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Pediatric psoriasis may have a distinct presentation
Children may have a distinctive presentation of psoriasis, compared with adults, Dr. Wynnis Tom said at a pediatric dermatology meeting sponsored by Rady Children’s Hospital–San Diego and UC San Diego School of Medicine.
Infants may present with diaper involvement, also known as “napkin psoriasis,” which may be confused with irritant dermatitis or perineal infections. Moreover, guttate psoriasis, which can be preceded by infectious triggers such as Streptococcus and appears as small, salmon-pink bumps on the skin, is more frequent in children than adults, said Dr. Tom, associate professor of dermatology and pediatrics at the university.
Patients with psoriasis are at higher risk for psychiatric disorders, especially depression and anxiety. A study by Varni et al. discussed QOL ratings by 208 children aged 4-17 years with moderate to severe plaque disease. The study demonstrated a significant negative QOL impact in patients with plaque psoriasis, comparable to the impairment of QOL from arthritis or asthma (Eur J Pediatr. 2011 Sep 30;171[3]485-92).
Dr. Tom talked about other comorbidities associated with psoriasis, including psoriatic arthritis, and encouraged physicians to inquire about morning stiffness, joint pains, swelling, and gait abnormalities. “Psoriatic arthritis occurs in about 10% of children, and it is essential to detect early to prevent permanent joint damage,” she said. “Over the past decade, psoriasis has resurfaced as a systemic disorder as it may be associated with obesity, metabolic syndrome, and inflammatory bowel disease.” Psoriasis also entails an increased risk for cardiovascular disease, myocardial infarction, and stroke.
Dr. Tom emphasized, “because of these risks, we need to extend comorbidity screening to the pediatric population.”
Management of pediatric psoriasis has focused on topical and systemic therapies, in addition to phototherapies. Most systemic agents are used off-label on the basis of experience rather than evidence. Clinical trials are currently underway to extend indications for systemic therapy to the pediatric age group, she said.
Dr. Tom disclosed she is an investigator for Promius Pharma, Celgene, and Janssen.
Children may have a distinctive presentation of psoriasis, compared with adults, Dr. Wynnis Tom said at a pediatric dermatology meeting sponsored by Rady Children’s Hospital–San Diego and UC San Diego School of Medicine.
Infants may present with diaper involvement, also known as “napkin psoriasis,” which may be confused with irritant dermatitis or perineal infections. Moreover, guttate psoriasis, which can be preceded by infectious triggers such as Streptococcus and appears as small, salmon-pink bumps on the skin, is more frequent in children than adults, said Dr. Tom, associate professor of dermatology and pediatrics at the university.
Patients with psoriasis are at higher risk for psychiatric disorders, especially depression and anxiety. A study by Varni et al. discussed QOL ratings by 208 children aged 4-17 years with moderate to severe plaque disease. The study demonstrated a significant negative QOL impact in patients with plaque psoriasis, comparable to the impairment of QOL from arthritis or asthma (Eur J Pediatr. 2011 Sep 30;171[3]485-92).
Dr. Tom talked about other comorbidities associated with psoriasis, including psoriatic arthritis, and encouraged physicians to inquire about morning stiffness, joint pains, swelling, and gait abnormalities. “Psoriatic arthritis occurs in about 10% of children, and it is essential to detect early to prevent permanent joint damage,” she said. “Over the past decade, psoriasis has resurfaced as a systemic disorder as it may be associated with obesity, metabolic syndrome, and inflammatory bowel disease.” Psoriasis also entails an increased risk for cardiovascular disease, myocardial infarction, and stroke.
Dr. Tom emphasized, “because of these risks, we need to extend comorbidity screening to the pediatric population.”
Management of pediatric psoriasis has focused on topical and systemic therapies, in addition to phototherapies. Most systemic agents are used off-label on the basis of experience rather than evidence. Clinical trials are currently underway to extend indications for systemic therapy to the pediatric age group, she said.
Dr. Tom disclosed she is an investigator for Promius Pharma, Celgene, and Janssen.
Children may have a distinctive presentation of psoriasis, compared with adults, Dr. Wynnis Tom said at a pediatric dermatology meeting sponsored by Rady Children’s Hospital–San Diego and UC San Diego School of Medicine.
Infants may present with diaper involvement, also known as “napkin psoriasis,” which may be confused with irritant dermatitis or perineal infections. Moreover, guttate psoriasis, which can be preceded by infectious triggers such as Streptococcus and appears as small, salmon-pink bumps on the skin, is more frequent in children than adults, said Dr. Tom, associate professor of dermatology and pediatrics at the university.
Patients with psoriasis are at higher risk for psychiatric disorders, especially depression and anxiety. A study by Varni et al. discussed QOL ratings by 208 children aged 4-17 years with moderate to severe plaque disease. The study demonstrated a significant negative QOL impact in patients with plaque psoriasis, comparable to the impairment of QOL from arthritis or asthma (Eur J Pediatr. 2011 Sep 30;171[3]485-92).
Dr. Tom talked about other comorbidities associated with psoriasis, including psoriatic arthritis, and encouraged physicians to inquire about morning stiffness, joint pains, swelling, and gait abnormalities. “Psoriatic arthritis occurs in about 10% of children, and it is essential to detect early to prevent permanent joint damage,” she said. “Over the past decade, psoriasis has resurfaced as a systemic disorder as it may be associated with obesity, metabolic syndrome, and inflammatory bowel disease.” Psoriasis also entails an increased risk for cardiovascular disease, myocardial infarction, and stroke.
Dr. Tom emphasized, “because of these risks, we need to extend comorbidity screening to the pediatric population.”
Management of pediatric psoriasis has focused on topical and systemic therapies, in addition to phototherapies. Most systemic agents are used off-label on the basis of experience rather than evidence. Clinical trials are currently underway to extend indications for systemic therapy to the pediatric age group, she said.
Dr. Tom disclosed she is an investigator for Promius Pharma, Celgene, and Janssen.
Fibrate could offer additional option for primary biliary cholangitis
AMSTERDAM – Patients with primary biliary cholangitis (PBC) who are not responding to first-line therapy with ursodeoxycholic acid (UDCA) may benefit from the addition of bezafibrate, randomized, double-blind, placebo-controlled study findings have suggested.
Almost one-third of the 50 patients who were treated with bezafibrate in addition to UDCA in the 2-year, phase III BEZURSO study met the primary endpoint for response, compared with none of the 50 patients in the control arm of the study.
The findings, presented as a late-breaking abstract at the International Liver Congress, sponsored by the European Association for the Study of the Liver (EASL), could be practice changing for a population of patients who have relatively few treatment options.
Although obeticholic acid was recently approved as a second-line treatment in combination with UDCA for PBC, one of the side effects of obeticholic acid is that it can cause pruritus, which is one of the symptoms of the condition as well. It can be tricky to explain to patients that there is a treatment but that this treatment might also increase their symptoms, Dr. Corpechot observed.
Between October 2012 and December 2014, mostly female patients (more than 92%), mean age 53 years, who were being treated with UDCA were recruited at 21 centers in France. For inclusion in the study, patients had to have an inadequate biochemical response to UDCA, which was defined by the Paris-2 criteria of an alkaline phosphatase (ALP) or an aspartate aminotransferase (AST) of more than 1.5 times the upper limit of normal (ULN), or a total bilirubin level of more than 17 micromol/L.
Patients were randomized to continue UDCA treatment (13-15 mg/kg per day) with or without the addition of bezafibrate, given as a 400-mg daily dose.
The primary endpoint was a complete biochemical response as defined by normal serum levels of total bilirubin, ALP, aminotransferases, albumin, and a normal prothrombin time at 2 years. The hypothesis was that 40% of the patients in the bezafibrate group and only 10% of patients in the UDCA group would reach this primary endpoint. The actual percentages were 30% and 10% (P less than .0001).
A significantly higher (67% vs. 0%) percentage of patients treated with the fibrate versus UDCA also achieved a normal serum ALP by 2 years, Dr. Corpechot reported, with a significant decrease seen by the third month of treatment.
The mean changes in all the biochemical parameters tested from baseline to the end of the study comparing the bezafibrate group with the control group were a respective –14% and +18% (P less than .0001) for total bilirubin, –60% and 0% for ALP (P less than .0001), –36% and 0% for alanine aminotransferase (P less than .0001), –8% and +8% for AST (P less than .05), –38% and +7% for gamma-glutamyl transferase (P less than .0001), 0% and –3% for albumin (P less than .05), and –16% and 0% for cholesterol (P less than .0001).
Other significant findings favoring the fibrate therapy were a significantly (–75% vs. 0%, P less than .01) decreased itch score (assessed with a visual analog scale) and a significantly lower (–10% vs. +10%, P less than .01) liver stiffness (assessed by transient elastography) at 2 years.
Importantly, the frequency of adverse events, including serious adverse events, did not differ significantly between the two groups.
Fibrates could thus offer a well tolerated and cheaper alternative, as they are already widely used in clinical practice, although they are not licensed for PBC treatment at the current time.
Dr. Tacke, professor of medicine in the department of gastroenterology, metabolic diseases and intensive care medicine at University Hospital Aachen, Germany, also noted that bezafibrate was a drug that “had been on the market for a very long time,” and was very inexpensive in comparison to obeticholic acid and, importantly, seemed to be very well tolerated in the study.
“One question the community will want to know is whether [bezafibrate] is as effective as obeticholic acid in the second-line treatment of PBC,” Dr. Tacke said. This is a question only a head-to-head study can answer and also it is not possible to say whether other fibrates may have the same benefit as bezafibrate as seen in this trial.
Although the study included only 100 patients, this was a relatively large study considering the disease area and that most patients given the primary treatment of UDCA will do well on it, Dr. Tacke acknowledged in an interview.
“What I like about this study is that they treated patients for 2 years and bezafibrate was given as an add-on treatment, so nobody was at risk for not receiving the UDCA, and they saw a very stable and solid improvement in the parameters studied,” Dr. Tacke said.
EASL launched new guidelines for the diagnosis and treatment of PBC to coincide with the meeting, which state that patients should be treated with UDCA for 1 year and then their biochemical response to treatment should assessed to see if they might need additional treatment. “Up to now, the second-line treatment recommended is obeticholic acid but off-label therapy is mentioned,” Dr. Tacke said.
He noted that there were small, nonrandomized studies with two fibrates – bezafibrate and fenofibrate – that have shown “very encouraging” results but that the current findings suggested that bezafibrate therapy may be an alternative, well-tolerated treatment option for patients failing to respond to standard UDCA therapy that could well be added into the guidelines when they are next revised.
The BEZURSO study was an investigator-led trial sponsored by the Assistance Publique – Hôpitaux de Paris. Dr. Corpechot disclosed financial relationships with Arrow Génériques, Intercept Pharma France, Mayoly-Spindler. Dr. Tacke had nothing to disclose.
AMSTERDAM – Patients with primary biliary cholangitis (PBC) who are not responding to first-line therapy with ursodeoxycholic acid (UDCA) may benefit from the addition of bezafibrate, randomized, double-blind, placebo-controlled study findings have suggested.
Almost one-third of the 50 patients who were treated with bezafibrate in addition to UDCA in the 2-year, phase III BEZURSO study met the primary endpoint for response, compared with none of the 50 patients in the control arm of the study.
The findings, presented as a late-breaking abstract at the International Liver Congress, sponsored by the European Association for the Study of the Liver (EASL), could be practice changing for a population of patients who have relatively few treatment options.
Although obeticholic acid was recently approved as a second-line treatment in combination with UDCA for PBC, one of the side effects of obeticholic acid is that it can cause pruritus, which is one of the symptoms of the condition as well. It can be tricky to explain to patients that there is a treatment but that this treatment might also increase their symptoms, Dr. Corpechot observed.
Between October 2012 and December 2014, mostly female patients (more than 92%), mean age 53 years, who were being treated with UDCA were recruited at 21 centers in France. For inclusion in the study, patients had to have an inadequate biochemical response to UDCA, which was defined by the Paris-2 criteria of an alkaline phosphatase (ALP) or an aspartate aminotransferase (AST) of more than 1.5 times the upper limit of normal (ULN), or a total bilirubin level of more than 17 micromol/L.
Patients were randomized to continue UDCA treatment (13-15 mg/kg per day) with or without the addition of bezafibrate, given as a 400-mg daily dose.
The primary endpoint was a complete biochemical response as defined by normal serum levels of total bilirubin, ALP, aminotransferases, albumin, and a normal prothrombin time at 2 years. The hypothesis was that 40% of the patients in the bezafibrate group and only 10% of patients in the UDCA group would reach this primary endpoint. The actual percentages were 30% and 10% (P less than .0001).
A significantly higher (67% vs. 0%) percentage of patients treated with the fibrate versus UDCA also achieved a normal serum ALP by 2 years, Dr. Corpechot reported, with a significant decrease seen by the third month of treatment.
The mean changes in all the biochemical parameters tested from baseline to the end of the study comparing the bezafibrate group with the control group were a respective –14% and +18% (P less than .0001) for total bilirubin, –60% and 0% for ALP (P less than .0001), –36% and 0% for alanine aminotransferase (P less than .0001), –8% and +8% for AST (P less than .05), –38% and +7% for gamma-glutamyl transferase (P less than .0001), 0% and –3% for albumin (P less than .05), and –16% and 0% for cholesterol (P less than .0001).
Other significant findings favoring the fibrate therapy were a significantly (–75% vs. 0%, P less than .01) decreased itch score (assessed with a visual analog scale) and a significantly lower (–10% vs. +10%, P less than .01) liver stiffness (assessed by transient elastography) at 2 years.
Importantly, the frequency of adverse events, including serious adverse events, did not differ significantly between the two groups.
Fibrates could thus offer a well tolerated and cheaper alternative, as they are already widely used in clinical practice, although they are not licensed for PBC treatment at the current time.
Dr. Tacke, professor of medicine in the department of gastroenterology, metabolic diseases and intensive care medicine at University Hospital Aachen, Germany, also noted that bezafibrate was a drug that “had been on the market for a very long time,” and was very inexpensive in comparison to obeticholic acid and, importantly, seemed to be very well tolerated in the study.
“One question the community will want to know is whether [bezafibrate] is as effective as obeticholic acid in the second-line treatment of PBC,” Dr. Tacke said. This is a question only a head-to-head study can answer and also it is not possible to say whether other fibrates may have the same benefit as bezafibrate as seen in this trial.
Although the study included only 100 patients, this was a relatively large study considering the disease area and that most patients given the primary treatment of UDCA will do well on it, Dr. Tacke acknowledged in an interview.
“What I like about this study is that they treated patients for 2 years and bezafibrate was given as an add-on treatment, so nobody was at risk for not receiving the UDCA, and they saw a very stable and solid improvement in the parameters studied,” Dr. Tacke said.
EASL launched new guidelines for the diagnosis and treatment of PBC to coincide with the meeting, which state that patients should be treated with UDCA for 1 year and then their biochemical response to treatment should assessed to see if they might need additional treatment. “Up to now, the second-line treatment recommended is obeticholic acid but off-label therapy is mentioned,” Dr. Tacke said.
He noted that there were small, nonrandomized studies with two fibrates – bezafibrate and fenofibrate – that have shown “very encouraging” results but that the current findings suggested that bezafibrate therapy may be an alternative, well-tolerated treatment option for patients failing to respond to standard UDCA therapy that could well be added into the guidelines when they are next revised.
The BEZURSO study was an investigator-led trial sponsored by the Assistance Publique – Hôpitaux de Paris. Dr. Corpechot disclosed financial relationships with Arrow Génériques, Intercept Pharma France, Mayoly-Spindler. Dr. Tacke had nothing to disclose.
AMSTERDAM – Patients with primary biliary cholangitis (PBC) who are not responding to first-line therapy with ursodeoxycholic acid (UDCA) may benefit from the addition of bezafibrate, randomized, double-blind, placebo-controlled study findings have suggested.
Almost one-third of the 50 patients who were treated with bezafibrate in addition to UDCA in the 2-year, phase III BEZURSO study met the primary endpoint for response, compared with none of the 50 patients in the control arm of the study.
The findings, presented as a late-breaking abstract at the International Liver Congress, sponsored by the European Association for the Study of the Liver (EASL), could be practice changing for a population of patients who have relatively few treatment options.
Although obeticholic acid was recently approved as a second-line treatment in combination with UDCA for PBC, one of the side effects of obeticholic acid is that it can cause pruritus, which is one of the symptoms of the condition as well. It can be tricky to explain to patients that there is a treatment but that this treatment might also increase their symptoms, Dr. Corpechot observed.
Between October 2012 and December 2014, mostly female patients (more than 92%), mean age 53 years, who were being treated with UDCA were recruited at 21 centers in France. For inclusion in the study, patients had to have an inadequate biochemical response to UDCA, which was defined by the Paris-2 criteria of an alkaline phosphatase (ALP) or an aspartate aminotransferase (AST) of more than 1.5 times the upper limit of normal (ULN), or a total bilirubin level of more than 17 micromol/L.
Patients were randomized to continue UDCA treatment (13-15 mg/kg per day) with or without the addition of bezafibrate, given as a 400-mg daily dose.
The primary endpoint was a complete biochemical response as defined by normal serum levels of total bilirubin, ALP, aminotransferases, albumin, and a normal prothrombin time at 2 years. The hypothesis was that 40% of the patients in the bezafibrate group and only 10% of patients in the UDCA group would reach this primary endpoint. The actual percentages were 30% and 10% (P less than .0001).
A significantly higher (67% vs. 0%) percentage of patients treated with the fibrate versus UDCA also achieved a normal serum ALP by 2 years, Dr. Corpechot reported, with a significant decrease seen by the third month of treatment.
The mean changes in all the biochemical parameters tested from baseline to the end of the study comparing the bezafibrate group with the control group were a respective –14% and +18% (P less than .0001) for total bilirubin, –60% and 0% for ALP (P less than .0001), –36% and 0% for alanine aminotransferase (P less than .0001), –8% and +8% for AST (P less than .05), –38% and +7% for gamma-glutamyl transferase (P less than .0001), 0% and –3% for albumin (P less than .05), and –16% and 0% for cholesterol (P less than .0001).
Other significant findings favoring the fibrate therapy were a significantly (–75% vs. 0%, P less than .01) decreased itch score (assessed with a visual analog scale) and a significantly lower (–10% vs. +10%, P less than .01) liver stiffness (assessed by transient elastography) at 2 years.
Importantly, the frequency of adverse events, including serious adverse events, did not differ significantly between the two groups.
Fibrates could thus offer a well tolerated and cheaper alternative, as they are already widely used in clinical practice, although they are not licensed for PBC treatment at the current time.
Dr. Tacke, professor of medicine in the department of gastroenterology, metabolic diseases and intensive care medicine at University Hospital Aachen, Germany, also noted that bezafibrate was a drug that “had been on the market for a very long time,” and was very inexpensive in comparison to obeticholic acid and, importantly, seemed to be very well tolerated in the study.
“One question the community will want to know is whether [bezafibrate] is as effective as obeticholic acid in the second-line treatment of PBC,” Dr. Tacke said. This is a question only a head-to-head study can answer and also it is not possible to say whether other fibrates may have the same benefit as bezafibrate as seen in this trial.
Although the study included only 100 patients, this was a relatively large study considering the disease area and that most patients given the primary treatment of UDCA will do well on it, Dr. Tacke acknowledged in an interview.
“What I like about this study is that they treated patients for 2 years and bezafibrate was given as an add-on treatment, so nobody was at risk for not receiving the UDCA, and they saw a very stable and solid improvement in the parameters studied,” Dr. Tacke said.
EASL launched new guidelines for the diagnosis and treatment of PBC to coincide with the meeting, which state that patients should be treated with UDCA for 1 year and then their biochemical response to treatment should assessed to see if they might need additional treatment. “Up to now, the second-line treatment recommended is obeticholic acid but off-label therapy is mentioned,” Dr. Tacke said.
He noted that there were small, nonrandomized studies with two fibrates – bezafibrate and fenofibrate – that have shown “very encouraging” results but that the current findings suggested that bezafibrate therapy may be an alternative, well-tolerated treatment option for patients failing to respond to standard UDCA therapy that could well be added into the guidelines when they are next revised.
The BEZURSO study was an investigator-led trial sponsored by the Assistance Publique – Hôpitaux de Paris. Dr. Corpechot disclosed financial relationships with Arrow Génériques, Intercept Pharma France, Mayoly-Spindler. Dr. Tacke had nothing to disclose.
AT ILC 2017
Key clinical point: Fibrates may offer another second-line treatment option for patients with primary biliary cholangitis (PBC), but their current use is off label.
Major finding: The primary endpoint of a complete biochemical response at 2 years was achieved by 30% and 0% of fibrate- and placebo-treated patients, respectively.
Data source: A multicenter, randomized, double-blind, placebo controlled phase III trial of bezafibrate added onto ursodeoxycholic acid (UDCA) versus UDCA in the treatment of 100 patients with PBC.
Disclosures: The BEZURSO study was an investigator-led trial sponsored by the Assistance Publique – Hôpitaux de Paris. Dr. Corpechot disclosed financial relationships with Arrow Génériques, Intercept Pharma France, Mayoly-Spindler. Dr. Tacke had nothing to disclose.
