografts, and 3.7% for soft tissue allografts. Non-processed soft tissue allografts were not found to have a statistically significantly different risk of revision compared to BPTB autografts. However, compared to BPTB autografts, allografts processed with more than 1.8Mrads irradiation had a more than 2 times higher risk of revision, and grafts processed with more than 1.8Mrads or high pressure chemical processing had a more than 4 to 6 times higher risk of revision. This was true even after adjustments for age, gender, and race.

ORLANDO, FL—Using soft tissue allografts for anterior cruciate ligament (ACL) reconstructions may increase the risks for a revision reconstruction postoperatively, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers analyzed data from the Kaiser Permanente ACLR Registry. Of the cases analyzed, 4,557 involved bone-patellar tendon-bone (BPTB) autografts, 3,751 soft tissue allograft, and 5,707 hamstring allograft.

After a 3-year follow-up, the overall revision rates were 2.5% for BPTB autographs, 3.5% for hamstring autografts, and 3.7% for soft tissue allografts. Non-processed soft tissue allografts were not found to have a statistically significantly different risk of revision compared to BPTB autografts. However, compared to BPTB autografts, allografts processed with more than 1.8Mrads irradiation had a more than 2 times higher risk of revision, and grafts processed with more than 1.8Mrads or high pressure chemical processing had a more than 4 to 6 times higher risk of revision. This was true even after adjustments for age, gender, and race.

ORLANDO, FL—Using soft tissue allografts for anterior cruciate ligament (ACL) reconstructions may increase the risks for a revision reconstruction postoperatively, according to research presented at the American Orthopedic Society for Sports Medicine’s Specialty Day.

Researchers analyzed data from the Kaiser Permanente ACLR Registry. Of the cases analyzed, 4,557 involved bone-patellar tendon-bone (BPTB) autografts, 3,751 soft tissue allograft, and 5,707 hamstring allograft.

After a 3-year follow-up, the overall revision rates were 2.5% for BPTB autographs, 3.5% for hamstring autografts, and 3.7% for soft tissue allografts. Non-processed soft tissue allografts were not found to have a statistically significantly different risk of revision compared to BPTB autografts. However, compared to BPTB autografts, allografts processed with more than 1.8Mrads irradiation had a more than 2 times higher risk of revision, and grafts processed with more than 1.8Mrads or high pressure chemical processing had a more than 4 to 6 times higher risk of revision. This was true even after adjustments for age, gender, and race.

Total shoulder arthroplasty (TSA) has demonstrated excellent long-term clinical outcomes for the treatment of advanced glenohumeral osteoarthritis (OA).^1-5 Glenohumeral OA is characterized by a broad spectrum of glenoid pathology. Both the morphology of the glenoid and humeral head subluxation are important preoperative factors to evaluate, as these have been shown to adversely impact shoulder arthroplasty outcomes.^6,7

Walch and colleagues⁸ have previously classified glenoid morphology in cases of advanced glenohumeral arthritis based on the preoperative computed tomography (CT) scans of individuals undergoing shoulder arthroplasty (Figures 1A-1E). The biconcave (B2) glenoid is characterized by asymmetric posterior bone loss and a posterior translated humeral head that is seated in a biconcave glenoid. The degree and extent of bone loss in the B2 glenoid can be highly variable, ranging from the classic interpretation, in which 50% of the native glenoid fossa is preserved, to the more extreme case with little remaining native anterior glenoid. Scalise and colleagues⁹ have reported that determining the premorbid native glenoid version with a 3-dimensional (3D) glenoid vault model can aid in differentiating a pathologic B2 glenoid from a nonpathologic type C glenoid.

The B2 glenoid in particular has been associated with poor shoulder arthroplasty outcomes and component survivorship.^6,10-12 There are many factors that are thought to contribute to this problem, such as glenoid component malposition, or undercorrection of the pathologic retroversion.^6,13,14 Walch and colleagues¹⁰ reported that if the neoglenoid retroversion was greater than 27°, there was a 44% incidence of loosening and/or instability and 60% of the dislocations were observed when the humeral head subluxation was greater than 80%. Cases with severe posterior glenoid bone deficiency present a unique challenge to the surgeon, and the ability to accurately and securely place an implant in the correct anatomic position can be compromised. Standard TSA has proven excellent outcomes in the setting of typical glenohumeral OA, but in the B2 glenoid with significant posterior bone erosion, additional attention must be given to ensure adequate correction of the bony deformity, soft tissue balancing, and implant stability.

Several strategies that have been proposed to address extreme bone loss in the B2 glenoid will be discussed in this review. These include hemiarthroplasty, TSA with asymmetric reaming of the high side, TSA with bone grafting of the posterior glenoid bone loss, TSA with an augmented glenoid component, and reverse shoulder arthroplasty (RSA). Importantly, while these techniques have been proposed for managing the B2 glenoid, currently there is no gold standard consensus for the treatment of this condition. The purpose of this review is to highlight important characteristics of the B2 glenoid morphology on clinical outcomes and discuss the current surgical management options for this condition.

Preoperative Planning

Being able to accurately determine the amount of retroversion is critical for preoperative planning. Friedman and colleagues¹⁵ initially described a method to measure glenoid retroversion; however, this is less accurate in B2 glenoids (Figures 2A, 2B). More recently, Rouleau and colleagues¹⁶ have validated and published methods to measure glenoid retroversion and subluxation in the B2 glenoid using 3 reference lines: the paleoglenoid (native glenoid surface), intermediate glenoid (line from anterior and posterior edge), and neoglenoid (eroded posterior surface) (Figure 2).

