Bryan T. Hanypsiak, MD

Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.³ Also, the mean life expectancy post-fragility fracture was only 527 days.³ Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.

RISK FACTORS AND CAUSES

The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.⁴ Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.⁵ A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.⁴ Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.⁶

Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.⁷ The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.⁷ Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.⁸ In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.⁹ The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.¹⁰

In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), H₂ receptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.¹¹ Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.¹² Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.¹³ Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.

Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.¹⁴ Proton pump inhibitors and H₂ receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.¹⁵ However, exposure lasting <7 years does not increase the risk of fracture.¹⁶ It is recommended that patients on long-term PPIs be referred for BMD testing.

An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.¹⁷ Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.¹⁸

Continue to: DIAGNOSIS...

Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.¹⁹ Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.²⁰

The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.¹⁹ The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.¹⁹ Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.²⁰ Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.²¹ Without testing, treatment of osteoporosis is very unlikely.

Table 1. T Score Criteria

Table 2. Z Score Criteria

The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.²² Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.

In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.²³ As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.

Continue to: TREATMENT...

NONPHARMACOLOGIC

Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.²⁴ The recommended daily total calcium intake is 1200 mg.²⁵ Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.²⁴Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.

Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.²⁴ Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.

PHARMACOLOGIC

After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.²⁶ Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.²⁷ Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.²⁸

Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.

Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.²⁹ In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.²⁹ Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.²⁹ Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.²⁶

Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.³⁰

Continue to: The recommended daily dose for abaloparatide...

The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.³¹ Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.³⁰ The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.

Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.³¹ It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.

Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.³² It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.

Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.³³ Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.

A summary of medications used to treat osteoporosis can be found in Table 3.

Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis

Abbreviation: CrCl, creatinine clearance.

CONCLUSION

With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.^34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.^34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.

Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.³ Also, the mean life expectancy post-fragility fracture was only 527 days.³ Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.

RISK FACTORS AND CAUSES

The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.⁴ Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.⁵ A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.⁴ Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.⁶

Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.⁷ The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.⁷ Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.⁸ In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.⁹ The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.¹⁰

In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), H₂ receptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.¹¹ Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.¹² Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.¹³ Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.

Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.¹⁴ Proton pump inhibitors and H₂ receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.¹⁵ However, exposure lasting <7 years does not increase the risk of fracture.¹⁶ It is recommended that patients on long-term PPIs be referred for BMD testing.

An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.¹⁷ Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.¹⁸

Continue to: DIAGNOSIS...

Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.¹⁹ Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.²⁰

The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.¹⁹ The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.¹⁹ Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.²⁰ Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.²¹ Without testing, treatment of osteoporosis is very unlikely.

Table 1. T Score Criteria

Table 2. Z Score Criteria

The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.²² Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.

In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.²³ As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.

Continue to: TREATMENT...

NONPHARMACOLOGIC

Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.²⁴ The recommended daily total calcium intake is 1200 mg.²⁵ Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.²⁴Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.

Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.²⁴ Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.

PHARMACOLOGIC

After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.²⁶ Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.²⁷ Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.²⁸

Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.

Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.²⁹ In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.²⁹ Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.²⁹ Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.²⁶

Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.³⁰

Continue to: The recommended daily dose for abaloparatide...

The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.³¹ Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.³⁰ The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.

Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.³¹ It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.

Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.³² It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.

Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.³³ Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.

A summary of medications used to treat osteoporosis can be found in Table 3.

Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis

Abbreviation: CrCl, creatinine clearance.

CONCLUSION

With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.^34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.^34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.

Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.³ Also, the mean life expectancy post-fragility fracture was only 527 days.³ Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.

RISK FACTORS AND CAUSES

The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.⁴ Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.⁵ A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.⁴ Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.⁶

Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.⁷ The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.⁷ Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.⁸ In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.⁹ The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.¹⁰

In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), H₂ receptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.¹¹ Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.¹² Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.¹³ Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.

Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.¹⁴ Proton pump inhibitors and H₂ receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.¹⁵ However, exposure lasting <7 years does not increase the risk of fracture.¹⁶ It is recommended that patients on long-term PPIs be referred for BMD testing.

An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.¹⁷ Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.¹⁸

Continue to: DIAGNOSIS...

Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.¹⁹ Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.²⁰

The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.¹⁹ The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.¹⁹ Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.²⁰ Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.²¹ Without testing, treatment of osteoporosis is very unlikely.

Table 1. T Score Criteria

Table 2. Z Score Criteria

The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.²² Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.

In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.²³ As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.

Continue to: TREATMENT...

NONPHARMACOLOGIC

Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.²⁴ The recommended daily total calcium intake is 1200 mg.²⁵ Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.²⁴Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.

Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.²⁴ Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.

PHARMACOLOGIC

After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.²⁶ Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.²⁷ Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.²⁸

Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.

Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.²⁹ In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.²⁹ Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.²⁹ Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.²⁶

Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.³⁰

Continue to: The recommended daily dose for abaloparatide...

The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.³¹ Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.³⁰ The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.

Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.³¹ It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.

Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.³² It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.

Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.³³ Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.

A summary of medications used to treat osteoporosis can be found in Table 3.

Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis

Abbreviation: CrCl, creatinine clearance.

CONCLUSION

With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.^34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.^34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.

“Hockey is a fast body-contact game played by men with clubs in their hands and knives laced to their feet, since the skates are razor sharp, and before the evening is over it is almost a certainty that someone will be hurt and will fleck the ice with a generous contribution of gore before he is led away to be hemstitched together again.” —Paul Gallico in Farewell to Sport (1938)

Ice hockey is a collision sport with player speeds in excess of 30 miles/hour, on a sheet of ice surrounded by unforgiving boards, with a vulcanized rubber puck moving at speeds approaching 100 miles/hour.^1-3 Understanding injuries specific to this fast-paced sport is an essential part of being a team physician at any level of competitive ice hockey. We are continuing to improve our ability to correctly identify and treat injuries in ice hockey players.^2,4 On the prevention side, rule changes in hockey have been implemented, such as raising the age to allow checking and penalties for deliberate hits to the head and checking from behind, to make the game safer to play.³ Additionally, advancements in biomechanical research and 3D modeling are providing new insights into the pathoanatomy of the hip joint, which can be utilized for surgical planning in hockey players and goalies suffering from symptomatic femoroacetabular impingement (FAI) of the hip.⁵

During the 2010 Winter Olympics, more than 30% of ice hockey players were injured, which was the highest percentage amongst all competing sports.⁶ They also tallied the highest percentage of player-to-player injuries during the Olympics of any sport. Consequently, the team physician covering ice hockey should be prepared to manage upper and lower extremity musculoskeletal injuries, but also concussions, cervical spine injuries, and ocular and dental trauma.² 

One of the earliest epidemiological studies of ice hockey injuries looked at elite Danish hockey players over 2 seasons and found that head trauma accounted for 28% of all injuries, followed by lower extremity injuries at 27% with upper extremity injuries accounting for 19%.⁷ More recent epidemiological studies have shown similar rates based on body region while further defining individual diagnoses and their incidence. This should help clinicians and researchers develop prevention strategies, as well as improve treatments to optimize player outcomes and return to sport.^8,9 Our group recently reviewed the evaluation and management of common head, neck, and shoulder injuries at all competitive levels of ice hockey, and this article serves to complement the former by focusing on lower extremity injuries (Table).²

Continue to: Hip and groin...

EVALUATION AND MANAGEMENT OF COMMON LOWER EXTREMITY HOCKEY INJURIES

HIP INJURIES

Hip and groin injuries are very common amongst this group of athletes and account for approximately 9% of all ice hockey injuries.¹ Unfortunately, they are also known for their high recurrence rates, which may be in part due to delayed diagnosis, inadequate rest and rehabilitation, as well as the extreme loads that are placed on the hip during competition.^10,11 In hockey, the most commonly reported hip injuries include goaltender’s hip, FAI, sports hernia/hockey groin syndrome, adductor strains, hip pointer, and quadriceps contusions. Dalton and colleagues¹² performed the largest epidemiological study to date on hip and groin injuries amongst National Collegiate Athletic Association ice hockey players and reported that the most common injury mechanism was noncontact in nature. Contact injuries accounted for 13% (55 of 421) in men’s ice hockey players while less than 4% (4 of 114) injuries in female ice hockey players, which is likely attributed to a no checking rule in the women’s division. Some of these hip and groin injuries are difficult to diagnose so it is important for the team physician to perform a thorough history and physical examination. Advanced imaging (magnetic resonance imaging [MRI] or a computed tomography (CT) scan with 3D reconstructions) may be necessary to make the correct diagnosis. This is important for providing proper treatment as well as setting player expectations for return to sport.¹²

^{Abbreviations: ACL, anterior cruciate ligament; BTB, bone-patellar tendon-bone; Cam, controlled ankle motion boot; MCL, medial collateral ligament; FAI, femoroacetabular impingement; NSAIDS, nonsteroidal anti-inflammatory drugs; ROM, range of motion.}

Throughout the hockey community, FAI is being examined as a possible source of symptomatic hip pain amongst players at all levels. A recent study, which utilized the National Hockey League (NHL) injury surveillance database, reported that FAI accounted for 5.3% of all hip and groin injuries.¹³ The etiology of FAI is thought to arise from a combination of genetic predisposition coupled with repetitive axial loading/hip flexion. This causes a bony overgrowth of the proximal femoral physes resulting in a cam deformity (Figure 1).^5,14 The abnormal bony anatomy allows for impingement between the acetabulum and proximal femur, which can injure the labrum and articular cartilage of the hip joint.