Identifying the four key findings in patients with suspected severe drug reactions
There are four key findings in patients with suspected severe drug reactions: a high risk medication, mucosal involvement, presence of pustules, and laboratory abnormalities, especially a CBC with differential and liver function tests, James R. Treat, MD, said at a pediatric dermatology meeting sponsored by Rady Children’s Hospital–San Diego and UC San Diego School of Medicine.
Several cutaneous drug reactions that were discussed during the conference included acute generalized exanthematous pustulosis (AGEP), a drug reaction with eosinophilia and systemic symptoms (DRESS), and Stevens-Johnson Syndrome (SJS) and toxic epidermal necrolysis (TEN).
AGEP is characterized by fever and generalized pustular eruption arising swiftly after administration of the causative drug. Such drugs include antibiotics, contrast agents, antifungals, and calcium channel blockers. Withdrawal of the offending drug and optimization of fluid and electrolyte balance are warranted in the management of AGEP. Topical steroids may decrease hospital length-of-stay and help with symptomatic treatment of AGEP, said Dr. Treat, a pediatric dermatologist at Children’s Hospital of Philadelphia and an assistant professor of pediatrics and dermatology at the Perelman School of Medicine at the University of Pennsylvania.
A DRESS, also known as drug hypersensitivity syndrome, or drug-induced hypersensitivity syndrome, is a skin eruption that generally occurs 2-6 weeks after the patient starts the offending medication. Clinical signs of this condition include ill-appearance, fever (greater than 100.4° F), facial and hand edema, lymphadenopathy, and lab abnormalities, including hypereosinophilia, atypical lymphocytosis, transaminitis, and human herpesvirus 6 reactivation. DRESS may be misdiagnosed as viral infection, Kawasaki’s disease, or SJS.
Commonly implicated drugs include antiepileptic drugs, antibiotics, HIV medications, and sulfa-containing medications.
“While withdrawal of the offending drug is promptly warranted, this condition may require other therapeutics, particularly if there is significant systemic involvement,” Dr. Treat emphasized. There is evidence that systemic steroids (1-2 mg/kg/day) and cyclosporine can help improve the disease course, although their use is off-label.
SJS and TEN are other severe cutaneous adverse reactions caused by Mycoplasma infection or medications, such as anticonvulsants, antibiotics, HIV medications, and sulfa-containing drugs. “These entities are characterized by an ill-appearing, febrile patient with painful skin and mucosal membrane involvement,” Dr. Treat described.
Mucosal predominance may be seen in cases associated with Mycoplasma and have been termed “Mycoplasma-induced rash and mucositis,” although the terminology is controversial. In a case series by Darren G. Gregory, MD, treatment with amniotic membrane transplantation applied to the eyelid margins, palpebral conjunctiva, and ocular surface during the acute phases of SJS and TEN has been shown to be effective, decreasing the risk of significant oculovisual sequelae (Ophthalmol. 2011 May;118[5]:908-14).
Diagnostic criteria have been detailed to classify each of these adverse reactions. Dr. Treat concluded his lecture with a discussion of a retrospective study by Bouvresse et al. that projected AGEP, DRESS, and SJS-TEN as distinct entities (Orphanet J Rare Dis. 2012. doi: 10.1186/1750-1172-7-72).
Dr. Treat reported having no relevant financial disclosures.
There are four key findings in patients with suspected severe drug reactions: a high risk medication, mucosal involvement, presence of pustules, and laboratory abnormalities, especially a CBC with differential and liver function tests, James R. Treat, MD, said at a pediatric dermatology meeting sponsored by Rady Children’s Hospital–San Diego and UC San Diego School of Medicine.
Several cutaneous drug reactions that were discussed during the conference included acute generalized exanthematous pustulosis (AGEP), a drug reaction with eosinophilia and systemic symptoms (DRESS), and Stevens-Johnson Syndrome (SJS) and toxic epidermal necrolysis (TEN).
AGEP is characterized by fever and generalized pustular eruption arising swiftly after administration of the causative drug. Such drugs include antibiotics, contrast agents, antifungals, and calcium channel blockers. Withdrawal of the offending drug and optimization of fluid and electrolyte balance are warranted in the management of AGEP. Topical steroids may decrease hospital length-of-stay and help with symptomatic treatment of AGEP, said Dr. Treat, a pediatric dermatologist at Children’s Hospital of Philadelphia and an assistant professor of pediatrics and dermatology at the Perelman School of Medicine at the University of Pennsylvania.
A DRESS, also known as drug hypersensitivity syndrome, or drug-induced hypersensitivity syndrome, is a skin eruption that generally occurs 2-6 weeks after the patient starts the offending medication. Clinical signs of this condition include ill-appearance, fever (greater than 100.4° F), facial and hand edema, lymphadenopathy, and lab abnormalities, including hypereosinophilia, atypical lymphocytosis, transaminitis, and human herpesvirus 6 reactivation. DRESS may be misdiagnosed as viral infection, Kawasaki’s disease, or SJS.
Commonly implicated drugs include antiepileptic drugs, antibiotics, HIV medications, and sulfa-containing medications.
“While withdrawal of the offending drug is promptly warranted, this condition may require other therapeutics, particularly if there is significant systemic involvement,” Dr. Treat emphasized. There is evidence that systemic steroids (1-2 mg/kg/day) and cyclosporine can help improve the disease course, although their use is off-label.
SJS and TEN are other severe cutaneous adverse reactions caused by Mycoplasma infection or medications, such as anticonvulsants, antibiotics, HIV medications, and sulfa-containing drugs. “These entities are characterized by an ill-appearing, febrile patient with painful skin and mucosal membrane involvement,” Dr. Treat described.
Mucosal predominance may be seen in cases associated with Mycoplasma and have been termed “Mycoplasma-induced rash and mucositis,” although the terminology is controversial. In a case series by Darren G. Gregory, MD, treatment with amniotic membrane transplantation applied to the eyelid margins, palpebral conjunctiva, and ocular surface during the acute phases of SJS and TEN has been shown to be effective, decreasing the risk of significant oculovisual sequelae (Ophthalmol. 2011 May;118[5]:908-14).
Diagnostic criteria have been detailed to classify each of these adverse reactions. Dr. Treat concluded his lecture with a discussion of a retrospective study by Bouvresse et al. that projected AGEP, DRESS, and SJS-TEN as distinct entities (Orphanet J Rare Dis. 2012. doi: 10.1186/1750-1172-7-72).
Dr. Treat reported having no relevant financial disclosures.
There are four key findings in patients with suspected severe drug reactions: a high risk medication, mucosal involvement, presence of pustules, and laboratory abnormalities, especially a CBC with differential and liver function tests, James R. Treat, MD, said at a pediatric dermatology meeting sponsored by Rady Children’s Hospital–San Diego and UC San Diego School of Medicine.
Several cutaneous drug reactions that were discussed during the conference included acute generalized exanthematous pustulosis (AGEP), a drug reaction with eosinophilia and systemic symptoms (DRESS), and Stevens-Johnson Syndrome (SJS) and toxic epidermal necrolysis (TEN).
AGEP is characterized by fever and generalized pustular eruption arising swiftly after administration of the causative drug. Such drugs include antibiotics, contrast agents, antifungals, and calcium channel blockers. Withdrawal of the offending drug and optimization of fluid and electrolyte balance are warranted in the management of AGEP. Topical steroids may decrease hospital length-of-stay and help with symptomatic treatment of AGEP, said Dr. Treat, a pediatric dermatologist at Children’s Hospital of Philadelphia and an assistant professor of pediatrics and dermatology at the Perelman School of Medicine at the University of Pennsylvania.
A DRESS, also known as drug hypersensitivity syndrome, or drug-induced hypersensitivity syndrome, is a skin eruption that generally occurs 2-6 weeks after the patient starts the offending medication. Clinical signs of this condition include ill-appearance, fever (greater than 100.4° F), facial and hand edema, lymphadenopathy, and lab abnormalities, including hypereosinophilia, atypical lymphocytosis, transaminitis, and human herpesvirus 6 reactivation. DRESS may be misdiagnosed as viral infection, Kawasaki’s disease, or SJS.
Commonly implicated drugs include antiepileptic drugs, antibiotics, HIV medications, and sulfa-containing medications.
“While withdrawal of the offending drug is promptly warranted, this condition may require other therapeutics, particularly if there is significant systemic involvement,” Dr. Treat emphasized. There is evidence that systemic steroids (1-2 mg/kg/day) and cyclosporine can help improve the disease course, although their use is off-label.
SJS and TEN are other severe cutaneous adverse reactions caused by Mycoplasma infection or medications, such as anticonvulsants, antibiotics, HIV medications, and sulfa-containing drugs. “These entities are characterized by an ill-appearing, febrile patient with painful skin and mucosal membrane involvement,” Dr. Treat described.
Mucosal predominance may be seen in cases associated with Mycoplasma and have been termed “Mycoplasma-induced rash and mucositis,” although the terminology is controversial. In a case series by Darren G. Gregory, MD, treatment with amniotic membrane transplantation applied to the eyelid margins, palpebral conjunctiva, and ocular surface during the acute phases of SJS and TEN has been shown to be effective, decreasing the risk of significant oculovisual sequelae (Ophthalmol. 2011 May;118[5]:908-14).
Diagnostic criteria have been detailed to classify each of these adverse reactions. Dr. Treat concluded his lecture with a discussion of a retrospective study by Bouvresse et al. that projected AGEP, DRESS, and SJS-TEN as distinct entities (Orphanet J Rare Dis. 2012. doi: 10.1186/1750-1172-7-72).
Dr. Treat reported having no relevant financial disclosures.
AATS Mitral Conclave Draws the Largest Crowd Ever
The fourth biennial the American Association for Thoracic Surgery (AATS) Mitral Conclave 2017 was attended by a large audience of cardiothoracic surgeons and other professionals from 67 countries on Thursday and Friday to hear the latest on repair and replacement of the mitral valve.
Conference chair David H. Adams, MD, of Mount Sinai Health System noted that this was the first time the AATS had directly managed the meeting. The conclave included more than 200 oral presentations and 207 e-posters.
The faculty included more than 70 international thought leaders in mitral valve repair, and the live sessions featured more than 200 lectures, abstracts, and video presentations. Twenty-two breakout sessions reported on more than 80 submitted abstracts.
Mastering videography skills also improves one’s minimally invasive skills, said Vinay Badhwar, MD, of West Virginia University. “To do mitral surgery robotically and do minimally invasive surgery, you have to become a videographer,” he said. The surgeon must also be engaged in carefully selecting his or her team, Dr. Badhwar added.
In seven different plenary sessions, international experts participated in panels that discussed management of complications and explored scenarios in which they would not intervene. A debate format modeled on the movie Thunderdome—“four men enter, one man leaves”—featured a spirited discussion on when to repair functional tricuspid regurgitation. Dr. Adams and Tirone E. David, MD, of Toronto General Hospital, took rather strident opposing views, with Dr. Adams advocating for repair. The goal, Dr. Adams said, is to provide normal tricuspid valve function for the long term. “We got aggressive because we were doing a lot of reoperations for tricuspid disease in patients who had mitral valve surgery,” Dr. Adams said.
One plenary roundtable tackled the subject of when to use mechanical valves instead of biological valves. “Has the pendulum swung too far away from mechanical valves and are there cases where mechanical valves should be the first choice?” Dr. Sundt, session chair, asked the panelists.
The panelists concurred that a patient’s individual needs would drive decision-making. Anelechi Anyanwu, MD, of Mount Sinai, said he’d be inclined to use a mechanical valve in a 25-year-old man with rheumatic mitral stenosis.* In younger patients, namely teenagers, valve selection depends on the activity level they’d pursue after surgery, said Pedro J. del Nido, MD, of Children’s Hospital Boston.
At the plenary on transcatheter mitral therapy, John Laschinger, MD, of the Food and Drug Administration, reviewed the approval process for new mitral devices. “It comes down to the benefit-risk determination where we look at the standard-of-care surgery and look to see if the device is an acceptable alternative – that is, if it is safer and more effective,” Dr. Laschinger said.
James S. Gammie, MD, of the University of Maryland, also reported on an analysis of 87,214 mitral procedures from the Society for Thoracic Surgeons database over the past 5 years. Among the revelations from this analysis are that 96.1% of procedures for leaflet prolapse involved annuloplasty and that 75.8% receive a bioprosthetic valve.
The plenary and breakouts also included seven different video sessions ranging from managing leaflet prolapse to adult congenital surgery and complex scenarios.
Robert A. Dion, MD, Genk, Belgium, delivered the Conclave Honored Lecture and received the Mitral Conclave Achievement Award. He talked about the operative team as a geese flight. “The geese flight is always a unit of hierarchy,” Dr. Dion said. “The figure of the geese flight is V and the chief chooses the lead goose for the capacity to fly high enough and fast enough.”
In the Honored Cardiology Lecture, Robert O. Bonow, MD, of Northwestern Memorial Hospital, explored clinical guidelines for mitral valve repair and replacement and their application in the clinic. “Both sets of guidelines in Europe and the United States make the clear point that is obvious to all of you but less so to cardiologists, that there are two forms of mitral valve disease: degenerative or primary, and functional, which is secondary,” he said. He called for thoracic surgeons to collaborate with their cardiology colleagues. “You and I have lots of work to do, not only in caring for our patients but also in starting to devise appropriate quality metrics, hopefully working together in a team-based approach,” Dr. Bonow said. “This is what gives the best patient care but also gives us the best recommendations for our policy issues. And I look forward to further enhancements from your field and mine as well.”
The AATS Mitral Conclave skips a year in 2018. Instead, New York will host the biennial AATS Aortic Symposium April 26–28 next year.
* CORRECTION: Dr. Anyanwu's remarks were corrected read "he’d be inclined to use a mechanical valve in a 25-year-old man with rheumatic mitral stenosis." 5/5/2017
The fourth biennial the American Association for Thoracic Surgery (AATS) Mitral Conclave 2017 was attended by a large audience of cardiothoracic surgeons and other professionals from 67 countries on Thursday and Friday to hear the latest on repair and replacement of the mitral valve.
Conference chair David H. Adams, MD, of Mount Sinai Health System noted that this was the first time the AATS had directly managed the meeting. The conclave included more than 200 oral presentations and 207 e-posters.
The faculty included more than 70 international thought leaders in mitral valve repair, and the live sessions featured more than 200 lectures, abstracts, and video presentations. Twenty-two breakout sessions reported on more than 80 submitted abstracts.
Mastering videography skills also improves one’s minimally invasive skills, said Vinay Badhwar, MD, of West Virginia University. “To do mitral surgery robotically and do minimally invasive surgery, you have to become a videographer,” he said. The surgeon must also be engaged in carefully selecting his or her team, Dr. Badhwar added.
In seven different plenary sessions, international experts participated in panels that discussed management of complications and explored scenarios in which they would not intervene. A debate format modeled on the movie Thunderdome—“four men enter, one man leaves”—featured a spirited discussion on when to repair functional tricuspid regurgitation. Dr. Adams and Tirone E. David, MD, of Toronto General Hospital, took rather strident opposing views, with Dr. Adams advocating for repair. The goal, Dr. Adams said, is to provide normal tricuspid valve function for the long term. “We got aggressive because we were doing a lot of reoperations for tricuspid disease in patients who had mitral valve surgery,” Dr. Adams said.
One plenary roundtable tackled the subject of when to use mechanical valves instead of biological valves. “Has the pendulum swung too far away from mechanical valves and are there cases where mechanical valves should be the first choice?” Dr. Sundt, session chair, asked the panelists.
The panelists concurred that a patient’s individual needs would drive decision-making. Anelechi Anyanwu, MD, of Mount Sinai, said he’d be inclined to use a mechanical valve in a 25-year-old man with rheumatic mitral stenosis.* In younger patients, namely teenagers, valve selection depends on the activity level they’d pursue after surgery, said Pedro J. del Nido, MD, of Children’s Hospital Boston.
At the plenary on transcatheter mitral therapy, John Laschinger, MD, of the Food and Drug Administration, reviewed the approval process for new mitral devices. “It comes down to the benefit-risk determination where we look at the standard-of-care surgery and look to see if the device is an acceptable alternative – that is, if it is safer and more effective,” Dr. Laschinger said.
James S. Gammie, MD, of the University of Maryland, also reported on an analysis of 87,214 mitral procedures from the Society for Thoracic Surgeons database over the past 5 years. Among the revelations from this analysis are that 96.1% of procedures for leaflet prolapse involved annuloplasty and that 75.8% receive a bioprosthetic valve.
The plenary and breakouts also included seven different video sessions ranging from managing leaflet prolapse to adult congenital surgery and complex scenarios.
Robert A. Dion, MD, Genk, Belgium, delivered the Conclave Honored Lecture and received the Mitral Conclave Achievement Award. He talked about the operative team as a geese flight. “The geese flight is always a unit of hierarchy,” Dr. Dion said. “The figure of the geese flight is V and the chief chooses the lead goose for the capacity to fly high enough and fast enough.”
In the Honored Cardiology Lecture, Robert O. Bonow, MD, of Northwestern Memorial Hospital, explored clinical guidelines for mitral valve repair and replacement and their application in the clinic. “Both sets of guidelines in Europe and the United States make the clear point that is obvious to all of you but less so to cardiologists, that there are two forms of mitral valve disease: degenerative or primary, and functional, which is secondary,” he said. He called for thoracic surgeons to collaborate with their cardiology colleagues. “You and I have lots of work to do, not only in caring for our patients but also in starting to devise appropriate quality metrics, hopefully working together in a team-based approach,” Dr. Bonow said. “This is what gives the best patient care but also gives us the best recommendations for our policy issues. And I look forward to further enhancements from your field and mine as well.”
The AATS Mitral Conclave skips a year in 2018. Instead, New York will host the biennial AATS Aortic Symposium April 26–28 next year.
* CORRECTION: Dr. Anyanwu's remarks were corrected read "he’d be inclined to use a mechanical valve in a 25-year-old man with rheumatic mitral stenosis." 5/5/2017
The fourth biennial the American Association for Thoracic Surgery (AATS) Mitral Conclave 2017 was attended by a large audience of cardiothoracic surgeons and other professionals from 67 countries on Thursday and Friday to hear the latest on repair and replacement of the mitral valve.
Conference chair David H. Adams, MD, of Mount Sinai Health System noted that this was the first time the AATS had directly managed the meeting. The conclave included more than 200 oral presentations and 207 e-posters.
The faculty included more than 70 international thought leaders in mitral valve repair, and the live sessions featured more than 200 lectures, abstracts, and video presentations. Twenty-two breakout sessions reported on more than 80 submitted abstracts.
Mastering videography skills also improves one’s minimally invasive skills, said Vinay Badhwar, MD, of West Virginia University. “To do mitral surgery robotically and do minimally invasive surgery, you have to become a videographer,” he said. The surgeon must also be engaged in carefully selecting his or her team, Dr. Badhwar added.
In seven different plenary sessions, international experts participated in panels that discussed management of complications and explored scenarios in which they would not intervene. A debate format modeled on the movie Thunderdome—“four men enter, one man leaves”—featured a spirited discussion on when to repair functional tricuspid regurgitation. Dr. Adams and Tirone E. David, MD, of Toronto General Hospital, took rather strident opposing views, with Dr. Adams advocating for repair. The goal, Dr. Adams said, is to provide normal tricuspid valve function for the long term. “We got aggressive because we were doing a lot of reoperations for tricuspid disease in patients who had mitral valve surgery,” Dr. Adams said.
One plenary roundtable tackled the subject of when to use mechanical valves instead of biological valves. “Has the pendulum swung too far away from mechanical valves and are there cases where mechanical valves should be the first choice?” Dr. Sundt, session chair, asked the panelists.
The panelists concurred that a patient’s individual needs would drive decision-making. Anelechi Anyanwu, MD, of Mount Sinai, said he’d be inclined to use a mechanical valve in a 25-year-old man with rheumatic mitral stenosis.* In younger patients, namely teenagers, valve selection depends on the activity level they’d pursue after surgery, said Pedro J. del Nido, MD, of Children’s Hospital Boston.
At the plenary on transcatheter mitral therapy, John Laschinger, MD, of the Food and Drug Administration, reviewed the approval process for new mitral devices. “It comes down to the benefit-risk determination where we look at the standard-of-care surgery and look to see if the device is an acceptable alternative – that is, if it is safer and more effective,” Dr. Laschinger said.
James S. Gammie, MD, of the University of Maryland, also reported on an analysis of 87,214 mitral procedures from the Society for Thoracic Surgeons database over the past 5 years. Among the revelations from this analysis are that 96.1% of procedures for leaflet prolapse involved annuloplasty and that 75.8% receive a bioprosthetic valve.
The plenary and breakouts also included seven different video sessions ranging from managing leaflet prolapse to adult congenital surgery and complex scenarios.
Robert A. Dion, MD, Genk, Belgium, delivered the Conclave Honored Lecture and received the Mitral Conclave Achievement Award. He talked about the operative team as a geese flight. “The geese flight is always a unit of hierarchy,” Dr. Dion said. “The figure of the geese flight is V and the chief chooses the lead goose for the capacity to fly high enough and fast enough.”