Preoperative evaluation starts with plain radiographs; however, additional imaging is needed, as the axillary view has shown to overestimate retroversion in 86% of patients (Figures 3A-3E).¹⁷ For a detailed evaluation of the glenoid retroversion and bone deficiency, CT scans with 3D reconstructions are useful.^18,19 The surgical plan should be guided by the location and extent of glenoid bone loss. One tool that has been developed to help in predicting premorbid glenoid version, inclination, and position of the joint line is the 3D virtual glenoid vault model.^9,20,21 This helps determine accurate premorbid glenoid anatomy and has been shown to assist in the selection of the optimal implant in an attempt to restore native glenoid anatomy, and avoid peg perforation.²¹ Patient-specific instrumentation (PSI) for shoulder arthroplasty is being used more frequently and has shown promise for more accurate glenoid component placement, particularly in the complex glenoid with severe bone deficiency. PSI involves creating a custom-fitted guide that is referenced to surface anatomy derived from the preoperative CT scan, which can then direct the surgeon toward optimal implant position with regard to glenoid component location, version and inclination (Figures 4A, 4B). Early reports show that PSI has resulted in a significant reduction in the frequency of malpositioned glenoid implants, with the greatest benefit observed in patients with retroversion in excess of 16°.²²

Surgical Management

Hemiarthroplasty

Shoulder hemiarthroplasty has been traditionally described as an option for younger, more active patients in whom longevity of the glenoid component is a concern, or in patients with inadequate glenoid bone stock to tolerate a glenoid component. While there are no reports of hemiarthroplasty specifically for patients with B2 glenoids, one study has examined the effect of glenoid morphology on the outcomes of hemiarthroplasty for shoulder osteoarthritis. Levine and colleagues⁷ reported inferior clinical outcomes after shoulder hemiarthroplasty in patients with eccentric posterior glenoid wear. Several authors have advocated a “ream-and-run” technique to create a concentric glenoid and re-center the humeral head while still maintaining the native glenoid.^23,24 However, in a recent series of 162 ream-and-run procedures, Gilmer and colleagues²⁵ reported that only 23% of patients with B2 glenoid geometry achieved a minimal clinically important change in patient-reported outcome scores and 14% required revision. Furthermore, Lynch and colleagues²⁶ found that progressive medial erosion and recurrent posterior glenoid erosion occur in a significant percentage of patients at early follow-up. Given these recent findings, the use of hemiarthroplasty alone or a ream-and-run procedure for patients with B2 glenoid morphology should be approached with caution.

Total Shoulder Arthroplasty

As with any TSA, the primary goals in treating patients with B2 glenoid defects are to provide the patient with a pain-free, stable, and functional shoulder (Figures 5A-5D). There are, however, a few challenges that are unique to TSA in the setting of B2 glenoid defects. Because the humeral head is often subluxated posteriorly into the defect, the anterior capsule and rotator cuff can tighten while the posterior aspect of the joint becomes lax. These soft tissues must be balanced during TSA in order to stabilize the shoulder and restore the appropriate length-tension relationship of the rotator cuff. The other primary concern is restoration of appropriate glenoid version and lateralization. To accomplish this, the most common techniques utilized are asymmetric reaming, bone graft augmentation, and glenoid component augmentation.^27,28

Asymmetric Reaming. One of the more readily utilized techniques for addressing the B2 glenoid during TSA is eccentric or asymmetric reaming. During this process, the anterior glenoid is preferentially reamed while little to no bone is removed posteriorly. This technique is generally felt to be sufficient to treat posterior defects up to 5 mm to 8 mm or retroversion up to 15°.²⁸ These upper limits have been confirmed in a number of cadaveric and simulated models.^29-31

The success of this technique hinges on excellent glenoid exposure. With appropriate retractors in place, the anterior capsulolabral complex, including the biceps insertion, is resected to improve visualization. The inferior capsule must be resected carefully to ensure exposure and better motion postoperatively. On the other hand, it is imperative to protect the posterior capsulolabral attachments because of the increased risk of posterior instability in patients with B2 glenoids.

Detailed imaging such as CT scans with 3D reconstructions have improved our understanding of the degree of the deformities in all directions, which can better guide the reaming. PSI and planning software developed to improve the surgeon’s ability to place the glenoid component centrally in the best possible position after version correction can be even more helpful. We find that using a burr to provisionally lower the high side (anterior) provides a more en face view, which subsequently makes the eccentric reaming easier. As a guide, we will not ream more than 1 cm of anterior bone or attempt to correct more than ~20° of retroversion. The goal should be to create a glenoid surface that is more neutral and congruent to the posterior surface of the glenoid component while not overmedializing the component.

Although eccentric reaming may be one of the more straightforward methods for addressing posterior glenoid erosion, it is not without a number of potential downsides. When attempting to correct defects >10 mm or retroversion beyond 15°, excessive medialization of the implant can occur. Although increasing the thickness of the glenoid component can compensate for small amounts of medialization, excessive medialization can lead to a number of issues.^27,28,32 As reaming progresses medially, the risk of keel penetration increases as the glenoid vault narrows.^30,32 Further medialization decreases posterior cortical support for the implant, which increases the risk of component loosening and subsidence.^33-35 The more medial the implant is placed, the smaller the surface of available bone for implant fixation. This often requires utilization of a smaller sized glenoid component that may result in component mismatch with the humeral implant. Finally, excessive medialization has the potential to under tension the rotator cuff, leading to decreased shoulder stability, strength, and function.