In the recent study by Ross and colleagues,¹⁵ the authors focused on symptomatic hip impingement in ice hockey goalies.¹⁵ Goaltender’s hip may be the result of the “butterfly style,” which is a technique of goaltending that emphasizes guarding the lower part of the goal. The goalie drops to his/her knees and internally rotates the hips to allow the leg pads to be parallel to the ice. This style acquired the name butterfly because of the resemblance of the spread goalie pads to a butterfly’s wings. Bedi and associates¹⁶ have evaluated hip biomechanics using 3D-generated bone models and showed in their study that arthroscopic treatment can improve hip kinematics and range of motion.

Plain radiographs showed that 90% (61 of 68) of hockey goalies had an elevated alpha angle signifying a femoral cam-type deformity.¹⁵ Goalies had a significantly lower mean lateral center-edge angle (27.3°  vs 29.6°; P = .03) and 13.2% of them were found to have acetabular dysplasia (lateral center-edge angle<20°) compared to only 3% of positional players. The CT scan measurements demonstrated that hockey goalies have a unique cam-type deformity that is located more lateral (1:00 o’clock vs 1:45 o’clock; P < .0001) along the proximal femur, an elevated maximum alpha angle (80.9° vs 68.6°; P < .0001) and loss of offset, when compared to positional players. These findings provide an anatomical basis in support of reports that goaltenders are more likely to experience intra-articular hip injuries compared to other positional players.¹³

Regardless of position, symptomatic FAI in a hockey player is generally a problem that slowly builds and is made worse with activity.¹⁷ On examination, the player may have limited hip flexion and internal rotation, as well as weakness compared to the contralateral side when testing hip flexion and abduction.^18,19 Plain radiographs plus MRI or CT allow for proper characterization and diagnosis (to include underlying chondrolabral pathology).^20,21

In the young athlete, initial management includes physical therapy, which focuses on core strengthening. Emphasis is placed on hip flexion and extension, as well as abduction and external rotation with the goal of reducing symptoms and avoiding injuries.²² A similar approach may be applied to the elite athlete, but failure of nonoperative management may necessitate surgical intervention. Hip arthroscopy continues to grow in popularity over open surgical dislocation with low complication rate and high return-to-play rate.^23-25

For the in-season athlete, attempts to continue to play can be assisted with the role of an intra-articular corticosteroid injection, which can help calm inflammation within the hip joint and mitigate pain, while rehabilitation focuses on core stabilization, postural retraining and focusing on any muscle imbalances that might be present. For positional players, ice time and shift duration can be adjusted to give the player’s hip a period of rest; meanwhile, for goaltenders, shot volumes in practice can be decreased.

Continue to: For athletes who...

For athletes who fail nonoperative care, surgical treatment varies depending on underlying hip pathology and may include femoroplasty, acetabuloplasty, and microfracture as well as labral repair or debridement. Though data are limited, Philippon and colleagues²⁶ have published promising results in a case series of 28 NHL players after surgical intervention for FAI. All players returned to sport at an average of 3.8 months and players who had surgery within 1 year of injury returned on average 1.1 months sooner than those who waited more than 1 year. Rehabilitation protocol varies between goaltenders compared to defensemen and offensive players due to the different demands required for blocking shots on goal.²⁷

One of the most challenging injuries to correctly identify in the hip area is athletic pubalgia (also referred to as sports hernia or core muscle injury) because pain in the groin may be referred from the lumbar spine, hip joint, urologic, or perineal etiologies.²⁸ Sports hernias involve dilatation of the external ring of the inguinal canal and thinning of the posterior wall. Players may report to the athletic trainer or team physician with a complaint of groin pain that is worse when pushing off with their skate or taking a slap shot.²⁹ On exam, pain can be reproduced by hip extension, contralateral torso rotation, or with a resisted sit-up with palpation of the inferolateral edge of the distal rectus abdominus.³⁰ An MRI with specific sequences centered over the pubic symphysis is usually warranted to aid in the workup of sports hernia. An MRI in these cases may also demonstrate avulsions of the rectus abdominus.³¹

Most of these injuries are managed conservatively but can warrant surgical intervention if the symptoms persist. In the study by Jakoi and colleagues,³² they identified 43 ice hockey players over an 8-year period (2001-2008) who had repairs of their sports hernias and assessed the statistics during the 2 years prior and 2 years after surgery. The authors found that 80% of these players were able to return to the ice for 2 or more full seasons. The return-to-sport rate was comparable to other sports after sports hernia repair, but players who had played in ≥7 seasons demonstrated a greater decrease in number of games played, goals, assists and time on ice compared to those who had played in ≤6 seasons prior to the time of injury. Between 1989 and 2000, 22 NHL players who failed to respond to nonoperative management of their groin injuries underwent surgical exploration.²⁹ At the time of surgical exploration, their hockey groin syndrome, consisted of small tears in the external oblique aponeurosis through which branches of the ilioinguinal or iliohypogastric could be identified. These surgical procedures were all through a standard inguinal approach and the perforating neurovascular structures were excised, while the main trunk of the ilioinguinal nerve was ablated and the external oblique aponeurosis was repaired and reinforced with Goretex (W.L. Gore & Associates Inc, Flagstaff, AZ). At follow-up, 18 of the 22 players (82%) had no pain and 19 (86%) were able to resume their careers in the NHL.²⁹ Ice hockey players with sports hernias or hockey groin syndrome often return to the sport, but it is important to identify these problems early so that surgical options can be discussed if the player fails conservative management. It is also critical to make sure that all pathology is identified, because in players with mixed sports hernia and FAI, return-to-play results improve when both issues are addressed. In a study of athletes (some of whom were ice hockey players), who had both FAI and sports hernia, and only hernia/pubalgia surgery was performed, 25% of these athletes returned to sport. If only FAI was addressed, 50% of the athletes returned to sport; however, when hernia and FAI were treated, 89% returned to play.³³

Adductor strains includes injury to the adductor muscles, pectineus, obturator externus and gracilis, and are prevalent in ice hockey players. A study of elite Swedish ice hockey players published in 1988 reported that adductor strains accounted for 10% (10 of 95) of all injuries.³⁴ Given the prevalence of these injuries, considerable research has been dedicated to understanding their mechanism and prevention.³⁵ Adductor strains within the ice hockey population have been attributed to the eccentric forces on the adductors when players attempt to decelerate the leg during a stride.³⁶ A study of NHL players revealed that a ratio <80% of adductor-to-abductor muscle is the best predictor of a groin strain.³⁷

These injuries are also well known for their recurrence rates, as was the case in an NHL study where 4 of the 9 adductor strains (44%) were recurrent injuries.³⁷ The authors attributed the recurrence to an incomplete rehabilitation program and an accelerated return to sport. This was followed by an NHL prevention program that spanned 2 seasons and analyzed 58 players whose adductor-to-abductor ratio was <80% and placed them into a 6-week intervention program during the preseason.³⁷ Only 3 players sustained an adductor strain in the 2 subsequent seasons after the intervention, compared to 11 strains in the previous 2 seasons. Thus, early identification of muscle strength imbalance coupled with an appropriate intervention program has proven to be an effective means of reducing adductor strains in this at-risk population.

Continue to: Contact injuries may...