In the Honored Cardiology Lecture, Robert O. Bonow, MD, of Northwestern Memorial Hospital, explored clinical guidelines for mitral valve repair and replacement and their application in the clinic. “Both sets of guidelines in Europe and the United States make the clear point that is obvious to all of you but less so to cardiologists, that there are two forms of mitral valve disease: degenerative or primary, and functional, which is secondary,” he said. He called for thoracic surgeons to collaborate with their cardiology colleagues. “You and I have lots of work to do, not only in caring for our patients but also in starting to devise appropriate quality metrics, hopefully working together in a team-based approach,” Dr. Bonow said. “This is what gives the best patient care but also gives us the best recommendations for our policy issues. And I look forward to further enhancements from your field and mine as well.”
The AATS Mitral Conclave skips a year in 2018. Instead, New York will host the biennial AATS Aortic Symposium April 26–28 next year.
* CORRECTION: Dr. Anyanwu's remarks were corrected read "he’d be inclined to use a mechanical valve in a 25-year-old man with rheumatic mitral stenosis." 5/5/2017
The End of a Season
Spring, it symbolizes a new beginning. The smell of fresh cut grass hangs in the air, and it’s my favorite time of the sports year. A new season has begun in baseball, and the NHL and NBA playoffs are underway. As a new season begins, two more draw to a close. In this fan’s opinion, there is nothing quite as exciting as playoff hockey, and this month AJO hopes to “Capital-ize” on that excitement by presenting the hockey issue.
In “The Ice Hockey Issue”, Popkin and colleagues present a review of upper extremity injuries in hockey, which will serve as a guide for sports medicine physicians covering hockey games. There’s even a segment covering dental and ocular injuries, in case you don’t have a dentist or ophthalmologist handy. While we typically no longer publish case reports, Degen and colleagues present a unique report detailing an unusual injury to a prominent NHL goaltender. AJO presents it to expand your diagnostic differential for neck injuries.
I had another reason in mind when I mentioned the end of a season in this month’s editorial. The new AJO has seen a lot of changes, and it is our Editorial Team’s goal to continuously improve the journal and to provide timely features that are directly relevant to your practice. We’ve updated our website, and we’ve added some features, such as QR codes and take-home points, to improve your reading experience. But our ability to further enhance the journal is limited in print, and our web statistics show that a large percentage of our readers view the articles on their smartphones.
As I’ve written before, these are challenging times for printed media. The digital age has arrived and technology has made traditional publications less appealing. Our younger readers now demand a portable, electronic, media-rich publication that provides information that directly benefits their practices. To provide this, we envision a digital journal that is immersed in a learning environment, with videos, technique guides, and supplementary materials just a click away.
A few months back, AJO tested the digital waters. Our trial met with a positive response, and so, it is with great excitement that we announce that beginning in 2018, AJO will be the first orthopedic journal to go “All Digital.”
To further our goal of creating material that directly impacts your practice, we will present each feature review article as a learning module. The articles will feature extensive photos and videos, PowerPoint presentations for download, test questions, and patient information sheets. We will publish authors’ preference cards and postoperative protocols.
We’re currently developing applications and tools to improve your interactive experience. In the coming months, look for announcements regarding new strategic partnerships and features that will become mainstays of our electronic environment.
I hope you share the excitement of a new beginning in the digital era. I know the transition will provide a greatly enhanced, valuable resource that will change the way we utilize journals in our practice.
Am J Orthop. 2017;46(3):122. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Spring, it symbolizes a new beginning. The smell of fresh cut grass hangs in the air, and it’s my favorite time of the sports year. A new season has begun in baseball, and the NHL and NBA playoffs are underway. As a new season begins, two more draw to a close. In this fan’s opinion, there is nothing quite as exciting as playoff hockey, and this month AJO hopes to “Capital-ize” on that excitement by presenting the hockey issue.
In “The Ice Hockey Issue”, Popkin and colleagues present a review of upper extremity injuries in hockey, which will serve as a guide for sports medicine physicians covering hockey games. There’s even a segment covering dental and ocular injuries, in case you don’t have a dentist or ophthalmologist handy. While we typically no longer publish case reports, Degen and colleagues present a unique report detailing an unusual injury to a prominent NHL goaltender. AJO presents it to expand your diagnostic differential for neck injuries.
I had another reason in mind when I mentioned the end of a season in this month’s editorial. The new AJO has seen a lot of changes, and it is our Editorial Team’s goal to continuously improve the journal and to provide timely features that are directly relevant to your practice. We’ve updated our website, and we’ve added some features, such as QR codes and take-home points, to improve your reading experience. But our ability to further enhance the journal is limited in print, and our web statistics show that a large percentage of our readers view the articles on their smartphones.
As I’ve written before, these are challenging times for printed media. The digital age has arrived and technology has made traditional publications less appealing. Our younger readers now demand a portable, electronic, media-rich publication that provides information that directly benefits their practices. To provide this, we envision a digital journal that is immersed in a learning environment, with videos, technique guides, and supplementary materials just a click away.
A few months back, AJO tested the digital waters. Our trial met with a positive response, and so, it is with great excitement that we announce that beginning in 2018, AJO will be the first orthopedic journal to go “All Digital.”
To further our goal of creating material that directly impacts your practice, we will present each feature review article as a learning module. The articles will feature extensive photos and videos, PowerPoint presentations for download, test questions, and patient information sheets. We will publish authors’ preference cards and postoperative protocols.
We’re currently developing applications and tools to improve your interactive experience. In the coming months, look for announcements regarding new strategic partnerships and features that will become mainstays of our electronic environment.
I hope you share the excitement of a new beginning in the digital era. I know the transition will provide a greatly enhanced, valuable resource that will change the way we utilize journals in our practice.
Am J Orthop. 2017;46(3):122. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Spring, it symbolizes a new beginning. The smell of fresh cut grass hangs in the air, and it’s my favorite time of the sports year. A new season has begun in baseball, and the NHL and NBA playoffs are underway. As a new season begins, two more draw to a close. In this fan’s opinion, there is nothing quite as exciting as playoff hockey, and this month AJO hopes to “Capital-ize” on that excitement by presenting the hockey issue.
In “The Ice Hockey Issue”, Popkin and colleagues present a review of upper extremity injuries in hockey, which will serve as a guide for sports medicine physicians covering hockey games. There’s even a segment covering dental and ocular injuries, in case you don’t have a dentist or ophthalmologist handy. While we typically no longer publish case reports, Degen and colleagues present a unique report detailing an unusual injury to a prominent NHL goaltender. AJO presents it to expand your diagnostic differential for neck injuries.
I had another reason in mind when I mentioned the end of a season in this month’s editorial. The new AJO has seen a lot of changes, and it is our Editorial Team’s goal to continuously improve the journal and to provide timely features that are directly relevant to your practice. We’ve updated our website, and we’ve added some features, such as QR codes and take-home points, to improve your reading experience. But our ability to further enhance the journal is limited in print, and our web statistics show that a large percentage of our readers view the articles on their smartphones.
As I’ve written before, these are challenging times for printed media. The digital age has arrived and technology has made traditional publications less appealing. Our younger readers now demand a portable, electronic, media-rich publication that provides information that directly benefits their practices. To provide this, we envision a digital journal that is immersed in a learning environment, with videos, technique guides, and supplementary materials just a click away.
A few months back, AJO tested the digital waters. Our trial met with a positive response, and so, it is with great excitement that we announce that beginning in 2018, AJO will be the first orthopedic journal to go “All Digital.”
To further our goal of creating material that directly impacts your practice, we will present each feature review article as a learning module. The articles will feature extensive photos and videos, PowerPoint presentations for download, test questions, and patient information sheets. We will publish authors’ preference cards and postoperative protocols.
We’re currently developing applications and tools to improve your interactive experience. In the coming months, look for announcements regarding new strategic partnerships and features that will become mainstays of our electronic environment.
I hope you share the excitement of a new beginning in the digital era. I know the transition will provide a greatly enhanced, valuable resource that will change the way we utilize journals in our practice.
Am J Orthop. 2017;46(3):122. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Head, Neck, and Shoulder Injuries in Ice Hockey: Current Concepts
Take-Home Points
- Hockey is a high-speed collision sport with one of the highest injury rates among all sports.
- Use of a helmet with visors or full-face shields significantly reduces the risk for eye injury.
- Broken portions of teeth should be found and placed in a protective medium such as saline, saliva, or milk for transport.
- A player with unresolved concussion symptoms should not be allowed to return to the ice.
- Shoulder dominance, which determines stick grip, is an important consideration in the treatment of shoulder instability in an ice hockey player.
On a surface of ice in Windsor, Nova Scotia in the middle of the 19th century, the modern game of ice hockey evolved.1 A blend of hurley, a Gaelic sport, and lacrosse, from the native Mi’kmaq culture, the sport of ice hockey gained rapidly in popularity throughout Canada and is now the country’s national sport. Hockey quickly spread to the United States and then Europe. It is presently played in 77 countries across the world.2
Hockey players can reach speeds of up to 48 km (~30 miles) per hour on razor-sharp skates on an ice surface surrounded by rigid plastic composite boards topped with plexiglass.3 They use sticks made of wood, aluminum, or a composite material to advance a 6-ounce vulcanized rubber puck on the opposing goal, and this puck sometimes reaches speeds over 160 km (~100 miles) per hour. Older, male players are allowed to make physical contact with their opposing counterparts to separate them from the puck (body-checking). Not surprisingly, the potential risk for injury in hockey is high. At the 2010 Winter Olympics, men’s ice hockey players had the highest rate of injury of any other competitors there—more than 30% were affected.4 
Hockey is played and enjoyed by athletes ranging widely in age. Youth hockey leagues accept players as young as 5 years. Hockey can become a lifelong recreational activity. In North America, old timers’ leagues have many players up to age 70 years.6 According to International Ice Hockey Federation data for 2016, more than 543,000 and 639,500 people play hockey in the United States and Canada, respectively.2 Most of the rules, protective equipment, skates, ice surfaces, and goal sizes are the same in men’s and women’s hockey.7 The major difference is in body-checking—this practice is not allowed at any age in women’s ice hockey.
In this article, we review the evaluation and management of common head, neck, and shoulder hockey injuries for physicians who provide medical support and coverage for youth, amateur, and senior hockey teams.
Evaluation and Management of Common Hockey Injuries
Eye Injuries
Although eye injuries are less common than musculoskeletal injuries and concussions in hockey, they are a serious risk for recreational and competitive players alike. Furthermore, recovery may be difficult, and eye injuries can have serious lifelong consequences.8 In hockey, the most commonly reported eye injuries are periorbital contusions and lacerations, hyphema, corneal and conjunctival abrasions, orbital fractures, and ruptured globes (Table 2).9,10 
As a contact sport, hockey often involves high-impact, blunt-force trauma. The trauma in hockey results from collisions with other players, the boards, hockey sticks, and pucks. It is therefore not surprising that the most common ocular injuries in this sport are periorbital contusions. Although most contusions cause only mild swelling and ecchymosis of the soft tissues around the eye, there is potential for serious consequences. In a Scandinavia study, Leivo and colleagues10 found that 9% of patients who sustained a periocular contusion also had a clinically significant secondary diagnosis, such as retinal tear or hemorrhage, eyelid laceration, vitreous hemorrhage, or retinal detachment. Although the study was hospital-based, and therefore biased toward more severe cases, its findings highlight the potential severity of eye injuries in hockey. Furthermore, the study found that the majority of players who sustained blunt trauma to the eye itself required lifelong follow-up because of increased risk for glaucoma. This is particularly true for hyphema, as this finding indicates significant damage to intraocular tissues.10Players can also sustain fractures of the orbital bones, including orbital blowout fractures. Typical signs and symptoms of blowout fractures include diplopia, proptosis or enophthalmos, infraorbital hypoesthesia, painful and decreased extraocular movement (particularly upgaze), and palpable crepitance caused by sinus air entering the lower eyelid.11 If orbital fracture is suspected, as it should be in any case in which the injured player experiences pain with eye movement or diplopia, the player should be referred to the ED for computed tomography (CT) and ophthalmologic evaluation.12 Continued participation seriously risks making the injury much worse, particularly should another impact occur. In addition, given the impact needed to cause orbital fractures, consideration must be given to the potential for a coexisting concussion injury.
Severe direct trauma to the eye—from a puck, a stick, or a fist—can result in a ruptured globe, a particularly serious injury that requires immediate surgical attention. Signs and symptoms of a ruptured globe are rarely subtle, but associated eyelid swelling or laceration may obscure the injury, delaying proper diagnosis and treatment. More obvious signs include severely reduced vision, hemorrhagic chemosis (swelling) of the conjunctiva, and an irregular or peaked pupil. If a rupture or any significant intraocular injury is suspected, it is crucial to avoid applying any pressure to the globe, as this can significantly worsen the damage to the intraocular tissues. Use of a helmet with protective shields and cages attached markedly reduces the risk for such injuries.13All eye injuries require prompt assessment, which allows for appropriate management and prevention of secondary damage.14 Initial evaluation of a patient with ocular trauma should begin with external examination for lacerations, swelling, or orbital rim step-off deformity. The physician should also check visual acuity in order to assess for significant vision impairment (counting fingers or reading a sign in the arena; confrontation visual fields). This should be done before attending to any periocular injuries, with the uninjured side serving as a control. Next, the physician should assess the extraocular eye movements as well as the size, shape, and reactivity of the pupils. Particular attention should be paid to detecting any deficit in extraocular movement or irregularity in pupil size, shape, or reactivity, as such findings are highly suggestive of serious injury to the globe.13 Hyphema (blood in anterior chamber of eye anterior to pupil) should be suspected if vision is reduced and the pupil cannot be clearly visualized. However, a bright red clot is not always apparent at time of injury or if the amount of blood is small. An irregular pupil, or a pupil that does not constrict well to light, is also a red flag for serious contusion injury to the eye, and requires ophthalmologic evaluation. It is important to keep in mind that blunt trauma severe enough to produce hyphema or an irregular and poorly reactive pupil is often associated with retinal damage as well, including retinal edema or detachment.
Minor injuries (eg, small foreign bodies, minor periocular contusions and lacerations) can often be managed rink-side. Foreign bodies not embedded in the cornea, but lodged under the upper eyelid, can sometimes be removed by everting the eyelid and sweeping with a moistened cotton swab or using diffuse, sterile saline irrigation.11 Corneal abrasions generally cause severe pain, photophobia, and tearing and are easily diagnosed with use of topical fluorescein and a blue light. A topical anesthetic can be extremely helpful in this setting, as it allows for proper pain-free evaluation, but should never be used in an ongoing manner for pain relief. Small lacerations of the brow can be sutured with 5-0 or 6-0 nylon or closed with 2-Octyl cyanoacrylate tissue adhesive (Dermabond). Eyelid lacerations, unless very small, are best managed by an ophthalmologist; care must be taken to rule out injury to the deeper orbital tissues and eye. If serious injury is suspected, or the eye cannot be appropriately evaluated, it should be stabilized and protected with a protective shield or plastic cup, and the player should be transferred to an ED for appropriate ophthalmologic evaluation.13Most eye injuries are accidental, caused by sticks or deflected pucks, but 18% are acquired in fights.8 Use of visors or full-face cages effectively minimizes the rate of eye injuries.8,13,15,16 In a cohort study of 282 elite amateur ice hockey players, the risk of eye injury was 4.7 times higher in players without face protection than in players who used half-face shields; there were no eye injuries in players who used full-face protection.13 For visors to prevent eye injury, they must be positioned to cover the eyes and the lower edge of the nose in all projections.10
Dental Injuries
The incidence and type of facial and dental injuries depend directly on the type of face protection used.11,17,18 In a study of face, head, and neck injuries in elite amateur ice hockey players, Stuart and colleagues13 found game-related injury rates of 158.9 per 1000 player-hours in players without face protection, 73.5 in players who used half-face shields, and 23.2 in players who used full-face shields. Players who wore full-face shields had facial, head, and neck injury rates of only 23.2 per 1000 player-game hours.13 Other studies clearly support the important role face shields play in lowering injury risk in hockey. Face and head injuries account for 20% to 40% of all hockey-related injuries,3,16,19 and dental injuries up to 11.5%.20 In a study from Finland, Lahti and colleagues19 found that over a 2-year period, 479 hockey players sustained injuries, including 650 separate dental injuries. The most commonly diagnosed dental injury was an uncomplicated crown fracture, and the most common cause was a hit with a hockey stick, which accounted for 52.7% and 40.3% of dental injuries in games and practices, respectively.19
In the management of dental fractures, the broken portions of teeth should be found and placed in a transportation-protective medium, such as saline, saliva, or milk,16 which can improve functional and esthetic replacement outcomes.21,22 Loose pieces of teeth should not be left in the player’s mouth. The residual tooth should be stabilized and exposure to air and occlusion limited. Dental fractures can affect the enamel, the enamel and dentin structures (uncomplicated fracture), or enamel, dentin, and pulp (complicated).23 Fractures involving only the enamel do not require urgent dental evaluation. Dentin or pulp involvement may cause temperature and air sensitivity.23 If a tooth is air-sensitive, the player should be referred to a specialist immediately.11
Direct trauma can cause instability without displacement (subluxation) or complete displacement of the tooth from its alveolar socket (avulsion).23 An avulsed tooth should be handled by the crown to avoid further damage to the root and periodontal ligament.16,24 The tooth should be rinsed gently with saline and reimplanted in its socket, ideally within 5 to 10 minutes,23with the athlete biting down gently on gauze to hold the tooth in place. A 1-mL supraperiosteal infiltration of 1% or 2% lidocaine hydrochloride (1:100,000 epinephrine) can be given into the apex of the tooth being anesthetized (Figure 1). 
Concussions
A concussion is a “complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.”25 Concussion is largely a functional disturbance instead of a structural injury, owing to the rotational and/or shearing forces involved. Many studies have identified concussion as the most common type of injury in all of youth hockey.26 Concussions account for up to 19% of all injuries in men’s collegiate hockey.3
Concussion can be challenging to diagnose on the ice. The most important factor in concussion management is symptom reporting by the athlete.27 Despite significant efforts in education and awareness, student athletes, especially hockey players, withhold reporting a possible concussion.28 Reasons for underreporting include fear of letting down other players and coaches, thinking the injury is not severe enough to warrant evaluation, and fear of losing standing with the current team or future teams.28 
As postinjury concussion assessments are ideal when comparisons can be made with preseason (baseline) scores, preseason testing is becoming standard in professional, college, junior, and high school hockey. This testing involves the Sport Concussion Assessment Tool, 3rd edition (SCAT3), and the King-Devick (K-D) test.30,31 Some youth leagues have baseline testing as well, though the frequency of baseline testing in their players is controversial,32 as the adolescent mind’s processing speed and memory increase exponentially.33 For these younger athletes, it may be necessary to perform baseline testing more frequently than annually.32 A physician can use baseline test results to help diagnose a concussion at the rink and then track the athlete’s recovery and help with return-to-play decisions.29 Vision involves almost half of the brain’s circuits,34 including areas vulnerable to head impact. A neuro-ophthalmologic test can assess for irregularities in accommodation, convergence, ocular muscle balance, pursuit, and saccades.29 The K-D test is a visual performance examination that allows easy and objective assessment of eye movements. Use of both the K-D test and the SCAT3 at the rink may increase the number of concussions detected.29,35 We recommend that physicians use both tests to assess for concussion at the hockey rink.
Initial treatment involves a period of physical rest and relative cognitive rest. Acute worsening of symptoms warrants urgent imaging to rule out a subdural or subarachnoid bleed. Once a player is symptom-free, a graded return-to-play protocol should be followed (Table 4). 
On the prevention side, great efforts have been made to improve hockey helmets. (Some manufacturers claim to have made concussion-proof helmets, but there is no evidence supporting this claim.6) Numerous investigators have reported a lower overall injury rate in players who wear a helmet and a full-face shield.6,13 In addition, rule changes aimed at decreasing head contact have been implemented to decrease the incidence of sport-related concussions.36 Moreover, education on proper helmet use and wear should be emphasized. A study of the effects of hockey helmet fit on cervical motion found that 7 (39%) of 18 players wore a game or competition helmet so loosely that it could be removed without unbuttoning its chinstrap.37 Improperly worn helmets cannot prevent injury as well as properly worn helmets can.