Bone Graft Augmentation. When posterior erosion becomes too excessive to address with eccentric reaming alone, defect augmentation is another option to consider (Figures 6A-6E). While technically more demanding, bone graft also provides the advantage of better re-creating the natural joint line and center of rotation of the glenohumeral joint.

For most defects, the resected humeral head provides the ideal source of graft. After initial reaming of the anterior glenoid, the defect must be sized and measured. We then recommend using a guided, cannulated system to place a central pin, lying perpendicular to the glenoid axis in neutral position. The anterior glenoid is then reamed enough to create a flat surface on which to attach the bone graft. The posterior surface is then gently burred to create a bleeding surface to enhance graft incorporation. The graft is then contoured to the defect and placed flush with the anterior glenoid. Cannulated screws are placed over guidewires to fix the graft. Using an arthroscopic cannula inserted posteriorly allows for easier placement of the guidewires and easier implantation of the screws. Although a reamer or burr can be used to contour the graft once it is fixed in place, this should be minimized to prevent loss of fixation. When the graft is fixed, we then cement the glenoid component into place.

Although good clinical results have been obtained with this technique, there is concern of incomplete graft healing and component loosening in the long term. Even in clinically asymptomatic and well functioning patients, some degree of radiographic lucency may be present in over 50% of cases.^31,36,37 Glenoid Component Augmentation. To address the issues related to lucency and nonunion of bone graft augmentation, several augmented glenoid components have been developed. Augmented glenoid components have the benefit of filling posterior defects and stabilizing the shoulder without requiring excessive medialization (as often occurs with eccentric reaming) or union of a bone-to-bone interface (as is required in bone graft augmentation).³⁸ Although many of the metal back designs experienced undesirably high failure rates and have since been recalled,³⁹ more modern all-polyethylene components hold promise. The 2 most commonly utilized designs are the posterior step augment (DePuy) and the posterior wedge (Exactech). Although biomechanical analyses of both designs have demonstrated increased stability during loading in cadaveric and simulation models, the step augment (DePuy) has demonstrated increased stability and resistance to loosening.^40,41 Although midterm results are not yet available for this newest generation of augmented components, short-term results with 2 to 3 years of follow-up have demonstrated excellent clinical outcomes.²⁸

Reverse Total Shoulder Arthroplasty

While most commonly indicated for patients with rotator cuff tear arthropathy, RSA has recently been advocated for older patients with osteoarthritis and B2 glenoids in the setting of an intact rotator cuff. The semi-constrained design of the RSA is a potential solution to the static posterior humeral head subluxation seen in patients with B2 glenoid geometry (Figure 6E).

Technically, RSA is often an easier solution than a TSA with bone grafting because there is usually enough glenoid bone stock for fixation. That said, we always get a CT scan with 3D reconstructions to better appreciate the anatomy. Note that in B2 glenoids, the bone loss is typically posterior and inferior. RSA in the setting of a B2 glenoid is one of the ideal indications to use PSI to ensure ideal placement of the central pin, which is the key to glenoid baseplate positioning. Even when using a RSA, eccentric reaming and/or bone grafting allow for more ideal component placement. Using the same eccentric reaming techniques described above, one should try to ream to place the baseplate at 10° of retroversion. In cases where retroversion cannot be corrected to 10°, graft can be taken from the humeral head, iliac crest, or allograft. A benefit to using bone graft with RSA as opposed to TSA is that the graft can be fashioned to the baseplate, impacted/compressed into the B2 glenoid, and then secured with a central compression screw and peripheral locking screws.

Mizuno and colleagues⁴¹ reported a retrospective series of 27 RSAs performed for primary glenohumeral osteoarthritis and biconcave glenoid. At a mean follow-up of nearly 5 years, the authors noted significant improvement in Constant scores and shoulder motion with minimal complications. There was no recurrence of posterior instability observed by the time of final follow-up.⁴¹

RSA is a promising treatment for primary glenohumeral arthritis with posterior glenoid bone loss and static posterior subluxation in elderly or less active patients, but the longevity of these implants has yet to be established for younger, more active patients and requires further study.

Conclusion

Reconstruction of the B2 glenoid presents a challenging clinical problem that has been associated with poor clinical outcomes and implant survivorship. The high failure rate from glenoid component loosening and subsequent premature implant failure can be substantially decreased with accurate glenoid component positioning and appropriate correction of the pathologic glenoid retroversion. Careful preoperative planning is essential for accurate preparation and execution of the optimal surgical plan. There are many surgical strategies to address the B2 glenoid, but no consensus on the optimal method exists, as the technique should be uniquely customized to the individual’s pathology and surgeon preference (Table). Cases with mild deformity may be corrected with eccentric reaming and TSA, while the more severe deformities may require posterior glenoid bone grafting and/or augmented implants to restore native version. Finally, the RSA is a reliable option to restore stability and address bone deficiency for the severe B2 glenoid in an older, lower demand patient.