Contact injuries may vary with checking into the boards being unique to men’s ice hockey. Hip pointers occur as a result of a direct compression injury to the iliac crest, which causes trauma to the bone but also to the overlying hip abductor musculature, and represent roughly 2.4% of ice hockey injuries.²³ The resulting contusion may cause a local hematoma formation. Early identification of the injury plus treatment with RICE (rest, ice, compression, elevation) coupled with crutches to limit weight-bearing status may minimize soft tissue trauma and swelling, and ultimately aid in pain control and return to sport.³⁸ Hip abductor strengthening, added padding over the injured area, as well as a compressive hip spica wrapping, have all been suggested to expedite return to play and help prevent recurrence of the hip pointer.⁸

KNEE INJURIES

Injury to the medial collateral ligament (MCL) is the most commonly reported knee injury (Figure 2) and second only to concussion amongst all injuries in National Collegiate Athletic Association ice hockey players.^8,39 The mechanism of injury typically involves a valgus force on the knee, which is often caused by collision into another player.³⁹ Valgus stress testing with the knee in 30° of flexion is used to grade the severity of injury (Grade I: 0-5 mm of medial opening; Grade II: 5-10 mm of medial opening; Grade III: >10 mm of medial opening).³⁹ One study that followed a single college hockey team for 8 seasons reported that 77% of injuries (10 of 13) occurred during player-to-player collision,³⁹ with 5 being Grade 1 injuries, 6 Grade 2 injuries, 1 Grade 3; information was missing for 1 player. Nonoperative management of incomplete injuries, grade 1 and 2 sprains, with RICE and early physical therapy intervention to work on knee range of motion and quadriceps strengthening typically helps the player return to sport within days for grade 1 and 2 injuries to 3 weeks for grade 2 injuries. Complete tears have been managed both operatively and nonoperatively with evidence to suggest better outcomes after surgical intervention if there is a concomitant ACL injury requiring reconstruction.^8,9

Anterior cruciate ligament (ACL) tears occur less frequently in hockey players compared to the players in other sports such as football and basketball.^38,40 Between 2006 and 2010, 47 players were identified by the NHL Injury Surveillance System as having sustained an ACL injury, which equates to an incidence of 9.4 ACL injuries per NHL season over this time span.⁴¹ The mechanism of ACL tears in ice hockey players appears to be different from other sports players based on a recent MRI study that evaluated players for concomitant injuries following ACL tear and noted significantly fewer bone bruises on the lateral femoral condyle compared to players in other sports.⁴² Early evaluation after injury with Lachman and/or pivot shift tests aids the diagnosis. Data from the NHL study identified 32 players (68%) with concomitant meniscal injuries and 32 (68%) had MCL injuries in conjunction with their ACL tears.⁴¹ Average length in the league prior to injury was 5.65 seasons. Twenty-nine of the injured players (61.7%) underwent reconstruction with a patellar tendon autograft, 13 (27.7%) had a hamstring autograft, and 5 (10.6%) had either a patellar tendon or hamstring allograft.⁴¹ Meniscus and ACL injuries were associated with a decreased length of career compared to age-matched controls and, notably, players >30 years at the time of injury had only a 67% rate of return to sport whereas those <30 years had a return-to-sport rate of 80%. Players who were able to return did so at an average of 9.8 months (range, 6-21 months) and had a significant reduction in total number of goals, assists, and points scored compared to controls. Decline in performance was typically associated with forwards and wings, while defensemen did not demonstrate the same decrease in performance following return to ice hockey.⁴¹

Meniscal tears are a well-documented concomitant injury with ruptures of the ACL, and the combination is a known pattern associated with shorter careers compared to isolated ACL tears in ice hockey players.⁴¹ The lateral meniscus is known for increased mobility compared to the medial meniscus and is more commonly injured (39% vs 8.5%) in ACL tears that occur in contact sports and downhill skiing.⁴² Ice hockey presents a scenario that is different from other contact sports because of the near frictionless interaction between the player’s ice skates and playing surface. This likely equates to a different injury mechanism and dissipation of energy after contact as well as non-contact injuries.³⁸ A recent study reviewed knee MRI findings associated with ACL tears in collegiate ice hockey players and compared to other sports known for their high rates of concomitant meniscal pathology. The authors reported a statistically significant decrease in lateral meniscus tears and bone-bruising patterns in ice hockey players with ACL injuries compared to athletes with ACL tears in other sports.⁴³ In contrast, an NHL study of ACL tears in professional ice hockey players found that 68% of players had concomitant meniscal tears (32 out of 47 players).⁴¹

Continue to: The presence of...

The presence of a meniscal tear on MRI is typically a surgical problem, especially if it occurred with an ACL injury. Meniscal repair is preferable, if possible, because there is a known association of increased cartilage contact pressures associated with meniscal debridement. Return to sport following meniscus injury hinges upon whether it is an isolated injury and how it is treated. If the meniscus injury occurs in isolation and can be treated with a debridement and partial resection alone, there is obviously a quicker return to sport as the player can be weight-bearing immediately following surgery. Return to skating after meniscal debridement and partial resection is usually 4 to 6 weeks, whereas meniscal repair protocols vary depending on surgeon; players may need 3 months to 4 months to return to the ice.

Quadriceps contusions are contact injuries that are not unique to ice hockey (Figure 3). They may result from player collision but also from direct blows from a hockey puck. A high velocity puck is known to cause immense trauma to the quadriceps muscles, which may result in localized bleeding and hematoma formation. If the player is able to anticipate the event, active contraction of the quadriceps muscle has been shown to absorb some of the energy and result in a less traumatic injury, but in a fast paced ice hockey game, the player’s anticipation is less likely than in other sports such as baseball.⁴⁴Interestingly, the degree of knee flexion after injury is predictive of injury severity with milder injuries associated with angles >90 and more severe injuries resulting in knee flexion angles <45° and typically an antalgic gait.⁴⁵ It is important to treat these injuries during the first 24 hours with the knee maintained in 120°of flexion, plus ice and compression, which can be achieved using a locked knee brace or elastic compression wrap. Quadriceps stretching and isometric strengthening should immediately follow the period of immobilization. The addition of NSAIDs may help prevent the formation of myositis ossificans. A study from West Point suggests that the average return to sport or activity ranges from 13 days (mild contusion) to 21 days (severe contusions), while others⁸ have indicated that if the injury is treated acutely and a player is able to regain motion and strength, return to ice hockey within a few days is possible.

FOOT AND ANKLE

Ice hockey has some unique injuries that can be attributed to the use of ice skates for play. One such injury is boot-top lacerations, which are fortunately rare as they can be a career-ending injury.⁴⁷ The spectrum of injury ranges from superficial abrasions to more severe soft tissue disruption, including the extensor tendons and neurovascular structures. The actual mechanism of injury involves an opponent’s skate blade cutting across the anterior ankle. One early case report described a protective method of having players place their skate tongues deep to their protective shin pads, instead of turning the tongues down.⁴⁷ Kevlar socks have also been shown to help prevent or minimize the damage from a skate blade.⁴⁸

Injury to the lateral ankle ligaments, anterior talofibular ligament or calcaneofibular ligament, are usually more common than the higher ankle sprains involving the syndesmosis. However, this is not the case in ice hockey. The rigidity of the ice skate at the level of the lateral ligaments seems to impart a protective mechanism to the lower ligaments, but this results in a higher incidence of syndesmotic injuries. These high ankle injuries are unfortunately more debilitating and often require a longer recovery period. In a study of these injuries in NHL players, syndesmotic sprains made up 74% of all ankle sprains, whereas only 18.4% of ankle sprains involved the syndesmosis in American football players..^49,50 The average number of days between injury and return to play is 45 days, and some authors believe that defensemen may have a harder time recovering because of the demands on their ankles by having to switch continuously between forward and backward skating.⁴⁹

Most patients are treated conservatively when their ankle plain radiographs show a congruent mortise and no evidence of syndesmotic widening. If the player expresses pain when squeezing the syndesmosis, it is helpful to obtain stress radiographs to further evaluate for syndesmotic injury. Nonoperative management includes RICE, immobilization in a rigid boot with crutches to protect weight-bearing with gradual advancements and eventually physical therapy to address any ankle stiffness, followed by dynamic functional activities. Treatment options for syndesmotic widening and failed conservative management includes both screw and plate options as well as suture buttons.^49,51,52

Ankle and foot fractures were historically a rare injury in ice hockey players based on radiograph evaluation; however, the recent study by Baker and colleagues⁴ demonstrated that MRI can be helpful in detecting subradiographic fractures. Most of the injuries detected after MRI were from being hit by a hockey puck; this was a novel mechanism that had not been previously reported in the literature.⁴ Of the injuries that resulted from a direct blow, 14 of 17 occurred on the medial aspect of the foot and ankle, which is believed to result another word? from a defender skating towards an offensive player and attempting to block shots on goal. In this study, all occult fractures involving the medial malleolus were eventually treated with open reduction and internal fixation and underwent routine healing.⁴ The navicular bone and base of the first metatarsal accounted for the remaining medial-sided fractures. In a recent analysis of risk factors for reoperation following operative fixation of foot fractures across the National Basketball Association, the National Football Leagues, Major League Baseball, and the National Hockey League only a total of 3 fractures involving the foot (1 navicular and 2 first metatarsal) were identified in NHL players over a 30-year period.⁵³ The study acknowledged a major limitation being a public source for identifying players with fractures.

Lace bite is another common ice hockey injury. It typically occurs at the beginning of a season or whenever a player is breaking in a new pair of skates. The cause of the lace bite is the rigid tongue in the skate that rubs against the anterior ankle. Skating causes inflammation in the area of the tibialis anterior tendon, and the player will complain of significant anterior ankle pain. First line treatment for lace bite is ice (Figure 4A), NSAID gel (eg, diclofenac 1%), and a Bunga lace-bite pad (Absolute Athletics). (Figure 4B).