Cervical Spine Injuries
Whereas American football is associated with a higher annual number of nonfatal catastrophic neck injuries, hockey has a 3 to 6 times higher incidence of cervical spine injuries and spinal cord damage.38,39 A Canadian Ice Hockey Spinal Injuries Registry review of the period 2006 to 2011 identified 44 cervical spine injuries, 7.3 per year on average.40 Severe injury, defined as complete motor and sensory loss, complete motor loss and incomplete sensory, or complete motor loss, occurred in 4 (9.1%) of the 44 injured players. In hockey, a major mechanism of cervical spine injury is an axial load to the slightly flexed spine.39 Of 355 hockey-related cervical spine injuries in a Canada study, 95 (35.5%) were caused by a check from behind.40,41 The Canadian neurosurgeons’ work led to rule changes prohibiting checks from behind, and this prohibition has reduced the incidence of cervical spine injuries in ice hockey.38,40
Team physicians should be comfortable managing serious neck and spine injuries on the ice. Initial evaluation should follow the standard ABCs (airway, breathing, circulation). The physician places a hand on each side of the head to stabilize the neck until the initial examination is complete. The goal is to minimize cervical spine motion until transportation to the hospital for advanced imaging and definitive treatment.37 The decision to remove or leave on the helmet is now controversial. Hockey helmets differ from football helmets in that their chinstraps do not afford significant cervical stabilization, and the helmets have less padding and cover less of the head; in addition, a shockingly high percentage of hockey players do not wear properly fitting helmets.37 In one study, 3-dimensional motion analysis of a hockey player during the logroll technique showed less transverse and sagittal cervical plane motion with the helmet removed than with the helmet (properly fitting or not) in place; the authors recommended removing the helmet to limit extraneous cervical spine motion during the technique.37 However, 2 other studies found that helmet removal can result in significantly increased cervical spine motion of the immobilized hockey player.42,43Recommendation 4 of the recently released interassociation consensus statement of the National Athletic Trainers’ Association reads, “Protective athletic equipment should be removed before transport to an emergency facility for an athlete-patient with suspected cervical spine instability.”44 This represents a shift from leaving the helmet and shoulder pads in place. For ice hockey players with suspected cervical spine injury, more research is needed on cervical motion during the entire sequence—partial logrolls, spine-boarding, placement of cervical collar before or after logroll, and different immobilization techniques for transport.37
The athlete must be carefully transferred to a spine board with either logroll or lift-and-slide. Although an extrication cervical collar can be placed before the spine board is placed, the effectiveness of this collar in executing the spine-board transfer is not proven.45 When the player is on the spine board, the head can be secured with pads and straps en route to the hospital.
Return-to-Play Criteria for Cervical Spine Injuries There is no clear consensus on return-to-play guidelines for cervical spine injuries in athletes.46 
Shoulder Injuries
For hockey players, the upper extremity traditionally has been considered a well-protected area.48 However, shoulder pads are considerably more flexible in hockey than in football and other collision sports. In addition, hockey gloves allow a fair amount of motion for stick handling, and the wrist may be in maximal flexion or extension when a hit against the boards or the ice occurs. Open-ice checking, board collisions, and hockey stick use have been postulated as reasons for the high incidence of upper extremity injuries in hockey. Researchers in Finland found that upper extremity injuries accounted for up to 31% of all hockey injuries.49 More than 50% of these injuries resulted from checking or board collisions. Furthermore, study findings highlighted a low rate of injury in younger players and indicated the rate increases with age.49,50
In hockey players, the acromioclavicular (AC) joint is the most commonly injured shoulder structure.51 The mechanism of injury can be a board collision or an open-ice hit, but most often is a direct blow to the shoulder. The collision disrupts the AC joint and can sprain or tear the coracoclavicular ligaments. The Rockwood classification is used to categorize AC joint injuries (Figure 2). 
Initial management involves icing the AC joint and placing a sling for comfort. Type I and type II injuries can be managed with progressive range-of-motion (ROM) exercises, strengthening, cryotherapy, and a period of rest. Treatment of type III injuries remains controversial,52 but in hockey players these injuries are almost always treated nonoperatively. Return to play requires full motion, normal strength, and minimal discomfort. Players return a few days to 2 weeks after a grade I injury; recovery from grade II injuries may take 2 to 3 weeks, and recovery from grade III injuries, 6 to 12 weeks. Surgical treatment is usually required in type IV and type V injuries, but we have had experience treating these injuries nonoperatively in high-level players. AC joint reinjury in hockey players is common, and surgical treatment should be approached cautiously, as delayed fracture after return to sport has been reported.53 Special precautions should be taken in collision athletes who undergo AC joint reconstruction. In the anatomical reconstruction described by Carofino and Mazzocca,54 2 holes are drilled in the clavicle; these holes are a potential source of fracture when the collision athlete returns to sport (Figure 3). 
Clavicle fracture is another common hockey injury.55 Studies have shown clavicle fractures proportionally occur most often in people 15 to 19 years old.49 The injury presents with pain and deformity over the clavicle; in more severe fractures, skin tenting is identified. Initial management of suspected clavicle fracture includes cryotherapy, sling, and radiographs. Radiographs should include an AP view and then a 45° cephalad view, which eliminates overshadowing from the ribs. Most clavicle fractures are successfully managed nonoperatively, though there is evidence that significantly displaced or comminuted fractures have better union rates and shoulder function when treated with open reduction and internal fixation.56 After a clavicle fracture, return to skating and noncontact practice usually takes 8 weeks, with return to full contact occurring around 12 weeks.
Sternoclavicular injuries are relatively uncommon, but potentially serious. Special attention should also be given to adolescent athletes with sternoclavicular pain. Although sternoclavicular dislocations have been reported in hockey players, instead these likely are fractures involving the medial clavicle physis.57 
The shoulder is the most commonly dislocated major joint, and the incidence of shoulder dislocation in elite hockey players is 8% to 21%.50,58 Anterior shoulder instability occurs from a fall with the shoulder in an abducted, externally rotated and extended position or from a direct anteriorly placed impact to the posterior shoulder. We recommend taking players off the ice for evaluation. Depending on physician comfort, the shoulder can be reduced in the training room, and the athlete sent for radiographs after reduction. If resources or support for closed reduction is not available at the rink, the athlete should be sent to the ED. Initial radiographic evaluation of a player with shoulder injury begins with plain radiographs, including a true AP (Grashey) view with the humerus in neutral, internal, and external rotation and an axillary view. The axillary radiograph is crucial in determining anterior or posterior dislocation. If the patient cannot tolerate the pain associated with having an axillary radiograph taken, a Velpeau radiograph can be used. This radiograph is taken with the patient’s arm in a sling and with the patient leaning back 30° while the x-ray beam is directed superior to inferior.
CT is performed for a suspected osseous injury. CT is more accurate than plain radiographs in showing glenoid and humeral fractures in the acute setting as well as the amount of bone loss in the case of chronic instability. Magnetic resonance arthrography is the imaging modality of choice for the diagnoses of capsulolabral injury.
After shoulder reduction, treatment with a sling, cryotherapy, and a nonsteroidal anti-inflammatory drug is initiated. In a Minnesota study of nonoperative management of shoulder instability, 9 of 10 hockey players were able to return to play the same season, and 6 of the 10 required surgery at the end of the season.59 
Compared with noncontact athletes, hockey players and other collision athletes are at increased risk for recurrence.60-62 For collision athletes who want to continue playing their sport after recurrent instability, surgery is recommended. A shoulder instability study in Toronto found that more than 54% of 24 professional hockey players had associated Hill-Sachs lesions, but only 3 shoulders (12.5%) had glenoid defects.50 Arthroscopic and open techniques both demonstrate good results, and identification of bone loss can help determine which surgery to recommend.63 Hockey players can usually return to sport 6 months after shoulder stabilization.
Another important consideration in managing shoulder instability in hockey players is shoulder dominance, which determines stick grip. A left-handed player places the right hand on top of the stick for support, but most of the motion associated with shooting the puck—including abduction and external rotation—occurs with the left shoulder. Thus, a left-handed player with a history of previous left-side shoulder dislocation may dislocate with each shot, but a right-handed player with left shoulder instability may have considerably less trouble on the ice.58Shoulder and rotator cuff contusions (RCCs) occur in hockey and other collision sports.49,64 RCCs almost always result from a direct blow to the shoulder, and present with shoulder function loss, weakness, and pain.
Summary
Hockey is a high-speed collision sport with one of the highest injury rates among all sports. Physicians caring for youth, amateur, and senior hockey teams see a range of acute head, neck, and shoulder injuries. Although treatment of eye injuries, dental injuries, and concussions is not always considered orthopedic care, an orthopedic surgeon who is covering hockey needs to be comfortable managing these injuries acutely. Quality rink-side care minimizes the impact of the injury, maximizes the functional result, and expedites the safe return of the injured player back to the ice.
Am J Orthop. 2017;46(3):123-134. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
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31. Galetta MS, Galetta KM, McCrossin J, et al. Saccades and memory: baseline associations of the King-Devick and SCAT2 SAC tests in professional ice hockey players. J Neurol Sci. 2013;328(1-2):28-31.
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36. Smith AM, Stuart MJ, Dodick DW, et al. Ice Hockey Summit II: zero tolerance for head hits and fighting. Curr Sports Med Rep. 2015;14(2):135-144.
37. Mihalik JP, Beard JR, Petschauer MA, Prentice WE, Guskiewicz KM. Effect of ice hockey helmet fit on cervical spine motion during an emergency log roll procedure. Clin J Sport Med. 2008;18(5):394-398.
38. Banerjee R, Palumbo MA, Fadale PD. Catastrophic cervical spine injuries in the collision sport athlete, part 1: epidemiology, functional anatomy, and diagnosis. Am J Sports Med. 2004;32(4):1077-1087.
39. Reynen PD, Clancy WG Jr. Cervical spine injury, hockey helmets, and face masks. Am J Sports Med. 1994;22(2):167-170.
40. Tator CH, Provvidenza C, Cassidy JD. Update and overview of spinal injuries in Canadian ice hockey, 1943 to 2011: the continuing need for injury prevention and education. Clin J Sport Med. 2016;26(3):232-238.
41. Tator CH, Edmonds VE, Lapczak L, Tator IB. Spinal injuries in ice hockey players, 1966-1987. Can J Surg. 1991;34(1):63-69.
42. Laprade RF, Schnetzler KA, Broxterman RJ, Wentorf F, Gilbert TJ. Cervical spine alignment in the immobilized ice hockey player. A computed tomographic analysis of the effects of helmet removal. Am J Sports Med. 2000;28(6):800-803.
43. Metz CM, Kuhn JE, Greenfield ML. Cervical spine alignment in immobilized hockey players: radiographic analysis with and without helmets and shoulder pads. Clin J Sport Med. 1998;8(2):92-95.
44. National Athletic Trainers’ Association. Appropriate prehospital management of the spine-injured athlete: updated from 1998 document. http://www.nata.org/sites/default/files/Executive-Summary-Spine-Injury-updated.pdf. Updated August 5, 2015. Accessed April 6, 2017.
45. Del Rossi G, Heffernan TP, Horodyski M, Rechtine GR. The effectiveness of extrication collars tested during the execution of spine-board transfer techniques. Spine J. 2004;4(6):619-623.
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Take-Home Points
- Hockey is a high-speed collision sport with one of the highest injury rates among all sports.
- Use of a helmet with visors or full-face shields significantly reduces the risk for eye injury.
- Broken portions of teeth should be found and placed in a protective medium such as saline, saliva, or milk for transport.
- A player with unresolved concussion symptoms should not be allowed to return to the ice.
- Shoulder dominance, which determines stick grip, is an important consideration in the treatment of shoulder instability in an ice hockey player.
On a surface of ice in Windsor, Nova Scotia in the middle of the 19th century, the modern game of ice hockey evolved.1 A blend of hurley, a Gaelic sport, and lacrosse, from the native Mi’kmaq culture, the sport of ice hockey gained rapidly in popularity throughout Canada and is now the country’s national sport. Hockey quickly spread to the United States and then Europe. It is presently played in 77 countries across the world.2
Hockey players can reach speeds of up to 48 km (~30 miles) per hour on razor-sharp skates on an ice surface surrounded by rigid plastic composite boards topped with plexiglass.3 They use sticks made of wood, aluminum, or a composite material to advance a 6-ounce vulcanized rubber puck on the opposing goal, and this puck sometimes reaches speeds over 160 km (~100 miles) per hour. Older, male players are allowed to make physical contact with their opposing counterparts to separate them from the puck (body-checking). Not surprisingly, the potential risk for injury in hockey is high. At the 2010 Winter Olympics, men’s ice hockey players had the highest rate of injury of any other competitors there—more than 30% were affected.4
Hockey is played and enjoyed by athletes ranging widely in age. Youth hockey leagues accept players as young as 5 years. Hockey can become a lifelong recreational activity. In North America, old timers’ leagues have many players up to age 70 years.6 According to International Ice Hockey Federation data for 2016, more than 543,000 and 639,500 people play hockey in the United States and Canada, respectively.2 Most of the rules, protective equipment, skates, ice surfaces, and goal sizes are the same in men’s and women’s hockey.7 The major difference is in body-checking—this practice is not allowed at any age in women’s ice hockey.
In this article, we review the evaluation and management of common head, neck, and shoulder hockey injuries for physicians who provide medical support and coverage for youth, amateur, and senior hockey teams.
Evaluation and Management of Common Hockey Injuries
Eye Injuries
Although eye injuries are less common than musculoskeletal injuries and concussions in hockey, they are a serious risk for recreational and competitive players alike. Furthermore, recovery may be difficult, and eye injuries can have serious lifelong consequences.8 In hockey, the most commonly reported eye injuries are periorbital contusions and lacerations, hyphema, corneal and conjunctival abrasions, orbital fractures, and ruptured globes (Table 2).9,10
As a contact sport, hockey often involves high-impact, blunt-force trauma. The trauma in hockey results from collisions with other players, the boards, hockey sticks, and pucks. It is therefore not surprising that the most common ocular injuries in this sport are periorbital contusions. Although most contusions cause only mild swelling and ecchymosis of the soft tissues around the eye, there is potential for serious consequences. In a Scandinavia study, Leivo and colleagues10 found that 9% of patients who sustained a periocular contusion also had a clinically significant secondary diagnosis, such as retinal tear or hemorrhage, eyelid laceration, vitreous hemorrhage, or retinal detachment. Although the study was hospital-based, and therefore biased toward more severe cases, its findings highlight the potential severity of eye injuries in hockey. Furthermore, the study found that the majority of players who sustained blunt trauma to the eye itself required lifelong follow-up because of increased risk for glaucoma. This is particularly true for hyphema, as this finding indicates significant damage to intraocular tissues.10Players can also sustain fractures of the orbital bones, including orbital blowout fractures. Typical signs and symptoms of blowout fractures include diplopia, proptosis or enophthalmos, infraorbital hypoesthesia, painful and decreased extraocular movement (particularly upgaze), and palpable crepitance caused by sinus air entering the lower eyelid.11 If orbital fracture is suspected, as it should be in any case in which the injured player experiences pain with eye movement or diplopia, the player should be referred to the ED for computed tomography (CT) and ophthalmologic evaluation.12 Continued participation seriously risks making the injury much worse, particularly should another impact occur. In addition, given the impact needed to cause orbital fractures, consideration must be given to the potential for a coexisting concussion injury.
Severe direct trauma to the eye—from a puck, a stick, or a fist—can result in a ruptured globe, a particularly serious injury that requires immediate surgical attention. Signs and symptoms of a ruptured globe are rarely subtle, but associated eyelid swelling or laceration may obscure the injury, delaying proper diagnosis and treatment. More obvious signs include severely reduced vision, hemorrhagic chemosis (swelling) of the conjunctiva, and an irregular or peaked pupil. If a rupture or any significant intraocular injury is suspected, it is crucial to avoid applying any pressure to the globe, as this can significantly worsen the damage to the intraocular tissues. Use of a helmet with protective shields and cages attached markedly reduces the risk for such injuries.13All eye injuries require prompt assessment, which allows for appropriate management and prevention of secondary damage.14 Initial evaluation of a patient with ocular trauma should begin with external examination for lacerations, swelling, or orbital rim step-off deformity. The physician should also check visual acuity in order to assess for significant vision impairment (counting fingers or reading a sign in the arena; confrontation visual fields). This should be done before attending to any periocular injuries, with the uninjured side serving as a control. Next, the physician should assess the extraocular eye movements as well as the size, shape, and reactivity of the pupils. Particular attention should be paid to detecting any deficit in extraocular movement or irregularity in pupil size, shape, or reactivity, as such findings are highly suggestive of serious injury to the globe.13 Hyphema (blood in anterior chamber of eye anterior to pupil) should be suspected if vision is reduced and the pupil cannot be clearly visualized. However, a bright red clot is not always apparent at time of injury or if the amount of blood is small. An irregular pupil, or a pupil that does not constrict well to light, is also a red flag for serious contusion injury to the eye, and requires ophthalmologic evaluation. It is important to keep in mind that blunt trauma severe enough to produce hyphema or an irregular and poorly reactive pupil is often associated with retinal damage as well, including retinal edema or detachment.
Minor injuries (eg, small foreign bodies, minor periocular contusions and lacerations) can often be managed rink-side. Foreign bodies not embedded in the cornea, but lodged under the upper eyelid, can sometimes be removed by everting the eyelid and sweeping with a moistened cotton swab or using diffuse, sterile saline irrigation.11 Corneal abrasions generally cause severe pain, photophobia, and tearing and are easily diagnosed with use of topical fluorescein and a blue light. A topical anesthetic can be extremely helpful in this setting, as it allows for proper pain-free evaluation, but should never be used in an ongoing manner for pain relief. Small lacerations of the brow can be sutured with 5-0 or 6-0 nylon or closed with 2-Octyl cyanoacrylate tissue adhesive (Dermabond). Eyelid lacerations, unless very small, are best managed by an ophthalmologist; care must be taken to rule out injury to the deeper orbital tissues and eye. If serious injury is suspected, or the eye cannot be appropriately evaluated, it should be stabilized and protected with a protective shield or plastic cup, and the player should be transferred to an ED for appropriate ophthalmologic evaluation.13Most eye injuries are accidental, caused by sticks or deflected pucks, but 18% are acquired in fights.8 Use of visors or full-face cages effectively minimizes the rate of eye injuries.8,13,15,16 In a cohort study of 282 elite amateur ice hockey players, the risk of eye injury was 4.7 times higher in players without face protection than in players who used half-face shields; there were no eye injuries in players who used full-face protection.13 For visors to prevent eye injury, they must be positioned to cover the eyes and the lower edge of the nose in all projections.10
Dental Injuries
The incidence and type of facial and dental injuries depend directly on the type of face protection used.11,17,18 In a study of face, head, and neck injuries in elite amateur ice hockey players, Stuart and colleagues13 found game-related injury rates of 158.9 per 1000 player-hours in players without face protection, 73.5 in players who used half-face shields, and 23.2 in players who used full-face shields. Players who wore full-face shields had facial, head, and neck injury rates of only 23.2 per 1000 player-game hours.13 Other studies clearly support the important role face shields play in lowering injury risk in hockey. Face and head injuries account for 20% to 40% of all hockey-related injuries,3,16,19 and dental injuries up to 11.5%.20 In a study from Finland, Lahti and colleagues19 found that over a 2-year period, 479 hockey players sustained injuries, including 650 separate dental injuries. The most commonly diagnosed dental injury was an uncomplicated crown fracture, and the most common cause was a hit with a hockey stick, which accounted for 52.7% and 40.3% of dental injuries in games and practices, respectively.19
In the management of dental fractures, the broken portions of teeth should be found and placed in a transportation-protective medium, such as saline, saliva, or milk,16 which can improve functional and esthetic replacement outcomes.21,22 Loose pieces of teeth should not be left in the player’s mouth. The residual tooth should be stabilized and exposure to air and occlusion limited. Dental fractures can affect the enamel, the enamel and dentin structures (uncomplicated fracture), or enamel, dentin, and pulp (complicated).23 Fractures involving only the enamel do not require urgent dental evaluation. Dentin or pulp involvement may cause temperature and air sensitivity.23 If a tooth is air-sensitive, the player should be referred to a specialist immediately.11
Direct trauma can cause instability without displacement (subluxation) or complete displacement of the tooth from its alveolar socket (avulsion).23 An avulsed tooth should be handled by the crown to avoid further damage to the root and periodontal ligament.16,24 The tooth should be rinsed gently with saline and reimplanted in its socket, ideally within 5 to 10 minutes,23with the athlete biting down gently on gauze to hold the tooth in place. A 1-mL supraperiosteal infiltration of 1% or 2% lidocaine hydrochloride (1:100,000 epinephrine) can be given into the apex of the tooth being anesthetized (Figure 1).
Concussions
A concussion is a “complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.”25 Concussion is largely a functional disturbance instead of a structural injury, owing to the rotational and/or shearing forces involved. Many studies have identified concussion as the most common type of injury in all of youth hockey.26 Concussions account for up to 19% of all injuries in men’s collegiate hockey.3
Concussion can be challenging to diagnose on the ice. The most important factor in concussion management is symptom reporting by the athlete.27 Despite significant efforts in education and awareness, student athletes, especially hockey players, withhold reporting a possible concussion.28 Reasons for underreporting include fear of letting down other players and coaches, thinking the injury is not severe enough to warrant evaluation, and fear of losing standing with the current team or future teams.28
As postinjury concussion assessments are ideal when comparisons can be made with preseason (baseline) scores, preseason testing is becoming standard in professional, college, junior, and high school hockey. This testing involves the Sport Concussion Assessment Tool, 3rd edition (SCAT3), and the King-Devick (K-D) test.30,31 Some youth leagues have baseline testing as well, though the frequency of baseline testing in their players is controversial,32 as the adolescent mind’s processing speed and memory increase exponentially.33 For these younger athletes, it may be necessary to perform baseline testing more frequently than annually.32 A physician can use baseline test results to help diagnose a concussion at the rink and then track the athlete’s recovery and help with return-to-play decisions.29 Vision involves almost half of the brain’s circuits,34 including areas vulnerable to head impact. A neuro-ophthalmologic test can assess for irregularities in accommodation, convergence, ocular muscle balance, pursuit, and saccades.29 The K-D test is a visual performance examination that allows easy and objective assessment of eye movements. Use of both the K-D test and the SCAT3 at the rink may increase the number of concussions detected.29,35 We recommend that physicians use both tests to assess for concussion at the hockey rink.