Total shoulder arthroplasty (TSA) has demonstrated excellent long-term clinical outcomes for the treatment of advanced glenohumeral osteoarthritis (OA).^1-5 Glenohumeral OA is characterized by a broad spectrum of glenoid pathology. Both the morphology of the glenoid and humeral head subluxation are important preoperative factors to evaluate, as these have been shown to adversely impact shoulder arthroplasty outcomes.^6,7

Walch and colleagues⁸ have previously classified glenoid morphology in cases of advanced glenohumeral arthritis based on the preoperative computed tomography (CT) scans of individuals undergoing shoulder arthroplasty (Figures 1A-1E). The biconcave (B2) glenoid is characterized by asymmetric posterior bone loss and a posterior translated humeral head that is seated in a biconcave glenoid. The degree and extent of bone loss in the B2 glenoid can be highly variable, ranging from the classic interpretation, in which 50% of the native glenoid fossa is preserved, to the more extreme case with little remaining native anterior glenoid. Scalise and colleagues⁹ have reported that determining the premorbid native glenoid version with a 3-dimensional (3D) glenoid vault model can aid in differentiating a pathologic B2 glenoid from a nonpathologic type C glenoid.

The B2 glenoid in particular has been associated with poor shoulder arthroplasty outcomes and component survivorship.^6,10-12 There are many factors that are thought to contribute to this problem, such as glenoid component malposition, or undercorrection of the pathologic retroversion.^6,13,14 Walch and colleagues¹⁰ reported that if the neoglenoid retroversion was greater than 27°, there was a 44% incidence of loosening and/or instability and 60% of the dislocations were observed when the humeral head subluxation was greater than 80%. Cases with severe posterior glenoid bone deficiency present a unique challenge to the surgeon, and the ability to accurately and securely place an implant in the correct anatomic position can be compromised. Standard TSA has proven excellent outcomes in the setting of typical glenohumeral OA, but in the B2 glenoid with significant posterior bone erosion, additional attention must be given to ensure adequate correction of the bony deformity, soft tissue balancing, and implant stability.

Several strategies that have been proposed to address extreme bone loss in the B2 glenoid will be discussed in this review. These include hemiarthroplasty, TSA with asymmetric reaming of the high side, TSA with bone grafting of the posterior glenoid bone loss, TSA with an augmented glenoid component, and reverse shoulder arthroplasty (RSA). Importantly, while these techniques have been proposed for managing the B2 glenoid, currently there is no gold standard consensus for the treatment of this condition. The purpose of this review is to highlight important characteristics of the B2 glenoid morphology on clinical outcomes and discuss the current surgical management options for this condition.

Preoperative Planning

Being able to accurately determine the amount of retroversion is critical for preoperative planning. Friedman and colleagues¹⁵ initially described a method to measure glenoid retroversion; however, this is less accurate in B2 glenoids (Figures 2A, 2B). More recently, Rouleau and colleagues¹⁶ have validated and published methods to measure glenoid retroversion and subluxation in the B2 glenoid using 3 reference lines: the paleoglenoid (native glenoid surface), intermediate glenoid (line from anterior and posterior edge), and neoglenoid (eroded posterior surface) (Figure 2).

Preoperative evaluation starts with plain radiographs; however, additional imaging is needed, as the axillary view has shown to overestimate retroversion in 86% of patients (Figures 3A-3E).¹⁷ For a detailed evaluation of the glenoid retroversion and bone deficiency, CT scans with 3D reconstructions are useful.^18,19 The surgical plan should be guided by the location and extent of glenoid bone loss. One tool that has been developed to help in predicting premorbid glenoid version, inclination, and position of the joint line is the 3D virtual glenoid vault model.^9,20,21 This helps determine accurate premorbid glenoid anatomy and has been shown to assist in the selection of the optimal implant in an attempt to restore native glenoid anatomy, and avoid peg perforation.²¹ Patient-specific instrumentation (PSI) for shoulder arthroplasty is being used more frequently and has shown promise for more accurate glenoid component placement, particularly in the complex glenoid with severe bone deficiency. PSI involves creating a custom-fitted guide that is referenced to surface anatomy derived from the preoperative CT scan, which can then direct the surgeon toward optimal implant position with regard to glenoid component location, version and inclination (Figures 4A, 4B). Early reports show that PSI has resulted in a significant reduction in the frequency of malpositioned glenoid implants, with the greatest benefit observed in patients with retroversion in excess of 16°.²²

Surgical Management

Hemiarthroplasty

Shoulder hemiarthroplasty has been traditionally described as an option for younger, more active patients in whom longevity of the glenoid component is a concern, or in patients with inadequate glenoid bone stock to tolerate a glenoid component. While there are no reports of hemiarthroplasty specifically for patients with B2 glenoids, one study has examined the effect of glenoid morphology on the outcomes of hemiarthroplasty for shoulder osteoarthritis. Levine and colleagues⁷ reported inferior clinical outcomes after shoulder hemiarthroplasty in patients with eccentric posterior glenoid wear. Several authors have advocated a “ream-and-run” technique to create a concentric glenoid and re-center the humeral head while still maintaining the native glenoid.^23,24 However, in a recent series of 162 ream-and-run procedures, Gilmer and colleagues²⁵ reported that only 23% of patients with B2 glenoid geometry achieved a minimal clinically important change in patient-reported outcome scores and 14% required revision. Furthermore, Lynch and colleagues²⁶ found that progressive medial erosion and recurrent posterior glenoid erosion occur in a significant percentage of patients at early follow-up. Given these recent findings, the use of hemiarthroplasty alone or a ream-and-run procedure for patients with B2 glenoid morphology should be approached with caution.