SUMMARY

Lower extremity injuries are common in ice hockey players, and a covering physician should be comfortable managing these injuries from breezers to skate. Proper evaluation and work-up is critical for early diagnosis and identification of pathology, which can minimize the impact of the injury and expedite a treatment plan to return the player safely to the ice and in the game.

“Hockey is a fast body-contact game played by men with clubs in their hands and knives laced to their feet, since the skates are razor sharp, and before the evening is over it is almost a certainty that someone will be hurt and will fleck the ice with a generous contribution of gore before he is led away to be hemstitched together again.” —Paul Gallico in Farewell to Sport (1938)

Ice hockey is a collision sport with player speeds in excess of 30 miles/hour, on a sheet of ice surrounded by unforgiving boards, with a vulcanized rubber puck moving at speeds approaching 100 miles/hour.^1-3 Understanding injuries specific to this fast-paced sport is an essential part of being a team physician at any level of competitive ice hockey. We are continuing to improve our ability to correctly identify and treat injuries in ice hockey players.^2,4 On the prevention side, rule changes in hockey have been implemented, such as raising the age to allow checking and penalties for deliberate hits to the head and checking from behind, to make the game safer to play.³ Additionally, advancements in biomechanical research and 3D modeling are providing new insights into the pathoanatomy of the hip joint, which can be utilized for surgical planning in hockey players and goalies suffering from symptomatic femoroacetabular impingement (FAI) of the hip.⁵

During the 2010 Winter Olympics, more than 30% of ice hockey players were injured, which was the highest percentage amongst all competing sports.⁶ They also tallied the highest percentage of player-to-player injuries during the Olympics of any sport. Consequently, the team physician covering ice hockey should be prepared to manage upper and lower extremity musculoskeletal injuries, but also concussions, cervical spine injuries, and ocular and dental trauma.² 

One of the earliest epidemiological studies of ice hockey injuries looked at elite Danish hockey players over 2 seasons and found that head trauma accounted for 28% of all injuries, followed by lower extremity injuries at 27% with upper extremity injuries accounting for 19%.⁷ More recent epidemiological studies have shown similar rates based on body region while further defining individual diagnoses and their incidence. This should help clinicians and researchers develop prevention strategies, as well as improve treatments to optimize player outcomes and return to sport.^8,9 Our group recently reviewed the evaluation and management of common head, neck, and shoulder injuries at all competitive levels of ice hockey, and this article serves to complement the former by focusing on lower extremity injuries (Table).²

Continue to: Hip and groin...

EVALUATION AND MANAGEMENT OF COMMON LOWER EXTREMITY HOCKEY INJURIES

HIP INJURIES

Hip and groin injuries are very common amongst this group of athletes and account for approximately 9% of all ice hockey injuries.¹ Unfortunately, they are also known for their high recurrence rates, which may be in part due to delayed diagnosis, inadequate rest and rehabilitation, as well as the extreme loads that are placed on the hip during competition.^10,11 In hockey, the most commonly reported hip injuries include goaltender’s hip, FAI, sports hernia/hockey groin syndrome, adductor strains, hip pointer, and quadriceps contusions. Dalton and colleagues¹² performed the largest epidemiological study to date on hip and groin injuries amongst National Collegiate Athletic Association ice hockey players and reported that the most common injury mechanism was noncontact in nature. Contact injuries accounted for 13% (55 of 421) in men’s ice hockey players while less than 4% (4 of 114) injuries in female ice hockey players, which is likely attributed to a no checking rule in the women’s division. Some of these hip and groin injuries are difficult to diagnose so it is important for the team physician to perform a thorough history and physical examination. Advanced imaging (magnetic resonance imaging [MRI] or a computed tomography (CT) scan with 3D reconstructions) may be necessary to make the correct diagnosis. This is important for providing proper treatment as well as setting player expectations for return to sport.¹²

^{Abbreviations: ACL, anterior cruciate ligament; BTB, bone-patellar tendon-bone; Cam, controlled ankle motion boot; MCL, medial collateral ligament; FAI, femoroacetabular impingement; NSAIDS, nonsteroidal anti-inflammatory drugs; ROM, range of motion.}

Throughout the hockey community, FAI is being examined as a possible source of symptomatic hip pain amongst players at all levels. A recent study, which utilized the National Hockey League (NHL) injury surveillance database, reported that FAI accounted for 5.3% of all hip and groin injuries.¹³ The etiology of FAI is thought to arise from a combination of genetic predisposition coupled with repetitive axial loading/hip flexion. This causes a bony overgrowth of the proximal femoral physes resulting in a cam deformity (Figure 1).^5,14 The abnormal bony anatomy allows for impingement between the acetabulum and proximal femur, which can injure the labrum and articular cartilage of the hip joint.

In the recent study by Ross and colleagues,¹⁵ the authors focused on symptomatic hip impingement in ice hockey goalies.¹⁵ Goaltender’s hip may be the result of the “butterfly style,” which is a technique of goaltending that emphasizes guarding the lower part of the goal. The goalie drops to his/her knees and internally rotates the hips to allow the leg pads to be parallel to the ice. This style acquired the name butterfly because of the resemblance of the spread goalie pads to a butterfly’s wings. Bedi and associates¹⁶ have evaluated hip biomechanics using 3D-generated bone models and showed in their study that arthroscopic treatment can improve hip kinematics and range of motion.

Plain radiographs showed that 90% (61 of 68) of hockey goalies had an elevated alpha angle signifying a femoral cam-type deformity.¹⁵ Goalies had a significantly lower mean lateral center-edge angle (27.3°  vs 29.6°; P = .03) and 13.2% of them were found to have acetabular dysplasia (lateral center-edge angle<20°) compared to only 3% of positional players. The CT scan measurements demonstrated that hockey goalies have a unique cam-type deformity that is located more lateral (1:00 o’clock vs 1:45 o’clock; P < .0001) along the proximal femur, an elevated maximum alpha angle (80.9° vs 68.6°; P < .0001) and loss of offset, when compared to positional players. These findings provide an anatomical basis in support of reports that goaltenders are more likely to experience intra-articular hip injuries compared to other positional players.¹³

Regardless of position, symptomatic FAI in a hockey player is generally a problem that slowly builds and is made worse with activity.¹⁷ On examination, the player may have limited hip flexion and internal rotation, as well as weakness compared to the contralateral side when testing hip flexion and abduction.^18,19 Plain radiographs plus MRI or CT allow for proper characterization and diagnosis (to include underlying chondrolabral pathology).^20,21

In the young athlete, initial management includes physical therapy, which focuses on core strengthening. Emphasis is placed on hip flexion and extension, as well as abduction and external rotation with the goal of reducing symptoms and avoiding injuries.²² A similar approach may be applied to the elite athlete, but failure of nonoperative management may necessitate surgical intervention. Hip arthroscopy continues to grow in popularity over open surgical dislocation with low complication rate and high return-to-play rate.^23-25

For the in-season athlete, attempts to continue to play can be assisted with the role of an intra-articular corticosteroid injection, which can help calm inflammation within the hip joint and mitigate pain, while rehabilitation focuses on core stabilization, postural retraining and focusing on any muscle imbalances that might be present. For positional players, ice time and shift duration can be adjusted to give the player’s hip a period of rest; meanwhile, for goaltenders, shot volumes in practice can be decreased.

Continue to: For athletes who...

For athletes who fail nonoperative care, surgical treatment varies depending on underlying hip pathology and may include femoroplasty, acetabuloplasty, and microfracture as well as labral repair or debridement. Though data are limited, Philippon and colleagues²⁶ have published promising results in a case series of 28 NHL players after surgical intervention for FAI. All players returned to sport at an average of 3.8 months and players who had surgery within 1 year of injury returned on average 1.1 months sooner than those who waited more than 1 year. Rehabilitation protocol varies between goaltenders compared to defensemen and offensive players due to the different demands required for blocking shots on goal.²⁷

One of the most challenging injuries to correctly identify in the hip area is athletic pubalgia (also referred to as sports hernia or core muscle injury) because pain in the groin may be referred from the lumbar spine, hip joint, urologic, or perineal etiologies.²⁸ Sports hernias involve dilatation of the external ring of the inguinal canal and thinning of the posterior wall. Players may report to the athletic trainer or team physician with a complaint of groin pain that is worse when pushing off with their skate or taking a slap shot.²⁹ On exam, pain can be reproduced by hip extension, contralateral torso rotation, or with a resisted sit-up with palpation of the inferolateral edge of the distal rectus abdominus.³⁰ An MRI with specific sequences centered over the pubic symphysis is usually warranted to aid in the workup of sports hernia. An MRI in these cases may also demonstrate avulsions of the rectus abdominus.³¹