Initial treatment involves a period of physical rest and relative cognitive rest. Acute worsening of symptoms warrants urgent imaging to rule out a subdural or subarachnoid bleed. Once a player is symptom-free, a graded return-to-play protocol should be followed (Table 4).
On the prevention side, great efforts have been made to improve hockey helmets. (Some manufacturers claim to have made concussion-proof helmets, but there is no evidence supporting this claim.6) Numerous investigators have reported a lower overall injury rate in players who wear a helmet and a full-face shield.6,13 In addition, rule changes aimed at decreasing head contact have been implemented to decrease the incidence of sport-related concussions.36 Moreover, education on proper helmet use and wear should be emphasized. A study of the effects of hockey helmet fit on cervical motion found that 7 (39%) of 18 players wore a game or competition helmet so loosely that it could be removed without unbuttoning its chinstrap.37 Improperly worn helmets cannot prevent injury as well as properly worn helmets can.
Cervical Spine Injuries
Whereas American football is associated with a higher annual number of nonfatal catastrophic neck injuries, hockey has a 3 to 6 times higher incidence of cervical spine injuries and spinal cord damage.38,39 A Canadian Ice Hockey Spinal Injuries Registry review of the period 2006 to 2011 identified 44 cervical spine injuries, 7.3 per year on average.40 Severe injury, defined as complete motor and sensory loss, complete motor loss and incomplete sensory, or complete motor loss, occurred in 4 (9.1%) of the 44 injured players. In hockey, a major mechanism of cervical spine injury is an axial load to the slightly flexed spine.39 Of 355 hockey-related cervical spine injuries in a Canada study, 95 (35.5%) were caused by a check from behind.40,41 The Canadian neurosurgeons’ work led to rule changes prohibiting checks from behind, and this prohibition has reduced the incidence of cervical spine injuries in ice hockey.38,40
Team physicians should be comfortable managing serious neck and spine injuries on the ice. Initial evaluation should follow the standard ABCs (airway, breathing, circulation). The physician places a hand on each side of the head to stabilize the neck until the initial examination is complete. The goal is to minimize cervical spine motion until transportation to the hospital for advanced imaging and definitive treatment.37 The decision to remove or leave on the helmet is now controversial. Hockey helmets differ from football helmets in that their chinstraps do not afford significant cervical stabilization, and the helmets have less padding and cover less of the head; in addition, a shockingly high percentage of hockey players do not wear properly fitting helmets.37 In one study, 3-dimensional motion analysis of a hockey player during the logroll technique showed less transverse and sagittal cervical plane motion with the helmet removed than with the helmet (properly fitting or not) in place; the authors recommended removing the helmet to limit extraneous cervical spine motion during the technique.37 However, 2 other studies found that helmet removal can result in significantly increased cervical spine motion of the immobilized hockey player.42,43Recommendation 4 of the recently released interassociation consensus statement of the National Athletic Trainers’ Association reads, “Protective athletic equipment should be removed before transport to an emergency facility for an athlete-patient with suspected cervical spine instability.”44 This represents a shift from leaving the helmet and shoulder pads in place. For ice hockey players with suspected cervical spine injury, more research is needed on cervical motion during the entire sequence—partial logrolls, spine-boarding, placement of cervical collar before or after logroll, and different immobilization techniques for transport.37
The athlete must be carefully transferred to a spine board with either logroll or lift-and-slide. Although an extrication cervical collar can be placed before the spine board is placed, the effectiveness of this collar in executing the spine-board transfer is not proven.45 When the player is on the spine board, the head can be secured with pads and straps en route to the hospital.
Return-to-Play Criteria for Cervical Spine Injuries There is no clear consensus on return-to-play guidelines for cervical spine injuries in athletes.46
Shoulder Injuries
For hockey players, the upper extremity traditionally has been considered a well-protected area.48 However, shoulder pads are considerably more flexible in hockey than in football and other collision sports. In addition, hockey gloves allow a fair amount of motion for stick handling, and the wrist may be in maximal flexion or extension when a hit against the boards or the ice occurs. Open-ice checking, board collisions, and hockey stick use have been postulated as reasons for the high incidence of upper extremity injuries in hockey. Researchers in Finland found that upper extremity injuries accounted for up to 31% of all hockey injuries.49 More than 50% of these injuries resulted from checking or board collisions. Furthermore, study findings highlighted a low rate of injury in younger players and indicated the rate increases with age.49,50
In hockey players, the acromioclavicular (AC) joint is the most commonly injured shoulder structure.51 The mechanism of injury can be a board collision or an open-ice hit, but most often is a direct blow to the shoulder. The collision disrupts the AC joint and can sprain or tear the coracoclavicular ligaments. The Rockwood classification is used to categorize AC joint injuries (Figure 2).
Initial management involves icing the AC joint and placing a sling for comfort. Type I and type II injuries can be managed with progressive range-of-motion (ROM) exercises, strengthening, cryotherapy, and a period of rest. Treatment of type III injuries remains controversial,52 but in hockey players these injuries are almost always treated nonoperatively. Return to play requires full motion, normal strength, and minimal discomfort. Players return a few days to 2 weeks after a grade I injury; recovery from grade II injuries may take 2 to 3 weeks, and recovery from grade III injuries, 6 to 12 weeks. Surgical treatment is usually required in type IV and type V injuries, but we have had experience treating these injuries nonoperatively in high-level players. AC joint reinjury in hockey players is common, and surgical treatment should be approached cautiously, as delayed fracture after return to sport has been reported.53 Special precautions should be taken in collision athletes who undergo AC joint reconstruction. In the anatomical reconstruction described by Carofino and Mazzocca,54 2 holes are drilled in the clavicle; these holes are a potential source of fracture when the collision athlete returns to sport (Figure 3).
Clavicle fracture is another common hockey injury.55 Studies have shown clavicle fractures proportionally occur most often in people 15 to 19 years old.49 The injury presents with pain and deformity over the clavicle; in more severe fractures, skin tenting is identified. Initial management of suspected clavicle fracture includes cryotherapy, sling, and radiographs. Radiographs should include an AP view and then a 45° cephalad view, which eliminates overshadowing from the ribs. Most clavicle fractures are successfully managed nonoperatively, though there is evidence that significantly displaced or comminuted fractures have better union rates and shoulder function when treated with open reduction and internal fixation.56 After a clavicle fracture, return to skating and noncontact practice usually takes 8 weeks, with return to full contact occurring around 12 weeks.
Sternoclavicular injuries are relatively uncommon, but potentially serious. Special attention should also be given to adolescent athletes with sternoclavicular pain. Although sternoclavicular dislocations have been reported in hockey players, instead these likely are fractures involving the medial clavicle physis.57
The shoulder is the most commonly dislocated major joint, and the incidence of shoulder dislocation in elite hockey players is 8% to 21%.50,58 Anterior shoulder instability occurs from a fall with the shoulder in an abducted, externally rotated and extended position or from a direct anteriorly placed impact to the posterior shoulder. We recommend taking players off the ice for evaluation. Depending on physician comfort, the shoulder can be reduced in the training room, and the athlete sent for radiographs after reduction. If resources or support for closed reduction is not available at the rink, the athlete should be sent to the ED. Initial radiographic evaluation of a player with shoulder injury begins with plain radiographs, including a true AP (Grashey) view with the humerus in neutral, internal, and external rotation and an axillary view. The axillary radiograph is crucial in determining anterior or posterior dislocation. If the patient cannot tolerate the pain associated with having an axillary radiograph taken, a Velpeau radiograph can be used. This radiograph is taken with the patient’s arm in a sling and with the patient leaning back 30° while the x-ray beam is directed superior to inferior.
CT is performed for a suspected osseous injury. CT is more accurate than plain radiographs in showing glenoid and humeral fractures in the acute setting as well as the amount of bone loss in the case of chronic instability. Magnetic resonance arthrography is the imaging modality of choice for the diagnoses of capsulolabral injury.
After shoulder reduction, treatment with a sling, cryotherapy, and a nonsteroidal anti-inflammatory drug is initiated. In a Minnesota study of nonoperative management of shoulder instability, 9 of 10 hockey players were able to return to play the same season, and 6 of the 10 required surgery at the end of the season.59
Compared with noncontact athletes, hockey players and other collision athletes are at increased risk for recurrence.60-62 For collision athletes who want to continue playing their sport after recurrent instability, surgery is recommended. A shoulder instability study in Toronto found that more than 54% of 24 professional hockey players had associated Hill-Sachs lesions, but only 3 shoulders (12.5%) had glenoid defects.50 Arthroscopic and open techniques both demonstrate good results, and identification of bone loss can help determine which surgery to recommend.63 Hockey players can usually return to sport 6 months after shoulder stabilization.
Another important consideration in managing shoulder instability in hockey players is shoulder dominance, which determines stick grip. A left-handed player places the right hand on top of the stick for support, but most of the motion associated with shooting the puck—including abduction and external rotation—occurs with the left shoulder. Thus, a left-handed player with a history of previous left-side shoulder dislocation may dislocate with each shot, but a right-handed player with left shoulder instability may have considerably less trouble on the ice.58Shoulder and rotator cuff contusions (RCCs) occur in hockey and other collision sports.49,64 RCCs almost always result from a direct blow to the shoulder, and present with shoulder function loss, weakness, and pain.
Summary
Hockey is a high-speed collision sport with one of the highest injury rates among all sports. Physicians caring for youth, amateur, and senior hockey teams see a range of acute head, neck, and shoulder injuries. Although treatment of eye injuries, dental injuries, and concussions is not always considered orthopedic care, an orthopedic surgeon who is covering hockey needs to be comfortable managing these injuries acutely. Quality rink-side care minimizes the impact of the injury, maximizes the functional result, and expedites the safe return of the injured player back to the ice.
Am J Orthop. 2017;46(3):123-134. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- Hockey is a high-speed collision sport with one of the highest injury rates among all sports.
- Use of a helmet with visors or full-face shields significantly reduces the risk for eye injury.
- Broken portions of teeth should be found and placed in a protective medium such as saline, saliva, or milk for transport.
- A player with unresolved concussion symptoms should not be allowed to return to the ice.
- Shoulder dominance, which determines stick grip, is an important consideration in the treatment of shoulder instability in an ice hockey player.
On a surface of ice in Windsor, Nova Scotia in the middle of the 19th century, the modern game of ice hockey evolved.1 A blend of hurley, a Gaelic sport, and lacrosse, from the native Mi’kmaq culture, the sport of ice hockey gained rapidly in popularity throughout Canada and is now the country’s national sport. Hockey quickly spread to the United States and then Europe. It is presently played in 77 countries across the world.2
Hockey players can reach speeds of up to 48 km (~30 miles) per hour on razor-sharp skates on an ice surface surrounded by rigid plastic composite boards topped with plexiglass.3 They use sticks made of wood, aluminum, or a composite material to advance a 6-ounce vulcanized rubber puck on the opposing goal, and this puck sometimes reaches speeds over 160 km (~100 miles) per hour. Older, male players are allowed to make physical contact with their opposing counterparts to separate them from the puck (body-checking). Not surprisingly, the potential risk for injury in hockey is high. At the 2010 Winter Olympics, men’s ice hockey players had the highest rate of injury of any other competitors there—more than 30% were affected.4
Hockey is played and enjoyed by athletes ranging widely in age. Youth hockey leagues accept players as young as 5 years. Hockey can become a lifelong recreational activity. In North America, old timers’ leagues have many players up to age 70 years.6 According to International Ice Hockey Federation data for 2016, more than 543,000 and 639,500 people play hockey in the United States and Canada, respectively.2 Most of the rules, protective equipment, skates, ice surfaces, and goal sizes are the same in men’s and women’s hockey.7 The major difference is in body-checking—this practice is not allowed at any age in women’s ice hockey.
In this article, we review the evaluation and management of common head, neck, and shoulder hockey injuries for physicians who provide medical support and coverage for youth, amateur, and senior hockey teams.
Evaluation and Management of Common Hockey Injuries
Eye Injuries
Although eye injuries are less common than musculoskeletal injuries and concussions in hockey, they are a serious risk for recreational and competitive players alike. Furthermore, recovery may be difficult, and eye injuries can have serious lifelong consequences.8 In hockey, the most commonly reported eye injuries are periorbital contusions and lacerations, hyphema, corneal and conjunctival abrasions, orbital fractures, and ruptured globes (Table 2).9,10
As a contact sport, hockey often involves high-impact, blunt-force trauma. The trauma in hockey results from collisions with other players, the boards, hockey sticks, and pucks. It is therefore not surprising that the most common ocular injuries in this sport are periorbital contusions. Although most contusions cause only mild swelling and ecchymosis of the soft tissues around the eye, there is potential for serious consequences. In a Scandinavia study, Leivo and colleagues10 found that 9% of patients who sustained a periocular contusion also had a clinically significant secondary diagnosis, such as retinal tear or hemorrhage, eyelid laceration, vitreous hemorrhage, or retinal detachment. Although the study was hospital-based, and therefore biased toward more severe cases, its findings highlight the potential severity of eye injuries in hockey. Furthermore, the study found that the majority of players who sustained blunt trauma to the eye itself required lifelong follow-up because of increased risk for glaucoma. This is particularly true for hyphema, as this finding indicates significant damage to intraocular tissues.10Players can also sustain fractures of the orbital bones, including orbital blowout fractures. Typical signs and symptoms of blowout fractures include diplopia, proptosis or enophthalmos, infraorbital hypoesthesia, painful and decreased extraocular movement (particularly upgaze), and palpable crepitance caused by sinus air entering the lower eyelid.11 If orbital fracture is suspected, as it should be in any case in which the injured player experiences pain with eye movement or diplopia, the player should be referred to the ED for computed tomography (CT) and ophthalmologic evaluation.12 Continued participation seriously risks making the injury much worse, particularly should another impact occur. In addition, given the impact needed to cause orbital fractures, consideration must be given to the potential for a coexisting concussion injury.
Severe direct trauma to the eye—from a puck, a stick, or a fist—can result in a ruptured globe, a particularly serious injury that requires immediate surgical attention. Signs and symptoms of a ruptured globe are rarely subtle, but associated eyelid swelling or laceration may obscure the injury, delaying proper diagnosis and treatment. More obvious signs include severely reduced vision, hemorrhagic chemosis (swelling) of the conjunctiva, and an irregular or peaked pupil. If a rupture or any significant intraocular injury is suspected, it is crucial to avoid applying any pressure to the globe, as this can significantly worsen the damage to the intraocular tissues. Use of a helmet with protective shields and cages attached markedly reduces the risk for such injuries.13All eye injuries require prompt assessment, which allows for appropriate management and prevention of secondary damage.14 Initial evaluation of a patient with ocular trauma should begin with external examination for lacerations, swelling, or orbital rim step-off deformity. The physician should also check visual acuity in order to assess for significant vision impairment (counting fingers or reading a sign in the arena; confrontation visual fields). This should be done before attending to any periocular injuries, with the uninjured side serving as a control. Next, the physician should assess the extraocular eye movements as well as the size, shape, and reactivity of the pupils. Particular attention should be paid to detecting any deficit in extraocular movement or irregularity in pupil size, shape, or reactivity, as such findings are highly suggestive of serious injury to the globe.13 Hyphema (blood in anterior chamber of eye anterior to pupil) should be suspected if vision is reduced and the pupil cannot be clearly visualized. However, a bright red clot is not always apparent at time of injury or if the amount of blood is small. An irregular pupil, or a pupil that does not constrict well to light, is also a red flag for serious contusion injury to the eye, and requires ophthalmologic evaluation. It is important to keep in mind that blunt trauma severe enough to produce hyphema or an irregular and poorly reactive pupil is often associated with retinal damage as well, including retinal edema or detachment.
Minor injuries (eg, small foreign bodies, minor periocular contusions and lacerations) can often be managed rink-side. Foreign bodies not embedded in the cornea, but lodged under the upper eyelid, can sometimes be removed by everting the eyelid and sweeping with a moistened cotton swab or using diffuse, sterile saline irrigation.11 Corneal abrasions generally cause severe pain, photophobia, and tearing and are easily diagnosed with use of topical fluorescein and a blue light. A topical anesthetic can be extremely helpful in this setting, as it allows for proper pain-free evaluation, but should never be used in an ongoing manner for pain relief. Small lacerations of the brow can be sutured with 5-0 or 6-0 nylon or closed with 2-Octyl cyanoacrylate tissue adhesive (Dermabond). Eyelid lacerations, unless very small, are best managed by an ophthalmologist; care must be taken to rule out injury to the deeper orbital tissues and eye. If serious injury is suspected, or the eye cannot be appropriately evaluated, it should be stabilized and protected with a protective shield or plastic cup, and the player should be transferred to an ED for appropriate ophthalmologic evaluation.13Most eye injuries are accidental, caused by sticks or deflected pucks, but 18% are acquired in fights.8 Use of visors or full-face cages effectively minimizes the rate of eye injuries.8,13,15,16 In a cohort study of 282 elite amateur ice hockey players, the risk of eye injury was 4.7 times higher in players without face protection than in players who used half-face shields; there were no eye injuries in players who used full-face protection.13 For visors to prevent eye injury, they must be positioned to cover the eyes and the lower edge of the nose in all projections.10
Dental Injuries
The incidence and type of facial and dental injuries depend directly on the type of face protection used.11,17,18 In a study of face, head, and neck injuries in elite amateur ice hockey players, Stuart and colleagues13 found game-related injury rates of 158.9 per 1000 player-hours in players without face protection, 73.5 in players who used half-face shields, and 23.2 in players who used full-face shields. Players who wore full-face shields had facial, head, and neck injury rates of only 23.2 per 1000 player-game hours.13 Other studies clearly support the important role face shields play in lowering injury risk in hockey. Face and head injuries account for 20% to 40% of all hockey-related injuries,3,16,19 and dental injuries up to 11.5%.20 In a study from Finland, Lahti and colleagues19 found that over a 2-year period, 479 hockey players sustained injuries, including 650 separate dental injuries. The most commonly diagnosed dental injury was an uncomplicated crown fracture, and the most common cause was a hit with a hockey stick, which accounted for 52.7% and 40.3% of dental injuries in games and practices, respectively.19
In the management of dental fractures, the broken portions of teeth should be found and placed in a transportation-protective medium, such as saline, saliva, or milk,16 which can improve functional and esthetic replacement outcomes.21,22 Loose pieces of teeth should not be left in the player’s mouth. The residual tooth should be stabilized and exposure to air and occlusion limited. Dental fractures can affect the enamel, the enamel and dentin structures (uncomplicated fracture), or enamel, dentin, and pulp (complicated).23 Fractures involving only the enamel do not require urgent dental evaluation. Dentin or pulp involvement may cause temperature and air sensitivity.23 If a tooth is air-sensitive, the player should be referred to a specialist immediately.11
Direct trauma can cause instability without displacement (subluxation) or complete displacement of the tooth from its alveolar socket (avulsion).23 An avulsed tooth should be handled by the crown to avoid further damage to the root and periodontal ligament.16,24 The tooth should be rinsed gently with saline and reimplanted in its socket, ideally within 5 to 10 minutes,23with the athlete biting down gently on gauze to hold the tooth in place. A 1-mL supraperiosteal infiltration of 1% or 2% lidocaine hydrochloride (1:100,000 epinephrine) can be given into the apex of the tooth being anesthetized (Figure 1).
Concussions
A concussion is a “complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.”25 Concussion is largely a functional disturbance instead of a structural injury, owing to the rotational and/or shearing forces involved. Many studies have identified concussion as the most common type of injury in all of youth hockey.26 Concussions account for up to 19% of all injuries in men’s collegiate hockey.3
Concussion can be challenging to diagnose on the ice. The most important factor in concussion management is symptom reporting by the athlete.27 Despite significant efforts in education and awareness, student athletes, especially hockey players, withhold reporting a possible concussion.28 Reasons for underreporting include fear of letting down other players and coaches, thinking the injury is not severe enough to warrant evaluation, and fear of losing standing with the current team or future teams.28
As postinjury concussion assessments are ideal when comparisons can be made with preseason (baseline) scores, preseason testing is becoming standard in professional, college, junior, and high school hockey. This testing involves the Sport Concussion Assessment Tool, 3rd edition (SCAT3), and the King-Devick (K-D) test.30,31 Some youth leagues have baseline testing as well, though the frequency of baseline testing in their players is controversial,32 as the adolescent mind’s processing speed and memory increase exponentially.33 For these younger athletes, it may be necessary to perform baseline testing more frequently than annually.32 A physician can use baseline test results to help diagnose a concussion at the rink and then track the athlete’s recovery and help with return-to-play decisions.29 Vision involves almost half of the brain’s circuits,34 including areas vulnerable to head impact. A neuro-ophthalmologic test can assess for irregularities in accommodation, convergence, ocular muscle balance, pursuit, and saccades.29 The K-D test is a visual performance examination that allows easy and objective assessment of eye movements. Use of both the K-D test and the SCAT3 at the rink may increase the number of concussions detected.29,35 We recommend that physicians use both tests to assess for concussion at the hockey rink.