Total Shoulder Arthroplasty

As with any TSA, the primary goals in treating patients with B2 glenoid defects are to provide the patient with a pain-free, stable, and functional shoulder (Figures 5A-5D). There are, however, a few challenges that are unique to TSA in the setting of B2 glenoid defects. Because the humeral head is often subluxated posteriorly into the defect, the anterior capsule and rotator cuff can tighten while the posterior aspect of the joint becomes lax. These soft tissues must be balanced during TSA in order to stabilize the shoulder and restore the appropriate length-tension relationship of the rotator cuff. The other primary concern is restoration of appropriate glenoid version and lateralization. To accomplish this, the most common techniques utilized are asymmetric reaming, bone graft augmentation, and glenoid component augmentation.^27,28

Asymmetric Reaming. One of the more readily utilized techniques for addressing the B2 glenoid during TSA is eccentric or asymmetric reaming. During this process, the anterior glenoid is preferentially reamed while little to no bone is removed posteriorly. This technique is generally felt to be sufficient to treat posterior defects up to 5 mm to 8 mm or retroversion up to 15°.²⁸ These upper limits have been confirmed in a number of cadaveric and simulated models.^29-31

The success of this technique hinges on excellent glenoid exposure. With appropriate retractors in place, the anterior capsulolabral complex, including the biceps insertion, is resected to improve visualization. The inferior capsule must be resected carefully to ensure exposure and better motion postoperatively. On the other hand, it is imperative to protect the posterior capsulolabral attachments because of the increased risk of posterior instability in patients with B2 glenoids.

Detailed imaging such as CT scans with 3D reconstructions have improved our understanding of the degree of the deformities in all directions, which can better guide the reaming. PSI and planning software developed to improve the surgeon’s ability to place the glenoid component centrally in the best possible position after version correction can be even more helpful. We find that using a burr to provisionally lower the high side (anterior) provides a more en face view, which subsequently makes the eccentric reaming easier. As a guide, we will not ream more than 1 cm of anterior bone or attempt to correct more than ~20° of retroversion. The goal should be to create a glenoid surface that is more neutral and congruent to the posterior surface of the glenoid component while not overmedializing the component.

Although eccentric reaming may be one of the more straightforward methods for addressing posterior glenoid erosion, it is not without a number of potential downsides. When attempting to correct defects >10 mm or retroversion beyond 15°, excessive medialization of the implant can occur. Although increasing the thickness of the glenoid component can compensate for small amounts of medialization, excessive medialization can lead to a number of issues.^27,28,32 As reaming progresses medially, the risk of keel penetration increases as the glenoid vault narrows.^30,32 Further medialization decreases posterior cortical support for the implant, which increases the risk of component loosening and subsidence.^33-35 The more medial the implant is placed, the smaller the surface of available bone for implant fixation. This often requires utilization of a smaller sized glenoid component that may result in component mismatch with the humeral implant. Finally, excessive medialization has the potential to under tension the rotator cuff, leading to decreased shoulder stability, strength, and function.

Bone Graft Augmentation. When posterior erosion becomes too excessive to address with eccentric reaming alone, defect augmentation is another option to consider (Figures 6A-6E). While technically more demanding, bone graft also provides the advantage of better re-creating the natural joint line and center of rotation of the glenohumeral joint.

For most defects, the resected humeral head provides the ideal source of graft. After initial reaming of the anterior glenoid, the defect must be sized and measured. We then recommend using a guided, cannulated system to place a central pin, lying perpendicular to the glenoid axis in neutral position. The anterior glenoid is then reamed enough to create a flat surface on which to attach the bone graft. The posterior surface is then gently burred to create a bleeding surface to enhance graft incorporation. The graft is then contoured to the defect and placed flush with the anterior glenoid. Cannulated screws are placed over guidewires to fix the graft. Using an arthroscopic cannula inserted posteriorly allows for easier placement of the guidewires and easier implantation of the screws. Although a reamer or burr can be used to contour the graft once it is fixed in place, this should be minimized to prevent loss of fixation. When the graft is fixed, we then cement the glenoid component into place.

Although good clinical results have been obtained with this technique, there is concern of incomplete graft healing and component loosening in the long term. Even in clinically asymptomatic and well functioning patients, some degree of radiographic lucency may be present in over 50% of cases.^31,36,37 Glenoid Component Augmentation. To address the issues related to lucency and nonunion of bone graft augmentation, several augmented glenoid components have been developed. Augmented glenoid components have the benefit of filling posterior defects and stabilizing the shoulder without requiring excessive medialization (as often occurs with eccentric reaming) or union of a bone-to-bone interface (as is required in bone graft augmentation).³⁸ Although many of the metal back designs experienced undesirably high failure rates and have since been recalled,³⁹ more modern all-polyethylene components hold promise. The 2 most commonly utilized designs are the posterior step augment (DePuy) and the posterior wedge (Exactech). Although biomechanical analyses of both designs have demonstrated increased stability during loading in cadaveric and simulation models, the step augment (DePuy) has demonstrated increased stability and resistance to loosening.^40,41 Although midterm results are not yet available for this newest generation of augmented components, short-term results with 2 to 3 years of follow-up have demonstrated excellent clinical outcomes.²⁸

Reverse Total Shoulder Arthroplasty

While most commonly indicated for patients with rotator cuff tear arthropathy, RSA has recently been advocated for older patients with osteoarthritis and B2 glenoids in the setting of an intact rotator cuff. The semi-constrained design of the RSA is a potential solution to the static posterior humeral head subluxation seen in patients with B2 glenoid geometry (Figure 6E).