Most of these injuries are managed conservatively but can warrant surgical intervention if the symptoms persist. In the study by Jakoi and colleagues,³² they identified 43 ice hockey players over an 8-year period (2001-2008) who had repairs of their sports hernias and assessed the statistics during the 2 years prior and 2 years after surgery. The authors found that 80% of these players were able to return to the ice for 2 or more full seasons. The return-to-sport rate was comparable to other sports after sports hernia repair, but players who had played in ≥7 seasons demonstrated a greater decrease in number of games played, goals, assists and time on ice compared to those who had played in ≤6 seasons prior to the time of injury. Between 1989 and 2000, 22 NHL players who failed to respond to nonoperative management of their groin injuries underwent surgical exploration.²⁹ At the time of surgical exploration, their hockey groin syndrome, consisted of small tears in the external oblique aponeurosis through which branches of the ilioinguinal or iliohypogastric could be identified. These surgical procedures were all through a standard inguinal approach and the perforating neurovascular structures were excised, while the main trunk of the ilioinguinal nerve was ablated and the external oblique aponeurosis was repaired and reinforced with Goretex (W.L. Gore & Associates Inc, Flagstaff, AZ). At follow-up, 18 of the 22 players (82%) had no pain and 19 (86%) were able to resume their careers in the NHL.²⁹ Ice hockey players with sports hernias or hockey groin syndrome often return to the sport, but it is important to identify these problems early so that surgical options can be discussed if the player fails conservative management. It is also critical to make sure that all pathology is identified, because in players with mixed sports hernia and FAI, return-to-play results improve when both issues are addressed. In a study of athletes (some of whom were ice hockey players), who had both FAI and sports hernia, and only hernia/pubalgia surgery was performed, 25% of these athletes returned to sport. If only FAI was addressed, 50% of the athletes returned to sport; however, when hernia and FAI were treated, 89% returned to play.³³

Adductor strains includes injury to the adductor muscles, pectineus, obturator externus and gracilis, and are prevalent in ice hockey players. A study of elite Swedish ice hockey players published in 1988 reported that adductor strains accounted for 10% (10 of 95) of all injuries.³⁴ Given the prevalence of these injuries, considerable research has been dedicated to understanding their mechanism and prevention.³⁵ Adductor strains within the ice hockey population have been attributed to the eccentric forces on the adductors when players attempt to decelerate the leg during a stride.³⁶ A study of NHL players revealed that a ratio <80% of adductor-to-abductor muscle is the best predictor of a groin strain.³⁷

These injuries are also well known for their recurrence rates, as was the case in an NHL study where 4 of the 9 adductor strains (44%) were recurrent injuries.³⁷ The authors attributed the recurrence to an incomplete rehabilitation program and an accelerated return to sport. This was followed by an NHL prevention program that spanned 2 seasons and analyzed 58 players whose adductor-to-abductor ratio was <80% and placed them into a 6-week intervention program during the preseason.³⁷ Only 3 players sustained an adductor strain in the 2 subsequent seasons after the intervention, compared to 11 strains in the previous 2 seasons. Thus, early identification of muscle strength imbalance coupled with an appropriate intervention program has proven to be an effective means of reducing adductor strains in this at-risk population.

Continue to: Contact injuries may...

Contact injuries may vary with checking into the boards being unique to men’s ice hockey. Hip pointers occur as a result of a direct compression injury to the iliac crest, which causes trauma to the bone but also to the overlying hip abductor musculature, and represent roughly 2.4% of ice hockey injuries.²³ The resulting contusion may cause a local hematoma formation. Early identification of the injury plus treatment with RICE (rest, ice, compression, elevation) coupled with crutches to limit weight-bearing status may minimize soft tissue trauma and swelling, and ultimately aid in pain control and return to sport.³⁸ Hip abductor strengthening, added padding over the injured area, as well as a compressive hip spica wrapping, have all been suggested to expedite return to play and help prevent recurrence of the hip pointer.⁸

KNEE INJURIES

Injury to the medial collateral ligament (MCL) is the most commonly reported knee injury (Figure 2) and second only to concussion amongst all injuries in National Collegiate Athletic Association ice hockey players.^8,39 The mechanism of injury typically involves a valgus force on the knee, which is often caused by collision into another player.³⁹ Valgus stress testing with the knee in 30° of flexion is used to grade the severity of injury (Grade I: 0-5 mm of medial opening; Grade II: 5-10 mm of medial opening; Grade III: >10 mm of medial opening).³⁹ One study that followed a single college hockey team for 8 seasons reported that 77% of injuries (10 of 13) occurred during player-to-player collision,³⁹ with 5 being Grade 1 injuries, 6 Grade 2 injuries, 1 Grade 3; information was missing for 1 player. Nonoperative management of incomplete injuries, grade 1 and 2 sprains, with RICE and early physical therapy intervention to work on knee range of motion and quadriceps strengthening typically helps the player return to sport within days for grade 1 and 2 injuries to 3 weeks for grade 2 injuries. Complete tears have been managed both operatively and nonoperatively with evidence to suggest better outcomes after surgical intervention if there is a concomitant ACL injury requiring reconstruction.^8,9

Anterior cruciate ligament (ACL) tears occur less frequently in hockey players compared to the players in other sports such as football and basketball.^38,40 Between 2006 and 2010, 47 players were identified by the NHL Injury Surveillance System as having sustained an ACL injury, which equates to an incidence of 9.4 ACL injuries per NHL season over this time span.⁴¹ The mechanism of ACL tears in ice hockey players appears to be different from other sports players based on a recent MRI study that evaluated players for concomitant injuries following ACL tear and noted significantly fewer bone bruises on the lateral femoral condyle compared to players in other sports.⁴² Early evaluation after injury with Lachman and/or pivot shift tests aids the diagnosis. Data from the NHL study identified 32 players (68%) with concomitant meniscal injuries and 32 (68%) had MCL injuries in conjunction with their ACL tears.⁴¹ Average length in the league prior to injury was 5.65 seasons. Twenty-nine of the injured players (61.7%) underwent reconstruction with a patellar tendon autograft, 13 (27.7%) had a hamstring autograft, and 5 (10.6%) had either a patellar tendon or hamstring allograft.⁴¹ Meniscus and ACL injuries were associated with a decreased length of career compared to age-matched controls and, notably, players >30 years at the time of injury had only a 67% rate of return to sport whereas those <30 years had a return-to-sport rate of 80%. Players who were able to return did so at an average of 9.8 months (range, 6-21 months) and had a significant reduction in total number of goals, assists, and points scored compared to controls. Decline in performance was typically associated with forwards and wings, while defensemen did not demonstrate the same decrease in performance following return to ice hockey.⁴¹

Meniscal tears are a well-documented concomitant injury with ruptures of the ACL, and the combination is a known pattern associated with shorter careers compared to isolated ACL tears in ice hockey players.⁴¹ The lateral meniscus is known for increased mobility compared to the medial meniscus and is more commonly injured (39% vs 8.5%) in ACL tears that occur in contact sports and downhill skiing.⁴² Ice hockey presents a scenario that is different from other contact sports because of the near frictionless interaction between the player’s ice skates and playing surface. This likely equates to a different injury mechanism and dissipation of energy after contact as well as non-contact injuries.³⁸ A recent study reviewed knee MRI findings associated with ACL tears in collegiate ice hockey players and compared to other sports known for their high rates of concomitant meniscal pathology. The authors reported a statistically significant decrease in lateral meniscus tears and bone-bruising patterns in ice hockey players with ACL injuries compared to athletes with ACL tears in other sports.⁴³ In contrast, an NHL study of ACL tears in professional ice hockey players found that 68% of players had concomitant meniscal tears (32 out of 47 players).⁴¹

Continue to: The presence of...

The presence of a meniscal tear on MRI is typically a surgical problem, especially if it occurred with an ACL injury. Meniscal repair is preferable, if possible, because there is a known association of increased cartilage contact pressures associated with meniscal debridement. Return to sport following meniscus injury hinges upon whether it is an isolated injury and how it is treated. If the meniscus injury occurs in isolation and can be treated with a debridement and partial resection alone, there is obviously a quicker return to sport as the player can be weight-bearing immediately following surgery. Return to skating after meniscal debridement and partial resection is usually 4 to 6 weeks, whereas meniscal repair protocols vary depending on surgeon; players may need 3 months to 4 months to return to the ice.