Initial treatment involves a period of physical rest and relative cognitive rest. Acute worsening of symptoms warrants urgent imaging to rule out a subdural or subarachnoid bleed. Once a player is symptom-free, a graded return-to-play protocol should be followed (Table 4).
On the prevention side, great efforts have been made to improve hockey helmets. (Some manufacturers claim to have made concussion-proof helmets, but there is no evidence supporting this claim.6) Numerous investigators have reported a lower overall injury rate in players who wear a helmet and a full-face shield.6,13 In addition, rule changes aimed at decreasing head contact have been implemented to decrease the incidence of sport-related concussions.36 Moreover, education on proper helmet use and wear should be emphasized. A study of the effects of hockey helmet fit on cervical motion found that 7 (39%) of 18 players wore a game or competition helmet so loosely that it could be removed without unbuttoning its chinstrap.37 Improperly worn helmets cannot prevent injury as well as properly worn helmets can.
Cervical Spine Injuries
Whereas American football is associated with a higher annual number of nonfatal catastrophic neck injuries, hockey has a 3 to 6 times higher incidence of cervical spine injuries and spinal cord damage.38,39 A Canadian Ice Hockey Spinal Injuries Registry review of the period 2006 to 2011 identified 44 cervical spine injuries, 7.3 per year on average.40 Severe injury, defined as complete motor and sensory loss, complete motor loss and incomplete sensory, or complete motor loss, occurred in 4 (9.1%) of the 44 injured players. In hockey, a major mechanism of cervical spine injury is an axial load to the slightly flexed spine.39 Of 355 hockey-related cervical spine injuries in a Canada study, 95 (35.5%) were caused by a check from behind.40,41 The Canadian neurosurgeons’ work led to rule changes prohibiting checks from behind, and this prohibition has reduced the incidence of cervical spine injuries in ice hockey.38,40
Team physicians should be comfortable managing serious neck and spine injuries on the ice. Initial evaluation should follow the standard ABCs (airway, breathing, circulation). The physician places a hand on each side of the head to stabilize the neck until the initial examination is complete. The goal is to minimize cervical spine motion until transportation to the hospital for advanced imaging and definitive treatment.37 The decision to remove or leave on the helmet is now controversial. Hockey helmets differ from football helmets in that their chinstraps do not afford significant cervical stabilization, and the helmets have less padding and cover less of the head; in addition, a shockingly high percentage of hockey players do not wear properly fitting helmets.37 In one study, 3-dimensional motion analysis of a hockey player during the logroll technique showed less transverse and sagittal cervical plane motion with the helmet removed than with the helmet (properly fitting or not) in place; the authors recommended removing the helmet to limit extraneous cervical spine motion during the technique.37 However, 2 other studies found that helmet removal can result in significantly increased cervical spine motion of the immobilized hockey player.42,43Recommendation 4 of the recently released interassociation consensus statement of the National Athletic Trainers’ Association reads, “Protective athletic equipment should be removed before transport to an emergency facility for an athlete-patient with suspected cervical spine instability.”44 This represents a shift from leaving the helmet and shoulder pads in place. For ice hockey players with suspected cervical spine injury, more research is needed on cervical motion during the entire sequence—partial logrolls, spine-boarding, placement of cervical collar before or after logroll, and different immobilization techniques for transport.37
The athlete must be carefully transferred to a spine board with either logroll or lift-and-slide. Although an extrication cervical collar can be placed before the spine board is placed, the effectiveness of this collar in executing the spine-board transfer is not proven.45 When the player is on the spine board, the head can be secured with pads and straps en route to the hospital.
Return-to-Play Criteria for Cervical Spine Injuries There is no clear consensus on return-to-play guidelines for cervical spine injuries in athletes.46
Shoulder Injuries
For hockey players, the upper extremity traditionally has been considered a well-protected area.48 However, shoulder pads are considerably more flexible in hockey than in football and other collision sports. In addition, hockey gloves allow a fair amount of motion for stick handling, and the wrist may be in maximal flexion or extension when a hit against the boards or the ice occurs. Open-ice checking, board collisions, and hockey stick use have been postulated as reasons for the high incidence of upper extremity injuries in hockey. Researchers in Finland found that upper extremity injuries accounted for up to 31% of all hockey injuries.49 More than 50% of these injuries resulted from checking or board collisions. Furthermore, study findings highlighted a low rate of injury in younger players and indicated the rate increases with age.49,50
In hockey players, the acromioclavicular (AC) joint is the most commonly injured shoulder structure.51 The mechanism of injury can be a board collision or an open-ice hit, but most often is a direct blow to the shoulder. The collision disrupts the AC joint and can sprain or tear the coracoclavicular ligaments. The Rockwood classification is used to categorize AC joint injuries (Figure 2).
Initial management involves icing the AC joint and placing a sling for comfort. Type I and type II injuries can be managed with progressive range-of-motion (ROM) exercises, strengthening, cryotherapy, and a period of rest. Treatment of type III injuries remains controversial,52 but in hockey players these injuries are almost always treated nonoperatively. Return to play requires full motion, normal strength, and minimal discomfort. Players return a few days to 2 weeks after a grade I injury; recovery from grade II injuries may take 2 to 3 weeks, and recovery from grade III injuries, 6 to 12 weeks. Surgical treatment is usually required in type IV and type V injuries, but we have had experience treating these injuries nonoperatively in high-level players. AC joint reinjury in hockey players is common, and surgical treatment should be approached cautiously, as delayed fracture after return to sport has been reported.53 Special precautions should be taken in collision athletes who undergo AC joint reconstruction. In the anatomical reconstruction described by Carofino and Mazzocca,54 2 holes are drilled in the clavicle; these holes are a potential source of fracture when the collision athlete returns to sport (Figure 3).
Clavicle fracture is another common hockey injury.55 Studies have shown clavicle fractures proportionally occur most often in people 15 to 19 years old.49 The injury presents with pain and deformity over the clavicle; in more severe fractures, skin tenting is identified. Initial management of suspected clavicle fracture includes cryotherapy, sling, and radiographs. Radiographs should include an AP view and then a 45° cephalad view, which eliminates overshadowing from the ribs. Most clavicle fractures are successfully managed nonoperatively, though there is evidence that significantly displaced or comminuted fractures have better union rates and shoulder function when treated with open reduction and internal fixation.56 After a clavicle fracture, return to skating and noncontact practice usually takes 8 weeks, with return to full contact occurring around 12 weeks.
Sternoclavicular injuries are relatively uncommon, but potentially serious. Special attention should also be given to adolescent athletes with sternoclavicular pain. Although sternoclavicular dislocations have been reported in hockey players, instead these likely are fractures involving the medial clavicle physis.57
The shoulder is the most commonly dislocated major joint, and the incidence of shoulder dislocation in elite hockey players is 8% to 21%.50,58 Anterior shoulder instability occurs from a fall with the shoulder in an abducted, externally rotated and extended position or from a direct anteriorly placed impact to the posterior shoulder. We recommend taking players off the ice for evaluation. Depending on physician comfort, the shoulder can be reduced in the training room, and the athlete sent for radiographs after reduction. If resources or support for closed reduction is not available at the rink, the athlete should be sent to the ED. Initial radiographic evaluation of a player with shoulder injury begins with plain radiographs, including a true AP (Grashey) view with the humerus in neutral, internal, and external rotation and an axillary view. The axillary radiograph is crucial in determining anterior or posterior dislocation. If the patient cannot tolerate the pain associated with having an axillary radiograph taken, a Velpeau radiograph can be used. This radiograph is taken with the patient’s arm in a sling and with the patient leaning back 30° while the x-ray beam is directed superior to inferior.
CT is performed for a suspected osseous injury. CT is more accurate than plain radiographs in showing glenoid and humeral fractures in the acute setting as well as the amount of bone loss in the case of chronic instability. Magnetic resonance arthrography is the imaging modality of choice for the diagnoses of capsulolabral injury.
After shoulder reduction, treatment with a sling, cryotherapy, and a nonsteroidal anti-inflammatory drug is initiated. In a Minnesota study of nonoperative management of shoulder instability, 9 of 10 hockey players were able to return to play the same season, and 6 of the 10 required surgery at the end of the season.59
Compared with noncontact athletes, hockey players and other collision athletes are at increased risk for recurrence.60-62 For collision athletes who want to continue playing their sport after recurrent instability, surgery is recommended. A shoulder instability study in Toronto found that more than 54% of 24 professional hockey players had associated Hill-Sachs lesions, but only 3 shoulders (12.5%) had glenoid defects.50 Arthroscopic and open techniques both demonstrate good results, and identification of bone loss can help determine which surgery to recommend.63 Hockey players can usually return to sport 6 months after shoulder stabilization.
Another important consideration in managing shoulder instability in hockey players is shoulder dominance, which determines stick grip. A left-handed player places the right hand on top of the stick for support, but most of the motion associated with shooting the puck—including abduction and external rotation—occurs with the left shoulder. Thus, a left-handed player with a history of previous left-side shoulder dislocation may dislocate with each shot, but a right-handed player with left shoulder instability may have considerably less trouble on the ice.58Shoulder and rotator cuff contusions (RCCs) occur in hockey and other collision sports.49,64 RCCs almost always result from a direct blow to the shoulder, and present with shoulder function loss, weakness, and pain.
Summary
Hockey is a high-speed collision sport with one of the highest injury rates among all sports. Physicians caring for youth, amateur, and senior hockey teams see a range of acute head, neck, and shoulder injuries. Although treatment of eye injuries, dental injuries, and concussions is not always considered orthopedic care, an orthopedic surgeon who is covering hockey needs to be comfortable managing these injuries acutely. Quality rink-side care minimizes the impact of the injury, maximizes the functional result, and expedites the safe return of the injured player back to the ice.
Am J Orthop. 2017;46(3):123-134. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Vaughan G. The Puck Starts Here: The Origin of Canada’s Great Winter Game, Ice Hockey. Fredericton, Canada: Goose Lane Editions; 1996.
2. IIHF member national associations. International Ice Hockey Federation website. http://www.iihf.com/iihf-home/the-iihf/members. Accessed April 6, 2017.
3. Flik K, Lyman S, Marx RG. American collegiate men’s ice hockey: an analysis of injuries. Am J Sports Med. 2005;33(2):183-187.
4. Engebretsen L, Steffen K, Alonso JM, et al. Sports injuries and illnesses during the Winter Olympic Games 2010. Br J Sports Med. 2010;44(11):772-780.
5. Deits J, Yard EE, Collins CL, Fields SK, Comstock RD. Patients with ice hockey injuries presenting to US emergency departments, 1990-2006. J Athl Train. 2010;45(5):467-474.
6. Brooks A, Loud KJ, Brenner JS, et al. Reducing injury risk from body checking in boys’ youth ice hockey. Pediatrics. 2014;133(6):1151-1157.
7. Agel J, Harvey EJ. A 7-year review of men’s and women’s ice hockey injuries in the NCAA. Can J Surg. 2010;53(5):319-323.
8. Micieli JA, Zurakowski D, Ahmed, II. Impact of visors on eye and orbital injuries in the National Hockey League. Can J Ophthalmol. 2014;49(3):243-248.
9. Pashby TJ. Ocular injuries in hockey. Int Ophthalmol Clin. 1988;28(3):228-231.
10. Leivo T, Haavisto AK, Sahraravand A. Sports-related eye injuries: the current picture. Acta Ophthalmol. 2015;93(3):224-231.
11. Cohn RM, Alaia MJ, Strauss EJ, Feldman AF. Rink-side management of ice hockey related injuries to the face, neck, and chest. Bull Hosp Jt Dis. 2013;71(4):253-256.
12. Reehal P. Facial injury in sport. Curr Sports Med Rep. 2010;9(1):27-34.
13. Stuart MJ, Smith AM, Malo-Ortiguera SA, Fischer TL, Larson DR. A comparison of facial protection and the incidence of head, neck, and facial injuries in Junior A hockey players. A function of individual playing time. Am J Sports Med. 2002;30(1):39-44.
14. MacEwen CJ, McLatchie GR. Eye injuries in sport. Scott Med J. 2010;55(2):22-24.
15. Stevens ST, Lassonde M, de Beaumont L, Keenan JP. The effect of visors on head and facial injury in National Hockey League players. J Sci Med Sport. 2006;9(3):238-242.
16. Moslener MD, Wadsworth LT. Ice hockey: a team physician’s perspective. Curr Sports Med Rep. 2010;9(3):134-138.
17. LaPrade RF, Burnett QM, Zarzour R, Moss R. The effect of the mandatory use of face masks on facial lacerations and head and neck injuries in ice hockey. A prospective study. Am J Sports Med. 1995;23(6):773-775.
18. Benson BW, Mohtadi NG, Rose MS, Meeuwisse WH. Head and neck injuries among ice hockey players wearing full face shields vs half face shields. JAMA. 1999;282(24):2328-2332.
19. Lahti H, Sane J, Ylipaavalniemi P. Dental injuries in ice hockey games and training. Med Sci Sports Exerc. 2002;34(3):400-402.
20. Sane J, Ylipaavalniemi P, Leppanen H. Maxillofacial and dental ice hockey injuries. Med Sci Sports Exerc. 1988;20(2):202-207.
21. Emerich K, Kaczmarek J. First aid for dental trauma caused by sports activities: state of knowledge, treatment and prevention. Sports Med. 2010;40(5):361-366.
22. Rosenberg H, Rosenberg H, Hickey M. Emergency management of a traumatic tooth avulsion. Ann Emerg Med. 2011;57(4):375-377.
23. Young EJ, Macias CR, Stephens L. Common dental injury management in athletes. Sports Health. 2015;7(3):250-255.
24. Andersson L, Andreasen JO, Day P, et al. International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 2. Avulsion of permanent teeth. Dent Traumatol. 2012;28(2):88-96.
25. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Clin J Sport Med. 2009;19(3):185-200.
26. Schneider KJ, Meeuwisse WH, Kang J, Schneider GM, Emery CA. Preseason reports of neck pain, dizziness, and headache as risk factors for concussion in male youth ice hockey players. Clin J Sport Med. 2013;23(4):267-272.
27. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Br J Sports Med. 2013;47(5):250-258.
28. Delaney JS, Lamfookon C, Bloom GA, Al-Kashmiri A, Correa JA. Why university athletes choose not to reveal their concussion symptoms during a practice or game. Clin J Sport Med. 2015;25(2):113-125.
29. Ventura RE, Balcer LJ, Galetta SL. The concussion toolbox: the role of vision in the assessment of concussion. Semin Neurol. 2015;35(5):599-606.
30. Vartiainen MV, Holm A, Peltonen K, Luoto TM, Iverson GL, Hokkanen L. King-Devick test normative reference values for professional male ice hockey players. Scand J Med Sci Sports. 2015;25(3):e327-e330.
31. Galetta MS, Galetta KM, McCrossin J, et al. Saccades and memory: baseline associations of the King-Devick and SCAT2 SAC tests in professional ice hockey players. J Neurol Sci. 2013;328(1-2):28-31.
32. Vernau BT, Grady MF, Goodman A, et al. Oculomotor and neurocognitive assessment of youth ice hockey players: baseline associations and observations after concussion. Dev Neuropsychol. 2015;40(1):7-11.
33. Fry AF, Hale S. Relationships among processing speed, working memory, and fluid intelligence in children. Biol Psychol. 2000;54(1-3):1-34.
34. Felleman DJ, Van Essen DC. Distributed hierarchical processing in the primate cerebral cortex. Cereb Cortex. 1991;1(1):1-47.
35. Guskiewicz KM, Register-Mihalik J, McCrory P, et al. Evidence-based approach to revising the SCAT2: introducing the SCAT3. Br J Sports Med. 2013;47(5):289-293.
36. Smith AM, Stuart MJ, Dodick DW, et al. Ice Hockey Summit II: zero tolerance for head hits and fighting. Curr Sports Med Rep. 2015;14(2):135-144.
37. Mihalik JP, Beard JR, Petschauer MA, Prentice WE, Guskiewicz KM. Effect of ice hockey helmet fit on cervical spine motion during an emergency log roll procedure. Clin J Sport Med. 2008;18(5):394-398.
38. Banerjee R, Palumbo MA, Fadale PD. Catastrophic cervical spine injuries in the collision sport athlete, part 1: epidemiology, functional anatomy, and diagnosis. Am J Sports Med. 2004;32(4):1077-1087.
39. Reynen PD, Clancy WG Jr. Cervical spine injury, hockey helmets, and face masks. Am J Sports Med. 1994;22(2):167-170.
40. Tator CH, Provvidenza C, Cassidy JD. Update and overview of spinal injuries in Canadian ice hockey, 1943 to 2011: the continuing need for injury prevention and education. Clin J Sport Med. 2016;26(3):232-238.
41. Tator CH, Edmonds VE, Lapczak L, Tator IB. Spinal injuries in ice hockey players, 1966-1987. Can J Surg. 1991;34(1):63-69.
42. Laprade RF, Schnetzler KA, Broxterman RJ, Wentorf F, Gilbert TJ. Cervical spine alignment in the immobilized ice hockey player. A computed tomographic analysis of the effects of helmet removal. Am J Sports Med. 2000;28(6):800-803.
43. Metz CM, Kuhn JE, Greenfield ML. Cervical spine alignment in immobilized hockey players: radiographic analysis with and without helmets and shoulder pads. Clin J Sport Med. 1998;8(2):92-95.
44. National Athletic Trainers’ Association. Appropriate prehospital management of the spine-injured athlete: updated from 1998 document. http://www.nata.org/sites/default/files/Executive-Summary-Spine-Injury-updated.pdf. Updated August 5, 2015. Accessed April 6, 2017.
45. Del Rossi G, Heffernan TP, Horodyski M, Rechtine GR. The effectiveness of extrication collars tested during the execution of spine-board transfer techniques. Spine J. 2004;4(6):619-623.
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47. Huang P, Anissipour A, McGee W, Lemak L. Return-to-play recommendations after cervical, thoracic, and lumbar spine injuries: a comprehensive review. Sports Health. 2016;8(1):19-25.
48. Shindle MK, Marx RG, Kelly BT, Bisson L, Burke CJ 3rd. Hockey injuries: a pediatric sport update. Curr Opin Pediatr. 2010;22(1):54-60.
49. Molsa J, Kujala U, Myllynen P, Torstila I, Airaksinen O. Injuries to the upper extremity in ice hockey: analysis of a series of 760 injuries. Am J Sports Med. 2003;31(5):751-757.
50. Dwyer T, Petrera M, Bleakney R, Theodoropoulos JS. Shoulder instability in ice hockey players: incidence, mechanism, and MRI findings. Clin Sports Med. 2013;32(4):803-813.
51. LaPrade RF, Wijdicks CA, Griffith CJ. Division I intercollegiate ice hockey team coverage. Br J Sports Med. 2009;43(13):1000-1005.
52. Willimon SC, Gaskill TR, Millett PJ. Acromioclavicular joint injuries: anatomy, diagnosis, and treatment. Phys Sportsmed. 2011;39(1):116-122.
53. Martetschlager F, Horan MP, Warth RJ, Millett PJ. Complications after anatomic fixation and reconstruction of the coracoclavicular ligaments. Am J Sports Med. 2013;41(12):2896-2903.
54. Carofino BC, Mazzocca AD. The anatomic coracoclavicular ligament reconstruction: surgical technique and indications. J Shoulder Elbow Surg. 2010;19(2 suppl):37-46.
55. Laprade RF, Surowiec RK, Sochanska AN, et al. Epidemiology, identification, treatment and return to play of musculoskeletal-based ice hockey injuries. Br J Sports Med. 2014;48(1):4-10.
56. Canadian Orthopaedic Trauma Society. Nonoperative treatment compared with plate fixation of displaced midshaft clavicular fractures. A multicenter, randomized clinical trial. J Bone Joint Surg Am. 2007;89(1):1-10.
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58. Hovelius L. Shoulder dislocation in Swedish ice hockey players. Am J Sports Med. 1978;6(6):373-377.
59. Buss DD, Lynch GP, Meyer CP, Huber SM, Freehill MQ. Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med. 2004;32(6):1430-1433.
60. Mazzocca AD, Brown FM Jr, Carreira DS, Hayden J, Romeo AA. Arthroscopic anterior shoulder stabilization of collision and contact athletes. Am J Sports Med. 2005;33(1):52-60.
61. Harris JD, Romeo AA. Arthroscopic management of the contact athlete with instability. Clin Sports Med. 2013;32(4):709-730.
62. Cho NS, Hwang JC, Rhee YG. Arthroscopic stabilization in anterior shoulder instability: collision athletes versus noncollision athletes. Arthroscopy. 2006;22(9):947-953.
63. Griffin JW, Brockmeier SF. Shoulder instability with concomitant bone loss in the athlete. Orthop Clin North Am. 2015;46(1):89-103.