Technically, RSA is often an easier solution than a TSA with bone grafting because there is usually enough glenoid bone stock for fixation. That said, we always get a CT scan with 3D reconstructions to better appreciate the anatomy. Note that in B2 glenoids, the bone loss is typically posterior and inferior. RSA in the setting of a B2 glenoid is one of the ideal indications to use PSI to ensure ideal placement of the central pin, which is the key to glenoid baseplate positioning. Even when using a RSA, eccentric reaming and/or bone grafting allow for more ideal component placement. Using the same eccentric reaming techniques described above, one should try to ream to place the baseplate at 10° of retroversion. In cases where retroversion cannot be corrected to 10°, graft can be taken from the humeral head, iliac crest, or allograft. A benefit to using bone graft with RSA as opposed to TSA is that the graft can be fashioned to the baseplate, impacted/compressed into the B2 glenoid, and then secured with a central compression screw and peripheral locking screws.

Mizuno and colleagues⁴¹ reported a retrospective series of 27 RSAs performed for primary glenohumeral osteoarthritis and biconcave glenoid. At a mean follow-up of nearly 5 years, the authors noted significant improvement in Constant scores and shoulder motion with minimal complications. There was no recurrence of posterior instability observed by the time of final follow-up.⁴¹

RSA is a promising treatment for primary glenohumeral arthritis with posterior glenoid bone loss and static posterior subluxation in elderly or less active patients, but the longevity of these implants has yet to be established for younger, more active patients and requires further study.

Conclusion

Reconstruction of the B2 glenoid presents a challenging clinical problem that has been associated with poor clinical outcomes and implant survivorship. The high failure rate from glenoid component loosening and subsequent premature implant failure can be substantially decreased with accurate glenoid component positioning and appropriate correction of the pathologic glenoid retroversion. Careful preoperative planning is essential for accurate preparation and execution of the optimal surgical plan. There are many surgical strategies to address the B2 glenoid, but no consensus on the optimal method exists, as the technique should be uniquely customized to the individual’s pathology and surgeon preference (Table). Cases with mild deformity may be corrected with eccentric reaming and TSA, while the more severe deformities may require posterior glenoid bone grafting and/or augmented implants to restore native version. Finally, the RSA is a reliable option to restore stability and address bone deficiency for the severe B2 glenoid in an older, lower demand patient.

Total shoulder arthroplasty (TSA) has demonstrated excellent long-term clinical outcomes for the treatment of advanced glenohumeral osteoarthritis (OA).^1-5 Glenohumeral OA is characterized by a broad spectrum of glenoid pathology. Both the morphology of the glenoid and humeral head subluxation are important preoperative factors to evaluate, as these have been shown to adversely impact shoulder arthroplasty outcomes.^6,7

Walch and colleagues⁸ have previously classified glenoid morphology in cases of advanced glenohumeral arthritis based on the preoperative computed tomography (CT) scans of individuals undergoing shoulder arthroplasty (Figures 1A-1E). The biconcave (B2) glenoid is characterized by asymmetric posterior bone loss and a posterior translated humeral head that is seated in a biconcave glenoid. The degree and extent of bone loss in the B2 glenoid can be highly variable, ranging from the classic interpretation, in which 50% of the native glenoid fossa is preserved, to the more extreme case with little remaining native anterior glenoid. Scalise and colleagues⁹ have reported that determining the premorbid native glenoid version with a 3-dimensional (3D) glenoid vault model can aid in differentiating a pathologic B2 glenoid from a nonpathologic type C glenoid.

The B2 glenoid in particular has been associated with poor shoulder arthroplasty outcomes and component survivorship.^6,10-12 There are many factors that are thought to contribute to this problem, such as glenoid component malposition, or undercorrection of the pathologic retroversion.^6,13,14 Walch and colleagues¹⁰ reported that if the neoglenoid retroversion was greater than 27°, there was a 44% incidence of loosening and/or instability and 60% of the dislocations were observed when the humeral head subluxation was greater than 80%. Cases with severe posterior glenoid bone deficiency present a unique challenge to the surgeon, and the ability to accurately and securely place an implant in the correct anatomic position can be compromised. Standard TSA has proven excellent outcomes in the setting of typical glenohumeral OA, but in the B2 glenoid with significant posterior bone erosion, additional attention must be given to ensure adequate correction of the bony deformity, soft tissue balancing, and implant stability.

Several strategies that have been proposed to address extreme bone loss in the B2 glenoid will be discussed in this review. These include hemiarthroplasty, TSA with asymmetric reaming of the high side, TSA with bone grafting of the posterior glenoid bone loss, TSA with an augmented glenoid component, and reverse shoulder arthroplasty (RSA). Importantly, while these techniques have been proposed for managing the B2 glenoid, currently there is no gold standard consensus for the treatment of this condition. The purpose of this review is to highlight important characteristics of the B2 glenoid morphology on clinical outcomes and discuss the current surgical management options for this condition.