Quadriceps contusions are contact injuries that are not unique to ice hockey (Figure 3). They may result from player collision but also from direct blows from a hockey puck. A high velocity puck is known to cause immense trauma to the quadriceps muscles, which may result in localized bleeding and hematoma formation. If the player is able to anticipate the event, active contraction of the quadriceps muscle has been shown to absorb some of the energy and result in a less traumatic injury, but in a fast paced ice hockey game, the player’s anticipation is less likely than in other sports such as baseball.⁴⁴Interestingly, the degree of knee flexion after injury is predictive of injury severity with milder injuries associated with angles >90 and more severe injuries resulting in knee flexion angles <45° and typically an antalgic gait.⁴⁵ It is important to treat these injuries during the first 24 hours with the knee maintained in 120°of flexion, plus ice and compression, which can be achieved using a locked knee brace or elastic compression wrap. Quadriceps stretching and isometric strengthening should immediately follow the period of immobilization. The addition of NSAIDs may help prevent the formation of myositis ossificans. A study from West Point suggests that the average return to sport or activity ranges from 13 days (mild contusion) to 21 days (severe contusions), while others⁸ have indicated that if the injury is treated acutely and a player is able to regain motion and strength, return to ice hockey within a few days is possible.

FOOT AND ANKLE

Ice hockey has some unique injuries that can be attributed to the use of ice skates for play. One such injury is boot-top lacerations, which are fortunately rare as they can be a career-ending injury.⁴⁷ The spectrum of injury ranges from superficial abrasions to more severe soft tissue disruption, including the extensor tendons and neurovascular structures. The actual mechanism of injury involves an opponent’s skate blade cutting across the anterior ankle. One early case report described a protective method of having players place their skate tongues deep to their protective shin pads, instead of turning the tongues down.⁴⁷ Kevlar socks have also been shown to help prevent or minimize the damage from a skate blade.⁴⁸

Injury to the lateral ankle ligaments, anterior talofibular ligament or calcaneofibular ligament, are usually more common than the higher ankle sprains involving the syndesmosis. However, this is not the case in ice hockey. The rigidity of the ice skate at the level of the lateral ligaments seems to impart a protective mechanism to the lower ligaments, but this results in a higher incidence of syndesmotic injuries. These high ankle injuries are unfortunately more debilitating and often require a longer recovery period. In a study of these injuries in NHL players, syndesmotic sprains made up 74% of all ankle sprains, whereas only 18.4% of ankle sprains involved the syndesmosis in American football players..^49,50 The average number of days between injury and return to play is 45 days, and some authors believe that defensemen may have a harder time recovering because of the demands on their ankles by having to switch continuously between forward and backward skating.⁴⁹

Most patients are treated conservatively when their ankle plain radiographs show a congruent mortise and no evidence of syndesmotic widening. If the player expresses pain when squeezing the syndesmosis, it is helpful to obtain stress radiographs to further evaluate for syndesmotic injury. Nonoperative management includes RICE, immobilization in a rigid boot with crutches to protect weight-bearing with gradual advancements and eventually physical therapy to address any ankle stiffness, followed by dynamic functional activities. Treatment options for syndesmotic widening and failed conservative management includes both screw and plate options as well as suture buttons.^49,51,52

Ankle and foot fractures were historically a rare injury in ice hockey players based on radiograph evaluation; however, the recent study by Baker and colleagues⁴ demonstrated that MRI can be helpful in detecting subradiographic fractures. Most of the injuries detected after MRI were from being hit by a hockey puck; this was a novel mechanism that had not been previously reported in the literature.⁴ Of the injuries that resulted from a direct blow, 14 of 17 occurred on the medial aspect of the foot and ankle, which is believed to result another word? from a defender skating towards an offensive player and attempting to block shots on goal. In this study, all occult fractures involving the medial malleolus were eventually treated with open reduction and internal fixation and underwent routine healing.⁴ The navicular bone and base of the first metatarsal accounted for the remaining medial-sided fractures. In a recent analysis of risk factors for reoperation following operative fixation of foot fractures across the National Basketball Association, the National Football Leagues, Major League Baseball, and the National Hockey League only a total of 3 fractures involving the foot (1 navicular and 2 first metatarsal) were identified in NHL players over a 30-year period.⁵³ The study acknowledged a major limitation being a public source for identifying players with fractures.

Lace bite is another common ice hockey injury. It typically occurs at the beginning of a season or whenever a player is breaking in a new pair of skates. The cause of the lace bite is the rigid tongue in the skate that rubs against the anterior ankle. Skating causes inflammation in the area of the tibialis anterior tendon, and the player will complain of significant anterior ankle pain. First line treatment for lace bite is ice (Figure 4A), NSAID gel (eg, diclofenac 1%), and a Bunga lace-bite pad (Absolute Athletics). (Figure 4B).

SUMMARY

Lower extremity injuries are common in ice hockey players, and a covering physician should be comfortable managing these injuries from breezers to skate. Proper evaluation and work-up is critical for early diagnosis and identification of pathology, which can minimize the impact of the injury and expedite a treatment plan to return the player safely to the ice and in the game.

“Hockey is a fast body-contact game played by men with clubs in their hands and knives laced to their feet, since the skates are razor sharp, and before the evening is over it is almost a certainty that someone will be hurt and will fleck the ice with a generous contribution of gore before he is led away to be hemstitched together again.” —Paul Gallico in Farewell to Sport (1938)

Ice hockey is a collision sport with player speeds in excess of 30 miles/hour, on a sheet of ice surrounded by unforgiving boards, with a vulcanized rubber puck moving at speeds approaching 100 miles/hour.^1-3 Understanding injuries specific to this fast-paced sport is an essential part of being a team physician at any level of competitive ice hockey. We are continuing to improve our ability to correctly identify and treat injuries in ice hockey players.^2,4 On the prevention side, rule changes in hockey have been implemented, such as raising the age to allow checking and penalties for deliberate hits to the head and checking from behind, to make the game safer to play.³ Additionally, advancements in biomechanical research and 3D modeling are providing new insights into the pathoanatomy of the hip joint, which can be utilized for surgical planning in hockey players and goalies suffering from symptomatic femoroacetabular impingement (FAI) of the hip.⁵

During the 2010 Winter Olympics, more than 30% of ice hockey players were injured, which was the highest percentage amongst all competing sports.⁶ They also tallied the highest percentage of player-to-player injuries during the Olympics of any sport. Consequently, the team physician covering ice hockey should be prepared to manage upper and lower extremity musculoskeletal injuries, but also concussions, cervical spine injuries, and ocular and dental trauma.² 

One of the earliest epidemiological studies of ice hockey injuries looked at elite Danish hockey players over 2 seasons and found that head trauma accounted for 28% of all injuries, followed by lower extremity injuries at 27% with upper extremity injuries accounting for 19%.⁷ More recent epidemiological studies have shown similar rates based on body region while further defining individual diagnoses and their incidence. This should help clinicians and researchers develop prevention strategies, as well as improve treatments to optimize player outcomes and return to sport.^8,9 Our group recently reviewed the evaluation and management of common head, neck, and shoulder injuries at all competitive levels of ice hockey, and this article serves to complement the former by focusing on lower extremity injuries (Table).²

Continue to: Hip and groin...

EVALUATION AND MANAGEMENT OF COMMON LOWER EXTREMITY HOCKEY INJURIES

HIP INJURIES

Hip and groin injuries are very common amongst this group of athletes and account for approximately 9% of all ice hockey injuries.¹ Unfortunately, they are also known for their high recurrence rates, which may be in part due to delayed diagnosis, inadequate rest and rehabilitation, as well as the extreme loads that are placed on the hip during competition.^10,11 In hockey, the most commonly reported hip injuries include goaltender’s hip, FAI, sports hernia/hockey groin syndrome, adductor strains, hip pointer, and quadriceps contusions. Dalton and colleagues¹² performed the largest epidemiological study to date on hip and groin injuries amongst National Collegiate Athletic Association ice hockey players and reported that the most common injury mechanism was noncontact in nature. Contact injuries accounted for 13% (55 of 421) in men’s ice hockey players while less than 4% (4 of 114) injuries in female ice hockey players, which is likely attributed to a no checking rule in the women’s division. Some of these hip and groin injuries are difficult to diagnose so it is important for the team physician to perform a thorough history and physical examination. Advanced imaging (magnetic resonance imaging [MRI] or a computed tomography (CT) scan with 3D reconstructions) may be necessary to make the correct diagnosis. This is important for providing proper treatment as well as setting player expectations for return to sport.¹²

^{Abbreviations: ACL, anterior cruciate ligament; BTB, bone-patellar tendon-bone; Cam, controlled ankle motion boot; MCL, medial collateral ligament; FAI, femoroacetabular impingement; NSAIDS, nonsteroidal anti-inflammatory drugs; ROM, range of motion.}

Throughout the hockey community, FAI is being examined as a possible source of symptomatic hip pain amongst players at all levels. A recent study, which utilized the National Hockey League (NHL) injury surveillance database, reported that FAI accounted for 5.3% of all hip and groin injuries.¹³ The etiology of FAI is thought to arise from a combination of genetic predisposition coupled with repetitive axial loading/hip flexion. This causes a bony overgrowth of the proximal femoral physes resulting in a cam deformity (Figure 1).^5,14 The abnormal bony anatomy allows for impingement between the acetabulum and proximal femur, which can injure the labrum and articular cartilage of the hip joint.