64. Cohen SB, Towers JD, Bradley JP. Rotator cuff contusions of the shoulder in professional football players: epidemiology and magnetic resonance imaging findings. Am J Sports Med. 2007;35(3):442-447.
65. Lorentzon R, Wedrèn H, Pietilä T. Incidence, nature, and causes of ice hockey injuries. A three-year prospective study of a Swedish elite ice hockey team. Am J Sports Med. 1988;16(4):392-396.
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74. Tuominen M, Stuart MJ, Aubry M, Kannus P, Parkkari J. Injuries in men’s international ice hockey: a 7-year study of the International Ice Hockey Federation Adult World Championship Tournaments and Olympic Winter Games. Br J Sports Med. 2015;49(1):30-36.
75. Heckman JD, Bucholz RW. In: Rockwood CA, Green DP, Heckman JD, Bucholz RW, eds. Rockwood and Green’s Fractures in Adults, Volume 1. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.
1. Vaughan G. The Puck Starts Here: The Origin of Canada’s Great Winter Game, Ice Hockey. Fredericton, Canada: Goose Lane Editions; 1996.
2. IIHF member national associations. International Ice Hockey Federation website. http://www.iihf.com/iihf-home/the-iihf/members. Accessed April 6, 2017.
3. Flik K, Lyman S, Marx RG. American collegiate men’s ice hockey: an analysis of injuries. Am J Sports Med. 2005;33(2):183-187.
4. Engebretsen L, Steffen K, Alonso JM, et al. Sports injuries and illnesses during the Winter Olympic Games 2010. Br J Sports Med. 2010;44(11):772-780.
5. Deits J, Yard EE, Collins CL, Fields SK, Comstock RD. Patients with ice hockey injuries presenting to US emergency departments, 1990-2006. J Athl Train. 2010;45(5):467-474.
6. Brooks A, Loud KJ, Brenner JS, et al. Reducing injury risk from body checking in boys’ youth ice hockey. Pediatrics. 2014;133(6):1151-1157.
7. Agel J, Harvey EJ. A 7-year review of men’s and women’s ice hockey injuries in the NCAA. Can J Surg. 2010;53(5):319-323.
8. Micieli JA, Zurakowski D, Ahmed, II. Impact of visors on eye and orbital injuries in the National Hockey League. Can J Ophthalmol. 2014;49(3):243-248.
9. Pashby TJ. Ocular injuries in hockey. Int Ophthalmol Clin. 1988;28(3):228-231.
10. Leivo T, Haavisto AK, Sahraravand A. Sports-related eye injuries: the current picture. Acta Ophthalmol. 2015;93(3):224-231.
11. Cohn RM, Alaia MJ, Strauss EJ, Feldman AF. Rink-side management of ice hockey related injuries to the face, neck, and chest. Bull Hosp Jt Dis. 2013;71(4):253-256.
12. Reehal P. Facial injury in sport. Curr Sports Med Rep. 2010;9(1):27-34.
13. Stuart MJ, Smith AM, Malo-Ortiguera SA, Fischer TL, Larson DR. A comparison of facial protection and the incidence of head, neck, and facial injuries in Junior A hockey players. A function of individual playing time. Am J Sports Med. 2002;30(1):39-44.
14. MacEwen CJ, McLatchie GR. Eye injuries in sport. Scott Med J. 2010;55(2):22-24.
15. Stevens ST, Lassonde M, de Beaumont L, Keenan JP. The effect of visors on head and facial injury in National Hockey League players. J Sci Med Sport. 2006;9(3):238-242.
16. Moslener MD, Wadsworth LT. Ice hockey: a team physician’s perspective. Curr Sports Med Rep. 2010;9(3):134-138.
17. LaPrade RF, Burnett QM, Zarzour R, Moss R. The effect of the mandatory use of face masks on facial lacerations and head and neck injuries in ice hockey. A prospective study. Am J Sports Med. 1995;23(6):773-775.
18. Benson BW, Mohtadi NG, Rose MS, Meeuwisse WH. Head and neck injuries among ice hockey players wearing full face shields vs half face shields. JAMA. 1999;282(24):2328-2332.
19. Lahti H, Sane J, Ylipaavalniemi P. Dental injuries in ice hockey games and training. Med Sci Sports Exerc. 2002;34(3):400-402.
20. Sane J, Ylipaavalniemi P, Leppanen H. Maxillofacial and dental ice hockey injuries. Med Sci Sports Exerc. 1988;20(2):202-207.
21. Emerich K, Kaczmarek J. First aid for dental trauma caused by sports activities: state of knowledge, treatment and prevention. Sports Med. 2010;40(5):361-366.
22. Rosenberg H, Rosenberg H, Hickey M. Emergency management of a traumatic tooth avulsion. Ann Emerg Med. 2011;57(4):375-377.
23. Young EJ, Macias CR, Stephens L. Common dental injury management in athletes. Sports Health. 2015;7(3):250-255.
24. Andersson L, Andreasen JO, Day P, et al. International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 2. Avulsion of permanent teeth. Dent Traumatol. 2012;28(2):88-96.
25. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Clin J Sport Med. 2009;19(3):185-200.
26. Schneider KJ, Meeuwisse WH, Kang J, Schneider GM, Emery CA. Preseason reports of neck pain, dizziness, and headache as risk factors for concussion in male youth ice hockey players. Clin J Sport Med. 2013;23(4):267-272.
27. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Br J Sports Med. 2013;47(5):250-258.
28. Delaney JS, Lamfookon C, Bloom GA, Al-Kashmiri A, Correa JA. Why university athletes choose not to reveal their concussion symptoms during a practice or game. Clin J Sport Med. 2015;25(2):113-125.
29. Ventura RE, Balcer LJ, Galetta SL. The concussion toolbox: the role of vision in the assessment of concussion. Semin Neurol. 2015;35(5):599-606.
30. Vartiainen MV, Holm A, Peltonen K, Luoto TM, Iverson GL, Hokkanen L. King-Devick test normative reference values for professional male ice hockey players. Scand J Med Sci Sports. 2015;25(3):e327-e330.
31. Galetta MS, Galetta KM, McCrossin J, et al. Saccades and memory: baseline associations of the King-Devick and SCAT2 SAC tests in professional ice hockey players. J Neurol Sci. 2013;328(1-2):28-31.
32. Vernau BT, Grady MF, Goodman A, et al. Oculomotor and neurocognitive assessment of youth ice hockey players: baseline associations and observations after concussion. Dev Neuropsychol. 2015;40(1):7-11.
33. Fry AF, Hale S. Relationships among processing speed, working memory, and fluid intelligence in children. Biol Psychol. 2000;54(1-3):1-34.
34. Felleman DJ, Van Essen DC. Distributed hierarchical processing in the primate cerebral cortex. Cereb Cortex. 1991;1(1):1-47.
35. Guskiewicz KM, Register-Mihalik J, McCrory P, et al. Evidence-based approach to revising the SCAT2: introducing the SCAT3. Br J Sports Med. 2013;47(5):289-293.
36. Smith AM, Stuart MJ, Dodick DW, et al. Ice Hockey Summit II: zero tolerance for head hits and fighting. Curr Sports Med Rep. 2015;14(2):135-144.
37. Mihalik JP, Beard JR, Petschauer MA, Prentice WE, Guskiewicz KM. Effect of ice hockey helmet fit on cervical spine motion during an emergency log roll procedure. Clin J Sport Med. 2008;18(5):394-398.
38. Banerjee R, Palumbo MA, Fadale PD. Catastrophic cervical spine injuries in the collision sport athlete, part 1: epidemiology, functional anatomy, and diagnosis. Am J Sports Med. 2004;32(4):1077-1087.
39. Reynen PD, Clancy WG Jr. Cervical spine injury, hockey helmets, and face masks. Am J Sports Med. 1994;22(2):167-170.
40. Tator CH, Provvidenza C, Cassidy JD. Update and overview of spinal injuries in Canadian ice hockey, 1943 to 2011: the continuing need for injury prevention and education. Clin J Sport Med. 2016;26(3):232-238.
41. Tator CH, Edmonds VE, Lapczak L, Tator IB. Spinal injuries in ice hockey players, 1966-1987. Can J Surg. 1991;34(1):63-69.
42. Laprade RF, Schnetzler KA, Broxterman RJ, Wentorf F, Gilbert TJ. Cervical spine alignment in the immobilized ice hockey player. A computed tomographic analysis of the effects of helmet removal. Am J Sports Med. 2000;28(6):800-803.
43. Metz CM, Kuhn JE, Greenfield ML. Cervical spine alignment in immobilized hockey players: radiographic analysis with and without helmets and shoulder pads. Clin J Sport Med. 1998;8(2):92-95.
44. National Athletic Trainers’ Association. Appropriate prehospital management of the spine-injured athlete: updated from 1998 document. http://www.nata.org/sites/default/files/Executive-Summary-Spine-Injury-updated.pdf. Updated August 5, 2015. Accessed April 6, 2017.
45. Del Rossi G, Heffernan TP, Horodyski M, Rechtine GR. The effectiveness of extrication collars tested during the execution of spine-board transfer techniques. Spine J. 2004;4(6):619-623.
46. Morganti C, Sweeney CA, Albanese SA, Burak C, Hosea T, Connolly PJ. Return to play after cervical spine injury. Spine. 2001;26(10):1131-1136.
47. Huang P, Anissipour A, McGee W, Lemak L. Return-to-play recommendations after cervical, thoracic, and lumbar spine injuries: a comprehensive review. Sports Health. 2016;8(1):19-25.
48. Shindle MK, Marx RG, Kelly BT, Bisson L, Burke CJ 3rd. Hockey injuries: a pediatric sport update. Curr Opin Pediatr. 2010;22(1):54-60.
49. Molsa J, Kujala U, Myllynen P, Torstila I, Airaksinen O. Injuries to the upper extremity in ice hockey: analysis of a series of 760 injuries. Am J Sports Med. 2003;31(5):751-757.
50. Dwyer T, Petrera M, Bleakney R, Theodoropoulos JS. Shoulder instability in ice hockey players: incidence, mechanism, and MRI findings. Clin Sports Med. 2013;32(4):803-813.
51. LaPrade RF, Wijdicks CA, Griffith CJ. Division I intercollegiate ice hockey team coverage. Br J Sports Med. 2009;43(13):1000-1005.
52. Willimon SC, Gaskill TR, Millett PJ. Acromioclavicular joint injuries: anatomy, diagnosis, and treatment. Phys Sportsmed. 2011;39(1):116-122.
53. Martetschlager F, Horan MP, Warth RJ, Millett PJ. Complications after anatomic fixation and reconstruction of the coracoclavicular ligaments. Am J Sports Med. 2013;41(12):2896-2903.
54. Carofino BC, Mazzocca AD. The anatomic coracoclavicular ligament reconstruction: surgical technique and indications. J Shoulder Elbow Surg. 2010;19(2 suppl):37-46.
55. Laprade RF, Surowiec RK, Sochanska AN, et al. Epidemiology, identification, treatment and return to play of musculoskeletal-based ice hockey injuries. Br J Sports Med. 2014;48(1):4-10.
56. Canadian Orthopaedic Trauma Society. Nonoperative treatment compared with plate fixation of displaced midshaft clavicular fractures. A multicenter, randomized clinical trial. J Bone Joint Surg Am. 2007;89(1):1-10.
57. Lee JT, Nasreddine AY, Black EM, Bae DS, Kocher MS. Posterior sternoclavicular joint injuries in skeletally immature patients. J Pediatr Orthop. 2014;34(4):369-375.
58. Hovelius L. Shoulder dislocation in Swedish ice hockey players. Am J Sports Med. 1978;6(6):373-377.
59. Buss DD, Lynch GP, Meyer CP, Huber SM, Freehill MQ. Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med. 2004;32(6):1430-1433.
60. Mazzocca AD, Brown FM Jr, Carreira DS, Hayden J, Romeo AA. Arthroscopic anterior shoulder stabilization of collision and contact athletes. Am J Sports Med. 2005;33(1):52-60.
61. Harris JD, Romeo AA. Arthroscopic management of the contact athlete with instability. Clin Sports Med. 2013;32(4):709-730.
62. Cho NS, Hwang JC, Rhee YG. Arthroscopic stabilization in anterior shoulder instability: collision athletes versus noncollision athletes. Arthroscopy. 2006;22(9):947-953.
63. Griffin JW, Brockmeier SF. Shoulder instability with concomitant bone loss in the athlete. Orthop Clin North Am. 2015;46(1):89-103.
64. Cohen SB, Towers JD, Bradley JP. Rotator cuff contusions of the shoulder in professional football players: epidemiology and magnetic resonance imaging findings. Am J Sports Med. 2007;35(3):442-447.
65. Lorentzon R, Wedrèn H, Pietilä T. Incidence, nature, and causes of ice hockey injuries. A three-year prospective study of a Swedish elite ice hockey team. Am J Sports Med. 1988;16(4):392-396.
66. Stuart MJ, Smith A. Injuries in Junior A ice hockey. A three-year prospective study. Am J Sports Med. 1995;23(4):458-461.
67. Voaklander DC, Saunders LD, Quinney HA, Macnab RB. Epidemiology of recreational and old-timer ice hockey injuries. Clin J Sport Med. 1996;6(1):15-21.
68. Mölsä J, Airaksinen O, Näsman O, Torstila I. Ice hockey injuries in Finland. A prospective epidemiologic study. Am J Sports Med. 1997;25(4):495-499.
69. Ferrara MS, Schurr KT. Intercollegiate ice hockey injuries: a casual analysis. Clin J Sport Med. 1999;9(1):30-33.
70. Pinto M, Kuhn JE, Greenfield ML, Hawkins RJ. Prospective analysis of ice hockey injuries at the Junior A level over the course of one season. Clin J Sport Med. 1999;9(2):70-74.
71. Emery CA, Meeuwisse WH. Injury rates, risk factors, and mechanisms of injury in minor hockey. Am J Sports Med. 2006;34(12):1960-1969.
72. Kuzuhara K, Shimamoto H, Mase Y. Ice hockey injuries in a Japanese elite team: a 3-year prospective study. J Athl Train. 2009;44(2):208-214.
73. Rishiraj N, Lloyd-Smith R, Lorenz T, Niven B, Michel M. University men’s ice hockey: rates and risk of injuries over 6-years. J Sports Med Phys Fitness. 2009;49(2):159-166.
74. Tuominen M, Stuart MJ, Aubry M, Kannus P, Parkkari J. Injuries in men’s international ice hockey: a 7-year study of the International Ice Hockey Federation Adult World Championship Tournaments and Olympic Winter Games. Br J Sports Med. 2015;49(1):30-36.
75. Heckman JD, Bucholz RW. In: Rockwood CA, Green DP, Heckman JD, Bucholz RW, eds. Rockwood and Green’s Fractures in Adults, Volume 1. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.
Arthroscopic Excision of Bipartite Patella With Preservation of Lateral Retinaculum in an Adolescent Ice Hockey Player
Take-Home Points
- Bipartite patella is an asymptomatic anatomical variant.
- Occasionally, some adolescent athletes can present with AKP, resulting in decreased participation and performance.
- Bipartite patella is classified in type I, inferior pole; type II, lateral margin; and type III, superior lateral pole, depending on where the accessory patellar fragment is.
- Nonoperative treatment is advocated first. If symptoms persist surgical treatment should be attempted.
In 2% to 3% of the general population, the finding of bipartite patella on knee radiographs is often incidental.1,2 During development, the patella normally originates in a primary ossification center. Occasionally, secondary ossification centers emerge around the margins of the primary center and typically join that center. In some cases, the secondary2 center remains separated, leading to patella partita and an accessory patellar fragment.3,4
The bipartite patella is connected to the primary patella by fibrocartilage. The fibrous attachment may become irritated or separated as a result of trauma, overuse, or strenuous activity.1,5-7 Saupe classification of bipartite patella is based on accessory patellar fragment location: type I, inferior pole; type II, lateral margin; and type III, superior lateral pole.8 When an individual with a bipartite patella becomes symptomatic, anterior knee pain (AKP) is the most common complaint—it has been described in adolescent athletes in numerous sports.7,9-11For most patients, first-line treatment is nonoperative management. A typical regimen includes reduced activity, use of nonsteroidal anti-inflammatory drugs, physical therapy, and isometric quadriceps-strengthening exercises.1,12 Other nonoperative approaches described in the literature are immobilization,5,10 steroid and anesthetic injection, and ultrasound therapy.13 If symptoms do not improve, surgical treatment should be considered. Surgical treatment options include open excision of fragment,3,9,12 arthroscopic excision of fragment,7,14,15 tension band wiring,5,16 open reduction and internal fixation,17 open or arthroscopic vastus lateralis release,18-20 and lateral retinacular release.21 However, the optimal surgical option remains controversial.
In this case report, we present a modification of an arthroscopic surgical technique for excising a symptomatic bipartite patella and report midterm clinical outcomes. The patient provided written informed consent for print and electronic publication of this report.
Case Report
A 16-year-old elite male ice hockey player presented to clinic with a 2-week history of left AKP. He could not recall a specific injury that triggered the symptoms. Radiographs were obtained at an outside institution, and knee patellar fracture was diagnosed. The patient, placed in a straight-leg immobilizer, later presented to a referral clinic for a second opinion and further evaluation. Physical examination revealed significant tenderness to palpation of the lateral aspect of the patella. Range of motion was symmetric and fully intact. Patellar mobility was excellent. However, the patient could not perform a straight-leg raise because of the pain.
We obtained anteroposterior and lateral radiographs (Figures 1A, 1B), which showed evidence of a Saupe type III bipartite patella with separation at the superolateral pole. 
Two years later, the patient returned with left AKP, again localized to the lateral aspect of the patella, over the bipartite fragment. The pain was significant with compression. Given the patient’s history, arthroscopic excision of the bipartite patella was recommended. After discussing all treatment options, the patient elected to proceed with the surgery.
Surgical Technique
The patient was positioned supine on the operating table. Medial and lateral parapatellar arthroscopic portals were created. Menisci, cruciate ligaments, and tibiofemoral articular cartilage were arthroscopically visualized and determined to be normal. The bipartite patella was easily visualized, and notably loose when probed. Grade 2 chondromalacia was present diffusely throughout the bipartite patella and on the far lateral aspect of the patella, at the fragment interface.
Attention was then turned to arthroscopic removal of the accessory patellar fragment (Figures 3A, 3B). 
Postoperative Rehabilitation
Rehabilitation focused on protection of the healing patella and accelerated rehabilitation for early return to play. Range-of-motion exercises and stationary bicycling were initiated on postoperative day 1. Weight-bearing was allowed as tolerated. Quadriceps sets, straight-leg raises, and ankle pumps were performed 5 times daily for 6 weeks. Six weeks after surgery, the patient was cleared, and he returned to full on-ice activities.
Outcomes
This study was approved by an Institutional Review Board. Preoperative and postoperative outcomes were obtained and stored in a data registry. The patient’s Lysholm score22 improved from 71 before surgery to 100 at 31-month follow-up. In addition, his subjective International Knee Documentation Committee score23 improved from 65.5 before surgery to 72.4 after surgery. At follow-up, patient satisfaction with outcome was 10/10. In addition, the patient had returned to playing hockey at a higher national level without functional limitation.
Discussion
The most important finding in this case is that arthroscopic excision of a bipartite patella with preservation of the lateral retinaculum in an elite adolescent hockey player resulted in improved subjective clinical outcomes scores and early return to competition. Arthroscopic excision was favored over open excision in this patient because of potential quicker recovery,14 less pain, and expedited return to competition. In addition, previous arthroscopic techniques were modified to shorten postoperative rehabilitation. The modified technique included preservation of the lateral retinaculum and total arthroscopic excision of the accessory bipartite patella fragment.
Although results of open techniques have been favorable,3,8,9 these procedures are far more invasive than arthroscopic techniques and may result in loss of quadriceps strength and prolonged rehabilitation.18 Weckström and colleagues12 followed 25 male military recruits for a minimum of 10 years after open excision of symptomatic bipartite patella. Mean Kujala score was 95 (range, 75-100), and median visual analog scale score for knee pain was 1.0 (range, 0.0-6.0). In a study by Bourne and Bianco,3 13 of 16 patients who were followed for an average of 7 years experienced complete pain relief with an average recovery time of 2 months.
Other studies have described the arthroscopic excision technique for symptomatic bipartite patella,7,14,15 but outcomes are underreported, especially for follow-ups longer than 2 years. Felli and colleagues7 described a case of arthroscopic excision and lateral release in a 23-year-old female professional volleyball player; at 1-year follow-up, the patient was symptom-free and back to full athletic participation. Azarbod and colleagues14 also reported on a patient who was symptom-free, 6 weeks after arthroscopic excision of bipartite patella. Carney and colleagues15 indicated that successful excision of bipartite patella was evident on 6-month radiographic follow-up. Our 31-month follow-up is the longest of any study on arthroscopic excision of bipartite patella. Clinical outcomes were excellent both in our patient’s case and in the earlier studies.