Preoperative Planning

Being able to accurately determine the amount of retroversion is critical for preoperative planning. Friedman and colleagues¹⁵ initially described a method to measure glenoid retroversion; however, this is less accurate in B2 glenoids (Figures 2A, 2B). More recently, Rouleau and colleagues¹⁶ have validated and published methods to measure glenoid retroversion and subluxation in the B2 glenoid using 3 reference lines: the paleoglenoid (native glenoid surface), intermediate glenoid (line from anterior and posterior edge), and neoglenoid (eroded posterior surface) (Figure 2).

Preoperative evaluation starts with plain radiographs; however, additional imaging is needed, as the axillary view has shown to overestimate retroversion in 86% of patients (Figures 3A-3E).¹⁷ For a detailed evaluation of the glenoid retroversion and bone deficiency, CT scans with 3D reconstructions are useful.^18,19 The surgical plan should be guided by the location and extent of glenoid bone loss. One tool that has been developed to help in predicting premorbid glenoid version, inclination, and position of the joint line is the 3D virtual glenoid vault model.^9,20,21 This helps determine accurate premorbid glenoid anatomy and has been shown to assist in the selection of the optimal implant in an attempt to restore native glenoid anatomy, and avoid peg perforation.²¹ Patient-specific instrumentation (PSI) for shoulder arthroplasty is being used more frequently and has shown promise for more accurate glenoid component placement, particularly in the complex glenoid with severe bone deficiency. PSI involves creating a custom-fitted guide that is referenced to surface anatomy derived from the preoperative CT scan, which can then direct the surgeon toward optimal implant position with regard to glenoid component location, version and inclination (Figures 4A, 4B). Early reports show that PSI has resulted in a significant reduction in the frequency of malpositioned glenoid implants, with the greatest benefit observed in patients with retroversion in excess of 16°.²²

Surgical Management

Hemiarthroplasty

Shoulder hemiarthroplasty has been traditionally described as an option for younger, more active patients in whom longevity of the glenoid component is a concern, or in patients with inadequate glenoid bone stock to tolerate a glenoid component. While there are no reports of hemiarthroplasty specifically for patients with B2 glenoids, one study has examined the effect of glenoid morphology on the outcomes of hemiarthroplasty for shoulder osteoarthritis. Levine and colleagues⁷ reported inferior clinical outcomes after shoulder hemiarthroplasty in patients with eccentric posterior glenoid wear. Several authors have advocated a “ream-and-run” technique to create a concentric glenoid and re-center the humeral head while still maintaining the native glenoid.^23,24 However, in a recent series of 162 ream-and-run procedures, Gilmer and colleagues²⁵ reported that only 23% of patients with B2 glenoid geometry achieved a minimal clinically important change in patient-reported outcome scores and 14% required revision. Furthermore, Lynch and colleagues²⁶ found that progressive medial erosion and recurrent posterior glenoid erosion occur in a significant percentage of patients at early follow-up. Given these recent findings, the use of hemiarthroplasty alone or a ream-and-run procedure for patients with B2 glenoid morphology should be approached with caution.

Total Shoulder Arthroplasty

As with any TSA, the primary goals in treating patients with B2 glenoid defects are to provide the patient with a pain-free, stable, and functional shoulder (Figures 5A-5D). There are, however, a few challenges that are unique to TSA in the setting of B2 glenoid defects. Because the humeral head is often subluxated posteriorly into the defect, the anterior capsule and rotator cuff can tighten while the posterior aspect of the joint becomes lax. These soft tissues must be balanced during TSA in order to stabilize the shoulder and restore the appropriate length-tension relationship of the rotator cuff. The other primary concern is restoration of appropriate glenoid version and lateralization. To accomplish this, the most common techniques utilized are asymmetric reaming, bone graft augmentation, and glenoid component augmentation.^27,28

Asymmetric Reaming. One of the more readily utilized techniques for addressing the B2 glenoid during TSA is eccentric or asymmetric reaming. During this process, the anterior glenoid is preferentially reamed while little to no bone is removed posteriorly. This technique is generally felt to be sufficient to treat posterior defects up to 5 mm to 8 mm or retroversion up to 15°.²⁸ These upper limits have been confirmed in a number of cadaveric and simulated models.^29-31

The success of this technique hinges on excellent glenoid exposure. With appropriate retractors in place, the anterior capsulolabral complex, including the biceps insertion, is resected to improve visualization. The inferior capsule must be resected carefully to ensure exposure and better motion postoperatively. On the other hand, it is imperative to protect the posterior capsulolabral attachments because of the increased risk of posterior instability in patients with B2 glenoids.

Detailed imaging such as CT scans with 3D reconstructions have improved our understanding of the degree of the deformities in all directions, which can better guide the reaming. PSI and planning software developed to improve the surgeon’s ability to place the glenoid component centrally in the best possible position after version correction can be even more helpful. We find that using a burr to provisionally lower the high side (anterior) provides a more en face view, which subsequently makes the eccentric reaming easier. As a guide, we will not ream more than 1 cm of anterior bone or attempt to correct more than ~20° of retroversion. The goal should be to create a glenoid surface that is more neutral and congruent to the posterior surface of the glenoid component while not overmedializing the component.