In the recent study by Ross and colleagues,¹⁵ the authors focused on symptomatic hip impingement in ice hockey goalies.¹⁵ Goaltender’s hip may be the result of the “butterfly style,” which is a technique of goaltending that emphasizes guarding the lower part of the goal. The goalie drops to his/her knees and internally rotates the hips to allow the leg pads to be parallel to the ice. This style acquired the name butterfly because of the resemblance of the spread goalie pads to a butterfly’s wings. Bedi and associates¹⁶ have evaluated hip biomechanics using 3D-generated bone models and showed in their study that arthroscopic treatment can improve hip kinematics and range of motion.

Plain radiographs showed that 90% (61 of 68) of hockey goalies had an elevated alpha angle signifying a femoral cam-type deformity.¹⁵ Goalies had a significantly lower mean lateral center-edge angle (27.3°  vs 29.6°; P = .03) and 13.2% of them were found to have acetabular dysplasia (lateral center-edge angle<20°) compared to only 3% of positional players. The CT scan measurements demonstrated that hockey goalies have a unique cam-type deformity that is located more lateral (1:00 o’clock vs 1:45 o’clock; P < .0001) along the proximal femur, an elevated maximum alpha angle (80.9° vs 68.6°; P < .0001) and loss of offset, when compared to positional players. These findings provide an anatomical basis in support of reports that goaltenders are more likely to experience intra-articular hip injuries compared to other positional players.¹³

Regardless of position, symptomatic FAI in a hockey player is generally a problem that slowly builds and is made worse with activity.¹⁷ On examination, the player may have limited hip flexion and internal rotation, as well as weakness compared to the contralateral side when testing hip flexion and abduction.^18,19 Plain radiographs plus MRI or CT allow for proper characterization and diagnosis (to include underlying chondrolabral pathology).^20,21

In the young athlete, initial management includes physical therapy, which focuses on core strengthening. Emphasis is placed on hip flexion and extension, as well as abduction and external rotation with the goal of reducing symptoms and avoiding injuries.²² A similar approach may be applied to the elite athlete, but failure of nonoperative management may necessitate surgical intervention. Hip arthroscopy continues to grow in popularity over open surgical dislocation with low complication rate and high return-to-play rate.^23-25

For the in-season athlete, attempts to continue to play can be assisted with the role of an intra-articular corticosteroid injection, which can help calm inflammation within the hip joint and mitigate pain, while rehabilitation focuses on core stabilization, postural retraining and focusing on any muscle imbalances that might be present. For positional players, ice time and shift duration can be adjusted to give the player’s hip a period of rest; meanwhile, for goaltenders, shot volumes in practice can be decreased.

Continue to: For athletes who...

For athletes who fail nonoperative care, surgical treatment varies depending on underlying hip pathology and may include femoroplasty, acetabuloplasty, and microfracture as well as labral repair or debridement. Though data are limited, Philippon and colleagues²⁶ have published promising results in a case series of 28 NHL players after surgical intervention for FAI. All players returned to sport at an average of 3.8 months and players who had surgery within 1 year of injury returned on average 1.1 months sooner than those who waited more than 1 year. Rehabilitation protocol varies between goaltenders compared to defensemen and offensive players due to the different demands required for blocking shots on goal.²⁷

One of the most challenging injuries to correctly identify in the hip area is athletic pubalgia (also referred to as sports hernia or core muscle injury) because pain in the groin may be referred from the lumbar spine, hip joint, urologic, or perineal etiologies.²⁸ Sports hernias involve dilatation of the external ring of the inguinal canal and thinning of the posterior wall. Players may report to the athletic trainer or team physician with a complaint of groin pain that is worse when pushing off with their skate or taking a slap shot.²⁹ On exam, pain can be reproduced by hip extension, contralateral torso rotation, or with a resisted sit-up with palpation of the inferolateral edge of the distal rectus abdominus.³⁰ An MRI with specific sequences centered over the pubic symphysis is usually warranted to aid in the workup of sports hernia. An MRI in these cases may also demonstrate avulsions of the rectus abdominus.³¹

Most of these injuries are managed conservatively but can warrant surgical intervention if the symptoms persist. In the study by Jakoi and colleagues,³² they identified 43 ice hockey players over an 8-year period (2001-2008) who had repairs of their sports hernias and assessed the statistics during the 2 years prior and 2 years after surgery. The authors found that 80% of these players were able to return to the ice for 2 or more full seasons. The return-to-sport rate was comparable to other sports after sports hernia repair, but players who had played in ≥7 seasons demonstrated a greater decrease in number of games played, goals, assists and time on ice compared to those who had played in ≤6 seasons prior to the time of injury. Between 1989 and 2000, 22 NHL players who failed to respond to nonoperative management of their groin injuries underwent surgical exploration.²⁹ At the time of surgical exploration, their hockey groin syndrome, consisted of small tears in the external oblique aponeurosis through which branches of the ilioinguinal or iliohypogastric could be identified. These surgical procedures were all through a standard inguinal approach and the perforating neurovascular structures were excised, while the main trunk of the ilioinguinal nerve was ablated and the external oblique aponeurosis was repaired and reinforced with Goretex (W.L. Gore & Associates Inc, Flagstaff, AZ). At follow-up, 18 of the 22 players (82%) had no pain and 19 (86%) were able to resume their careers in the NHL.²⁹ Ice hockey players with sports hernias or hockey groin syndrome often return to the sport, but it is important to identify these problems early so that surgical options can be discussed if the player fails conservative management. It is also critical to make sure that all pathology is identified, because in players with mixed sports hernia and FAI, return-to-play results improve when both issues are addressed. In a study of athletes (some of whom were ice hockey players), who had both FAI and sports hernia, and only hernia/pubalgia surgery was performed, 25% of these athletes returned to sport. If only FAI was addressed, 50% of the athletes returned to sport; however, when hernia and FAI were treated, 89% returned to play.³³

Adductor strains includes injury to the adductor muscles, pectineus, obturator externus and gracilis, and are prevalent in ice hockey players. A study of elite Swedish ice hockey players published in 1988 reported that adductor strains accounted for 10% (10 of 95) of all injuries.³⁴ Given the prevalence of these injuries, considerable research has been dedicated to understanding their mechanism and prevention.³⁵ Adductor strains within the ice hockey population have been attributed to the eccentric forces on the adductors when players attempt to decelerate the leg during a stride.³⁶ A study of NHL players revealed that a ratio <80% of adductor-to-abductor muscle is the best predictor of a groin strain.³⁷

These injuries are also well known for their recurrence rates, as was the case in an NHL study where 4 of the 9 adductor strains (44%) were recurrent injuries.³⁷ The authors attributed the recurrence to an incomplete rehabilitation program and an accelerated return to sport. This was followed by an NHL prevention program that spanned 2 seasons and analyzed 58 players whose adductor-to-abductor ratio was <80% and placed them into a 6-week intervention program during the preseason.³⁷ Only 3 players sustained an adductor strain in the 2 subsequent seasons after the intervention, compared to 11 strains in the previous 2 seasons. Thus, early identification of muscle strength imbalance coupled with an appropriate intervention program has proven to be an effective means of reducing adductor strains in this at-risk population.

Continue to: Contact injuries may...

Contact injuries may vary with checking into the boards being unique to men’s ice hockey. Hip pointers occur as a result of a direct compression injury to the iliac crest, which causes trauma to the bone but also to the overlying hip abductor musculature, and represent roughly 2.4% of ice hockey injuries.²³ The resulting contusion may cause a local hematoma formation. Early identification of the injury plus treatment with RICE (rest, ice, compression, elevation) coupled with crutches to limit weight-bearing status may minimize soft tissue trauma and swelling, and ultimately aid in pain control and return to sport.³⁸ Hip abductor strengthening, added padding over the injured area, as well as a compressive hip spica wrapping, have all been suggested to expedite return to play and help prevent recurrence of the hip pointer.⁸

KNEE INJURIES

Injury to the medial collateral ligament (MCL) is the most commonly reported knee injury (Figure 2) and second only to concussion amongst all injuries in National Collegiate Athletic Association ice hockey players.^8,39 The mechanism of injury typically involves a valgus force on the knee, which is often caused by collision into another player.³⁹ Valgus stress testing with the knee in 30° of flexion is used to grade the severity of injury (Grade I: 0-5 mm of medial opening; Grade II: 5-10 mm of medial opening; Grade III: >10 mm of medial opening).³⁹ One study that followed a single college hockey team for 8 seasons reported that 77% of injuries (10 of 13) occurred during player-to-player collision,³⁹ with 5 being Grade 1 injuries, 6 Grade 2 injuries, 1 Grade 3; information was missing for 1 player. Nonoperative management of incomplete injuries, grade 1 and 2 sprains, with RICE and early physical therapy intervention to work on knee range of motion and quadriceps strengthening typically helps the player return to sport within days for grade 1 and 2 injuries to 3 weeks for grade 2 injuries. Complete tears have been managed both operatively and nonoperatively with evidence to suggest better outcomes after surgical intervention if there is a concomitant ACL injury requiring reconstruction.^8,9

Anterior cruciate ligament (ACL) tears occur less frequently in hockey players compared to the players in other sports such as football and basketball.^38,40 Between 2006 and 2010, 47 players were identified by the NHL Injury Surveillance System as having sustained an ACL injury, which equates to an incidence of 9.4 ACL injuries per NHL season over this time span.⁴¹ The mechanism of ACL tears in ice hockey players appears to be different from other sports players based on a recent MRI study that evaluated players for concomitant injuries following ACL tear and noted significantly fewer bone bruises on the lateral femoral condyle compared to players in other sports.⁴² Early evaluation after injury with Lachman and/or pivot shift tests aids the diagnosis. Data from the NHL study identified 32 players (68%) with concomitant meniscal injuries and 32 (68%) had MCL injuries in conjunction with their ACL tears.⁴¹ Average length in the league prior to injury was 5.65 seasons. Twenty-nine of the injured players (61.7%) underwent reconstruction with a patellar tendon autograft, 13 (27.7%) had a hamstring autograft, and 5 (10.6%) had either a patellar tendon or hamstring allograft.⁴¹ Meniscus and ACL injuries were associated with a decreased length of career compared to age-matched controls and, notably, players >30 years at the time of injury had only a 67% rate of return to sport whereas those <30 years had a return-to-sport rate of 80%. Players who were able to return did so at an average of 9.8 months (range, 6-21 months) and had a significant reduction in total number of goals, assists, and points scored compared to controls. Decline in performance was typically associated with forwards and wings, while defensemen did not demonstrate the same decrease in performance following return to ice hockey.⁴¹

Meniscal tears are a well-documented concomitant injury with ruptures of the ACL, and the combination is a known pattern associated with shorter careers compared to isolated ACL tears in ice hockey players.⁴¹ The lateral meniscus is known for increased mobility compared to the medial meniscus and is more commonly injured (39% vs 8.5%) in ACL tears that occur in contact sports and downhill skiing.⁴² Ice hockey presents a scenario that is different from other contact sports because of the near frictionless interaction between the player’s ice skates and playing surface. This likely equates to a different injury mechanism and dissipation of energy after contact as well as non-contact injuries.³⁸ A recent study reviewed knee MRI findings associated with ACL tears in collegiate ice hockey players and compared to other sports known for their high rates of concomitant meniscal pathology. The authors reported a statistically significant decrease in lateral meniscus tears and bone-bruising patterns in ice hockey players with ACL injuries compared to athletes with ACL tears in other sports.⁴³ In contrast, an NHL study of ACL tears in professional ice hockey players found that 68% of players had concomitant meniscal tears (32 out of 47 players).⁴¹

Continue to: The presence of...

The presence of a meniscal tear on MRI is typically a surgical problem, especially if it occurred with an ACL injury. Meniscal repair is preferable, if possible, because there is a known association of increased cartilage contact pressures associated with meniscal debridement. Return to sport following meniscus injury hinges upon whether it is an isolated injury and how it is treated. If the meniscus injury occurs in isolation and can be treated with a debridement and partial resection alone, there is obviously a quicker return to sport as the player can be weight-bearing immediately following surgery. Return to skating after meniscal debridement and partial resection is usually 4 to 6 weeks, whereas meniscal repair protocols vary depending on surgeon; players may need 3 months to 4 months to return to the ice.

Quadriceps contusions are contact injuries that are not unique to ice hockey (Figure 3). They may result from player collision but also from direct blows from a hockey puck. A high velocity puck is known to cause immense trauma to the quadriceps muscles, which may result in localized bleeding and hematoma formation. If the player is able to anticipate the event, active contraction of the quadriceps muscle has been shown to absorb some of the energy and result in a less traumatic injury, but in a fast paced ice hockey game, the player’s anticipation is less likely than in other sports such as baseball.⁴⁴Interestingly, the degree of knee flexion after injury is predictive of injury severity with milder injuries associated with angles >90 and more severe injuries resulting in knee flexion angles <45° and typically an antalgic gait.⁴⁵ It is important to treat these injuries during the first 24 hours with the knee maintained in 120°of flexion, plus ice and compression, which can be achieved using a locked knee brace or elastic compression wrap. Quadriceps stretching and isometric strengthening should immediately follow the period of immobilization. The addition of NSAIDs may help prevent the formation of myositis ossificans. A study from West Point suggests that the average return to sport or activity ranges from 13 days (mild contusion) to 21 days (severe contusions), while others⁸ have indicated that if the injury is treated acutely and a player is able to regain motion and strength, return to ice hockey within a few days is possible.

FOOT AND ANKLE

Ice hockey has some unique injuries that can be attributed to the use of ice skates for play. One such injury is boot-top lacerations, which are fortunately rare as they can be a career-ending injury.⁴⁷ The spectrum of injury ranges from superficial abrasions to more severe soft tissue disruption, including the extensor tendons and neurovascular structures. The actual mechanism of injury involves an opponent’s skate blade cutting across the anterior ankle. One early case report described a protective method of having players place their skate tongues deep to their protective shin pads, instead of turning the tongues down.⁴⁷ Kevlar socks have also been shown to help prevent or minimize the damage from a skate blade.⁴⁸

Injury to the lateral ankle ligaments, anterior talofibular ligament or calcaneofibular ligament, are usually more common than the higher ankle sprains involving the syndesmosis. However, this is not the case in ice hockey. The rigidity of the ice skate at the level of the lateral ligaments seems to impart a protective mechanism to the lower ligaments, but this results in a higher incidence of syndesmotic injuries. These high ankle injuries are unfortunately more debilitating and often require a longer recovery period. In a study of these injuries in NHL players, syndesmotic sprains made up 74% of all ankle sprains, whereas only 18.4% of ankle sprains involved the syndesmosis in American football players..^49,50 The average number of days between injury and return to play is 45 days, and some authors believe that defensemen may have a harder time recovering because of the demands on their ankles by having to switch continuously between forward and backward skating.⁴⁹

Most patients are treated conservatively when their ankle plain radiographs show a congruent mortise and no evidence of syndesmotic widening. If the player expresses pain when squeezing the syndesmosis, it is helpful to obtain stress radiographs to further evaluate for syndesmotic injury. Nonoperative management includes RICE, immobilization in a rigid boot with crutches to protect weight-bearing with gradual advancements and eventually physical therapy to address any ankle stiffness, followed by dynamic functional activities. Treatment options for syndesmotic widening and failed conservative management includes both screw and plate options as well as suture buttons.^49,51,52

Ankle and foot fractures were historically a rare injury in ice hockey players based on radiograph evaluation; however, the recent study by Baker and colleagues⁴ demonstrated that MRI can be helpful in detecting subradiographic fractures. Most of the injuries detected after MRI were from being hit by a hockey puck; this was a novel mechanism that had not been previously reported in the literature.⁴ Of the injuries that resulted from a direct blow, 14 of 17 occurred on the medial aspect of the foot and ankle, which is believed to result another word? from a defender skating towards an offensive player and attempting to block shots on goal. In this study, all occult fractures involving the medial malleolus were eventually treated with open reduction and internal fixation and underwent routine healing.⁴ The navicular bone and base of the first metatarsal accounted for the remaining medial-sided fractures. In a recent analysis of risk factors for reoperation following operative fixation of foot fractures across the National Basketball Association, the National Football Leagues, Major League Baseball, and the National Hockey League only a total of 3 fractures involving the foot (1 navicular and 2 first metatarsal) were identified in NHL players over a 30-year period.⁵³ The study acknowledged a major limitation being a public source for identifying players with fractures.

Lace bite is another common ice hockey injury. It typically occurs at the beginning of a season or whenever a player is breaking in a new pair of skates. The cause of the lace bite is the rigid tongue in the skate that rubs against the anterior ankle. Skating causes inflammation in the area of the tibialis anterior tendon, and the player will complain of significant anterior ankle pain. First line treatment for lace bite is ice (Figure 4A), NSAID gel (eg, diclofenac 1%), and a Bunga lace-bite pad (Absolute Athletics). (Figure 4B).

SUMMARY

Lower extremity injuries are common in ice hockey players, and a covering physician should be comfortable managing these injuries from breezers to skate. Proper evaluation and work-up is critical for early diagnosis and identification of pathology, which can minimize the impact of the injury and expedite a treatment plan to return the player safely to the ice and in the game.