Although eccentric reaming may be one of the more straightforward methods for addressing posterior glenoid erosion, it is not without a number of potential downsides. When attempting to correct defects >10 mm or retroversion beyond 15°, excessive medialization of the implant can occur. Although increasing the thickness of the glenoid component can compensate for small amounts of medialization, excessive medialization can lead to a number of issues.^27,28,32 As reaming progresses medially, the risk of keel penetration increases as the glenoid vault narrows.^30,32 Further medialization decreases posterior cortical support for the implant, which increases the risk of component loosening and subsidence.^33-35 The more medial the implant is placed, the smaller the surface of available bone for implant fixation. This often requires utilization of a smaller sized glenoid component that may result in component mismatch with the humeral implant. Finally, excessive medialization has the potential to under tension the rotator cuff, leading to decreased shoulder stability, strength, and function.

Bone Graft Augmentation. When posterior erosion becomes too excessive to address with eccentric reaming alone, defect augmentation is another option to consider (Figures 6A-6E). While technically more demanding, bone graft also provides the advantage of better re-creating the natural joint line and center of rotation of the glenohumeral joint.

For most defects, the resected humeral head provides the ideal source of graft. After initial reaming of the anterior glenoid, the defect must be sized and measured. We then recommend using a guided, cannulated system to place a central pin, lying perpendicular to the glenoid axis in neutral position. The anterior glenoid is then reamed enough to create a flat surface on which to attach the bone graft. The posterior surface is then gently burred to create a bleeding surface to enhance graft incorporation. The graft is then contoured to the defect and placed flush with the anterior glenoid. Cannulated screws are placed over guidewires to fix the graft. Using an arthroscopic cannula inserted posteriorly allows for easier placement of the guidewires and easier implantation of the screws. Although a reamer or burr can be used to contour the graft once it is fixed in place, this should be minimized to prevent loss of fixation. When the graft is fixed, we then cement the glenoid component into place.

Although good clinical results have been obtained with this technique, there is concern of incomplete graft healing and component loosening in the long term. Even in clinically asymptomatic and well functioning patients, some degree of radiographic lucency may be present in over 50% of cases.^31,36,37 Glenoid Component Augmentation. To address the issues related to lucency and nonunion of bone graft augmentation, several augmented glenoid components have been developed. Augmented glenoid components have the benefit of filling posterior defects and stabilizing the shoulder without requiring excessive medialization (as often occurs with eccentric reaming) or union of a bone-to-bone interface (as is required in bone graft augmentation).³⁸ Although many of the metal back designs experienced undesirably high failure rates and have since been recalled,³⁹ more modern all-polyethylene components hold promise. The 2 most commonly utilized designs are the posterior step augment (DePuy) and the posterior wedge (Exactech). Although biomechanical analyses of both designs have demonstrated increased stability during loading in cadaveric and simulation models, the step augment (DePuy) has demonstrated increased stability and resistance to loosening.^40,41 Although midterm results are not yet available for this newest generation of augmented components, short-term results with 2 to 3 years of follow-up have demonstrated excellent clinical outcomes.²⁸

Reverse Total Shoulder Arthroplasty

While most commonly indicated for patients with rotator cuff tear arthropathy, RSA has recently been advocated for older patients with osteoarthritis and B2 glenoids in the setting of an intact rotator cuff. The semi-constrained design of the RSA is a potential solution to the static posterior humeral head subluxation seen in patients with B2 glenoid geometry (Figure 6E).

Technically, RSA is often an easier solution than a TSA with bone grafting because there is usually enough glenoid bone stock for fixation. That said, we always get a CT scan with 3D reconstructions to better appreciate the anatomy. Note that in B2 glenoids, the bone loss is typically posterior and inferior. RSA in the setting of a B2 glenoid is one of the ideal indications to use PSI to ensure ideal placement of the central pin, which is the key to glenoid baseplate positioning. Even when using a RSA, eccentric reaming and/or bone grafting allow for more ideal component placement. Using the same eccentric reaming techniques described above, one should try to ream to place the baseplate at 10° of retroversion. In cases where retroversion cannot be corrected to 10°, graft can be taken from the humeral head, iliac crest, or allograft. A benefit to using bone graft with RSA as opposed to TSA is that the graft can be fashioned to the baseplate, impacted/compressed into the B2 glenoid, and then secured with a central compression screw and peripheral locking screws.

Mizuno and colleagues⁴¹ reported a retrospective series of 27 RSAs performed for primary glenohumeral osteoarthritis and biconcave glenoid. At a mean follow-up of nearly 5 years, the authors noted significant improvement in Constant scores and shoulder motion with minimal complications. There was no recurrence of posterior instability observed by the time of final follow-up.⁴¹

RSA is a promising treatment for primary glenohumeral arthritis with posterior glenoid bone loss and static posterior subluxation in elderly or less active patients, but the longevity of these implants has yet to be established for younger, more active patients and requires further study.

Conclusion

Reconstruction of the B2 glenoid presents a challenging clinical problem that has been associated with poor clinical outcomes and implant survivorship. The high failure rate from glenoid component loosening and subsequent premature implant failure can be substantially decreased with accurate glenoid component positioning and appropriate correction of the pathologic glenoid retroversion. Careful preoperative planning is essential for accurate preparation and execution of the optimal surgical plan. There are many surgical strategies to address the B2 glenoid, but no consensus on the optimal method exists, as the technique should be uniquely customized to the individual’s pathology and surgeon preference (Table). Cases with mild deformity may be corrected with eccentric reaming and TSA, while the more severe deformities may require posterior glenoid bone grafting and/or augmented implants to restore native version. Finally, the RSA is a reliable option to restore stability and address bone deficiency for the severe B2 glenoid in an older, lower demand patient.