Our patient was a high-level hockey player who wanted to return to competition as quickly as possible. Conservative management, including physical therapy, initially resolved his symptoms and allowed him to resume on-ice activities after 6 weeks. In time, however, his symptoms returned and began limiting his on-ice performance. Arthroscopic removal of the bipartite patella accessory fragment allowed him to return to full on-ice activities after 6 weeks. His case provides evidence that arthroscopic management of bipartite patella with preservation of the vastus lateralis and lateral retinaculum may be an excellent treatment option for patients who want to return to athletics as quickly as possible.
Our technique of arthroscopic excision with preservation of lateral retinaculum is an excellent treatment option for symptomatic bipartite patella. This option, combined with an aggressive rehabilitation protocol, allows for pain relief and expedited return to competition.
Am J Orthop. 2017;46(3):135-138. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Atesok K, Doral MN, Lowe J, Finsterbush A. Symptomatic bipartite patella: treatment alternatives. J Am Acad Orthop Surg. 2008;16(8):455-461.
2. Insall J. Current concepts review: patellar pain. J Bone Joint Surg Am. 1982;64(1):147-152.
3. Bourne MH, Bianco AJ Jr. Bipartite patella in the adolescent: results of surgical excision. J Pediatr Orthop. 1990;10(1):69-73.
4. Oohashi Y, Koshino T, Oohashi Y. Clinical features and classification of bipartite or tripartite patella. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1465-1469.
5. Okuno H, Sugita T, Kawamata T, Ohnuma M, Yamada N, Yoshizumi Y. Traumatic separation of a type I bipartite patella: a report of four knees. Clin Orthop Relat Res. 2004;(420):257-260.
6. Yoo JH, Kim EH, Ryu HK. Arthroscopic removal of separated bipartite patella causing snapping knee syndrome. Orthopedics. 2008;31(7):717.
7. Felli L, Fiore M, Biglieni L. Arthroscopic treatment of symptomatic bipartite patella. Knee Surg Sports Traumatol Arthrosc. 2011;19(3):398-399.
8. Green WT Jr. Painful bipartite patellae. A report of three cases. Clin Orthop Relat Res. 1975;(110):197-200.
9. Ishikawa H, Sakurai A, Hirata S, et al. Painful bipartite patella in young athletes. The diagnostic value of skyline views taken in squatting position and the results of surgical excision. Clin Orthop Relat Res. 1994;(305):223-228.
10. Stocker RL, van Laer L. Injury of a bipartite patella in a young upcoming sportsman. Arch Orthop Trauma Surg. 2011;131(1):75-78.
11. Wong CK. Bipartite patella in a young athlete. J Orthop Sports Phys Ther. 2009;39(7):560.
12. Weckström M, Parviainen M, Pihlajamäki HK. Excision of painful bipartite patella: good long-term outcome in young adults. Clin Orthop Relat Res. 2008;466(11):2848-2855.
13. Kumahashi N, Uchio Y, Iwasa J, Kawasaki K, Adachi N, Ochi M. Bone union of painful bipartite patella after treatment with low-intensity pulsed ultrasound: report of two cases. Knee. 2008;15(1):50-53.
14. Azarbod P, Agar G, Patel V. Arthroscopic excision of a painful bipartite patella fragment. Arthroscopy. 2005;21(8):1006.
15. Carney J, Thompson D, O’Daniel J, Cassidy J. Arthroscopic excision of a painful bipartite patella fragment. Am J Orthop. 2010;39(1):40-43.
16. Tauber M, Matis N, Resch H. Traumatic separation of an uncommon bipartite patella type: a case report. Knee Surg Sports Traumatol Arthrosc. 2007;15(1):83-87.
17. Werner S, Durkan M, Jones J, Quilici S, Crawford D. Symptomatic bipartite patella: three subtypes, three representative cases. J Knee Surg. 2013;26(suppl 1):S72-S76.
18. Adachi N, Ochi M, Yamaguchi H, Uchio Y, Kuriwaka M. Vastus lateralis release for painful bipartite patella. Arthroscopy. 2002;18(4):404-411.
19. Maeno S, Hashimoto D, Otani T, Masumoto K, Hui C. The “coiling-up procedure”: a novel technique for extra-articular arthroscopy. Arthroscopy. 2010;26(11):1551-1555.
20. Ogata K. Painful bipartite patella. A new approach to operative treatment. J Bone Joint Surg Am. 1994;76(4):573-578.
21. Mori Y, Okumo H, Iketani H, Kuroki Y. Efficacy of lateral retinacular release for painful bipartite patella. Am J Sports Med. 1995;23(1):13-18.
22. Lysholm J, Gillquist J. Evaluation of knee ligament surgery results with special emphasis on use of a scoring scale. Am J Sports Med. 1982;10(3):150-154
23. Grevnerts HT, Terwee CB, Kvist J. The measurement properties of the IKDC-subjective knee form. Knee Surg Sports Traumatol Arthrosc. 2015;23(12):3698-3706.
Take-Home Points
- Bipartite patella is an asymptomatic anatomical variant.
- Occasionally, some adolescent athletes can present with AKP, resulting in decreased participation and performance.
- Bipartite patella is classified in type I, inferior pole; type II, lateral margin; and type III, superior lateral pole, depending on where the accessory patellar fragment is.
- Nonoperative treatment is advocated first. If symptoms persist surgical treatment should be attempted.
In 2% to 3% of the general population, the finding of bipartite patella on knee radiographs is often incidental.1,2 During development, the patella normally originates in a primary ossification center. Occasionally, secondary ossification centers emerge around the margins of the primary center and typically join that center. In some cases, the secondary2 center remains separated, leading to patella partita and an accessory patellar fragment.3,4
The bipartite patella is connected to the primary patella by fibrocartilage. The fibrous attachment may become irritated or separated as a result of trauma, overuse, or strenuous activity.1,5-7 Saupe classification of bipartite patella is based on accessory patellar fragment location: type I, inferior pole; type II, lateral margin; and type III, superior lateral pole.8 When an individual with a bipartite patella becomes symptomatic, anterior knee pain (AKP) is the most common complaint—it has been described in adolescent athletes in numerous sports.7,9-11For most patients, first-line treatment is nonoperative management. A typical regimen includes reduced activity, use of nonsteroidal anti-inflammatory drugs, physical therapy, and isometric quadriceps-strengthening exercises.1,12 Other nonoperative approaches described in the literature are immobilization,5,10 steroid and anesthetic injection, and ultrasound therapy.13 If symptoms do not improve, surgical treatment should be considered. Surgical treatment options include open excision of fragment,3,9,12 arthroscopic excision of fragment,7,14,15 tension band wiring,5,16 open reduction and internal fixation,17 open or arthroscopic vastus lateralis release,18-20 and lateral retinacular release.21 However, the optimal surgical option remains controversial.
In this case report, we present a modification of an arthroscopic surgical technique for excising a symptomatic bipartite patella and report midterm clinical outcomes. The patient provided written informed consent for print and electronic publication of this report.
Case Report
A 16-year-old elite male ice hockey player presented to clinic with a 2-week history of left AKP. He could not recall a specific injury that triggered the symptoms. Radiographs were obtained at an outside institution, and knee patellar fracture was diagnosed. The patient, placed in a straight-leg immobilizer, later presented to a referral clinic for a second opinion and further evaluation. Physical examination revealed significant tenderness to palpation of the lateral aspect of the patella. Range of motion was symmetric and fully intact. Patellar mobility was excellent. However, the patient could not perform a straight-leg raise because of the pain.
We obtained anteroposterior and lateral radiographs (Figures 1A, 1B), which showed evidence of a Saupe type III bipartite patella with separation at the superolateral pole.
Two years later, the patient returned with left AKP, again localized to the lateral aspect of the patella, over the bipartite fragment. The pain was significant with compression. Given the patient’s history, arthroscopic excision of the bipartite patella was recommended. After discussing all treatment options, the patient elected to proceed with the surgery.
Surgical Technique
The patient was positioned supine on the operating table. Medial and lateral parapatellar arthroscopic portals were created. Menisci, cruciate ligaments, and tibiofemoral articular cartilage were arthroscopically visualized and determined to be normal. The bipartite patella was easily visualized, and notably loose when probed. Grade 2 chondromalacia was present diffusely throughout the bipartite patella and on the far lateral aspect of the patella, at the fragment interface.
Attention was then turned to arthroscopic removal of the accessory patellar fragment (Figures 3A, 3B).
Postoperative Rehabilitation
Rehabilitation focused on protection of the healing patella and accelerated rehabilitation for early return to play. Range-of-motion exercises and stationary bicycling were initiated on postoperative day 1. Weight-bearing was allowed as tolerated. Quadriceps sets, straight-leg raises, and ankle pumps were performed 5 times daily for 6 weeks. Six weeks after surgery, the patient was cleared, and he returned to full on-ice activities.
Outcomes
This study was approved by an Institutional Review Board. Preoperative and postoperative outcomes were obtained and stored in a data registry. The patient’s Lysholm score22 improved from 71 before surgery to 100 at 31-month follow-up. In addition, his subjective International Knee Documentation Committee score23 improved from 65.5 before surgery to 72.4 after surgery. At follow-up, patient satisfaction with outcome was 10/10. In addition, the patient had returned to playing hockey at a higher national level without functional limitation.
Discussion
The most important finding in this case is that arthroscopic excision of a bipartite patella with preservation of the lateral retinaculum in an elite adolescent hockey player resulted in improved subjective clinical outcomes scores and early return to competition. Arthroscopic excision was favored over open excision in this patient because of potential quicker recovery,14 less pain, and expedited return to competition. In addition, previous arthroscopic techniques were modified to shorten postoperative rehabilitation. The modified technique included preservation of the lateral retinaculum and total arthroscopic excision of the accessory bipartite patella fragment.
Although results of open techniques have been favorable,3,8,9 these procedures are far more invasive than arthroscopic techniques and may result in loss of quadriceps strength and prolonged rehabilitation.18 Weckström and colleagues12 followed 25 male military recruits for a minimum of 10 years after open excision of symptomatic bipartite patella. Mean Kujala score was 95 (range, 75-100), and median visual analog scale score for knee pain was 1.0 (range, 0.0-6.0). In a study by Bourne and Bianco,3 13 of 16 patients who were followed for an average of 7 years experienced complete pain relief with an average recovery time of 2 months.
Other studies have described the arthroscopic excision technique for symptomatic bipartite patella,7,14,15 but outcomes are underreported, especially for follow-ups longer than 2 years. Felli and colleagues7 described a case of arthroscopic excision and lateral release in a 23-year-old female professional volleyball player; at 1-year follow-up, the patient was symptom-free and back to full athletic participation. Azarbod and colleagues14 also reported on a patient who was symptom-free, 6 weeks after arthroscopic excision of bipartite patella. Carney and colleagues15 indicated that successful excision of bipartite patella was evident on 6-month radiographic follow-up. Our 31-month follow-up is the longest of any study on arthroscopic excision of bipartite patella. Clinical outcomes were excellent both in our patient’s case and in the earlier studies.
Our patient was a high-level hockey player who wanted to return to competition as quickly as possible. Conservative management, including physical therapy, initially resolved his symptoms and allowed him to resume on-ice activities after 6 weeks. In time, however, his symptoms returned and began limiting his on-ice performance. Arthroscopic removal of the bipartite patella accessory fragment allowed him to return to full on-ice activities after 6 weeks. His case provides evidence that arthroscopic management of bipartite patella with preservation of the vastus lateralis and lateral retinaculum may be an excellent treatment option for patients who want to return to athletics as quickly as possible.
Our technique of arthroscopic excision with preservation of lateral retinaculum is an excellent treatment option for symptomatic bipartite patella. This option, combined with an aggressive rehabilitation protocol, allows for pain relief and expedited return to competition.
Am J Orthop. 2017;46(3):135-138. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- Bipartite patella is an asymptomatic anatomical variant.
- Occasionally, some adolescent athletes can present with AKP, resulting in decreased participation and performance.
- Bipartite patella is classified in type I, inferior pole; type II, lateral margin; and type III, superior lateral pole, depending on where the accessory patellar fragment is.
- Nonoperative treatment is advocated first. If symptoms persist surgical treatment should be attempted.
In 2% to 3% of the general population, the finding of bipartite patella on knee radiographs is often incidental.1,2 During development, the patella normally originates in a primary ossification center. Occasionally, secondary ossification centers emerge around the margins of the primary center and typically join that center. In some cases, the secondary2 center remains separated, leading to patella partita and an accessory patellar fragment.3,4
The bipartite patella is connected to the primary patella by fibrocartilage. The fibrous attachment may become irritated or separated as a result of trauma, overuse, or strenuous activity.1,5-7 Saupe classification of bipartite patella is based on accessory patellar fragment location: type I, inferior pole; type II, lateral margin; and type III, superior lateral pole.8 When an individual with a bipartite patella becomes symptomatic, anterior knee pain (AKP) is the most common complaint—it has been described in adolescent athletes in numerous sports.7,9-11For most patients, first-line treatment is nonoperative management. A typical regimen includes reduced activity, use of nonsteroidal anti-inflammatory drugs, physical therapy, and isometric quadriceps-strengthening exercises.1,12 Other nonoperative approaches described in the literature are immobilization,5,10 steroid and anesthetic injection, and ultrasound therapy.13 If symptoms do not improve, surgical treatment should be considered. Surgical treatment options include open excision of fragment,3,9,12 arthroscopic excision of fragment,7,14,15 tension band wiring,5,16 open reduction and internal fixation,17 open or arthroscopic vastus lateralis release,18-20 and lateral retinacular release.21 However, the optimal surgical option remains controversial.
In this case report, we present a modification of an arthroscopic surgical technique for excising a symptomatic bipartite patella and report midterm clinical outcomes. The patient provided written informed consent for print and electronic publication of this report.
Case Report
A 16-year-old elite male ice hockey player presented to clinic with a 2-week history of left AKP. He could not recall a specific injury that triggered the symptoms. Radiographs were obtained at an outside institution, and knee patellar fracture was diagnosed. The patient, placed in a straight-leg immobilizer, later presented to a referral clinic for a second opinion and further evaluation. Physical examination revealed significant tenderness to palpation of the lateral aspect of the patella. Range of motion was symmetric and fully intact. Patellar mobility was excellent. However, the patient could not perform a straight-leg raise because of the pain.
We obtained anteroposterior and lateral radiographs (Figures 1A, 1B), which showed evidence of a Saupe type III bipartite patella with separation at the superolateral pole.
Two years later, the patient returned with left AKP, again localized to the lateral aspect of the patella, over the bipartite fragment. The pain was significant with compression. Given the patient’s history, arthroscopic excision of the bipartite patella was recommended. After discussing all treatment options, the patient elected to proceed with the surgery.
Surgical Technique
The patient was positioned supine on the operating table. Medial and lateral parapatellar arthroscopic portals were created. Menisci, cruciate ligaments, and tibiofemoral articular cartilage were arthroscopically visualized and determined to be normal. The bipartite patella was easily visualized, and notably loose when probed. Grade 2 chondromalacia was present diffusely throughout the bipartite patella and on the far lateral aspect of the patella, at the fragment interface.
Attention was then turned to arthroscopic removal of the accessory patellar fragment (Figures 3A, 3B).
Postoperative Rehabilitation
Rehabilitation focused on protection of the healing patella and accelerated rehabilitation for early return to play. Range-of-motion exercises and stationary bicycling were initiated on postoperative day 1. Weight-bearing was allowed as tolerated. Quadriceps sets, straight-leg raises, and ankle pumps were performed 5 times daily for 6 weeks. Six weeks after surgery, the patient was cleared, and he returned to full on-ice activities.
Outcomes
This study was approved by an Institutional Review Board. Preoperative and postoperative outcomes were obtained and stored in a data registry. The patient’s Lysholm score22 improved from 71 before surgery to 100 at 31-month follow-up. In addition, his subjective International Knee Documentation Committee score23 improved from 65.5 before surgery to 72.4 after surgery. At follow-up, patient satisfaction with outcome was 10/10. In addition, the patient had returned to playing hockey at a higher national level without functional limitation.
Discussion
The most important finding in this case is that arthroscopic excision of a bipartite patella with preservation of the lateral retinaculum in an elite adolescent hockey player resulted in improved subjective clinical outcomes scores and early return to competition. Arthroscopic excision was favored over open excision in this patient because of potential quicker recovery,14 less pain, and expedited return to competition. In addition, previous arthroscopic techniques were modified to shorten postoperative rehabilitation. The modified technique included preservation of the lateral retinaculum and total arthroscopic excision of the accessory bipartite patella fragment.
Although results of open techniques have been favorable,3,8,9 these procedures are far more invasive than arthroscopic techniques and may result in loss of quadriceps strength and prolonged rehabilitation.18 Weckström and colleagues12 followed 25 male military recruits for a minimum of 10 years after open excision of symptomatic bipartite patella. Mean Kujala score was 95 (range, 75-100), and median visual analog scale score for knee pain was 1.0 (range, 0.0-6.0). In a study by Bourne and Bianco,3 13 of 16 patients who were followed for an average of 7 years experienced complete pain relief with an average recovery time of 2 months.
Other studies have described the arthroscopic excision technique for symptomatic bipartite patella,7,14,15 but outcomes are underreported, especially for follow-ups longer than 2 years. Felli and colleagues7 described a case of arthroscopic excision and lateral release in a 23-year-old female professional volleyball player; at 1-year follow-up, the patient was symptom-free and back to full athletic participation. Azarbod and colleagues14 also reported on a patient who was symptom-free, 6 weeks after arthroscopic excision of bipartite patella. Carney and colleagues15 indicated that successful excision of bipartite patella was evident on 6-month radiographic follow-up. Our 31-month follow-up is the longest of any study on arthroscopic excision of bipartite patella. Clinical outcomes were excellent both in our patient’s case and in the earlier studies.
Our patient was a high-level hockey player who wanted to return to competition as quickly as possible. Conservative management, including physical therapy, initially resolved his symptoms and allowed him to resume on-ice activities after 6 weeks. In time, however, his symptoms returned and began limiting his on-ice performance. Arthroscopic removal of the bipartite patella accessory fragment allowed him to return to full on-ice activities after 6 weeks. His case provides evidence that arthroscopic management of bipartite patella with preservation of the vastus lateralis and lateral retinaculum may be an excellent treatment option for patients who want to return to athletics as quickly as possible.
Our technique of arthroscopic excision with preservation of lateral retinaculum is an excellent treatment option for symptomatic bipartite patella. This option, combined with an aggressive rehabilitation protocol, allows for pain relief and expedited return to competition.
Am J Orthop. 2017;46(3):135-138. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Atesok K, Doral MN, Lowe J, Finsterbush A. Symptomatic bipartite patella: treatment alternatives. J Am Acad Orthop Surg. 2008;16(8):455-461.
2. Insall J. Current concepts review: patellar pain. J Bone Joint Surg Am. 1982;64(1):147-152.
3. Bourne MH, Bianco AJ Jr. Bipartite patella in the adolescent: results of surgical excision. J Pediatr Orthop. 1990;10(1):69-73.
4. Oohashi Y, Koshino T, Oohashi Y. Clinical features and classification of bipartite or tripartite patella. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1465-1469.
5. Okuno H, Sugita T, Kawamata T, Ohnuma M, Yamada N, Yoshizumi Y. Traumatic separation of a type I bipartite patella: a report of four knees. Clin Orthop Relat Res. 2004;(420):257-260.
6. Yoo JH, Kim EH, Ryu HK. Arthroscopic removal of separated bipartite patella causing snapping knee syndrome. Orthopedics. 2008;31(7):717.
7. Felli L, Fiore M, Biglieni L. Arthroscopic treatment of symptomatic bipartite patella. Knee Surg Sports Traumatol Arthrosc. 2011;19(3):398-399.
8. Green WT Jr. Painful bipartite patellae. A report of three cases. Clin Orthop Relat Res. 1975;(110):197-200.
9. Ishikawa H, Sakurai A, Hirata S, et al. Painful bipartite patella in young athletes. The diagnostic value of skyline views taken in squatting position and the results of surgical excision. Clin Orthop Relat Res. 1994;(305):223-228.
10. Stocker RL, van Laer L. Injury of a bipartite patella in a young upcoming sportsman. Arch Orthop Trauma Surg. 2011;131(1):75-78.
11. Wong CK. Bipartite patella in a young athlete. J Orthop Sports Phys Ther. 2009;39(7):560.
12. Weckström M, Parviainen M, Pihlajamäki HK. Excision of painful bipartite patella: good long-term outcome in young adults. Clin Orthop Relat Res. 2008;466(11):2848-2855.
13. Kumahashi N, Uchio Y, Iwasa J, Kawasaki K, Adachi N, Ochi M. Bone union of painful bipartite patella after treatment with low-intensity pulsed ultrasound: report of two cases. Knee. 2008;15(1):50-53.
14. Azarbod P, Agar G, Patel V. Arthroscopic excision of a painful bipartite patella fragment. Arthroscopy. 2005;21(8):1006.
15. Carney J, Thompson D, O’Daniel J, Cassidy J. Arthroscopic excision of a painful bipartite patella fragment. Am J Orthop. 2010;39(1):40-43.
16. Tauber M, Matis N, Resch H. Traumatic separation of an uncommon bipartite patella type: a case report. Knee Surg Sports Traumatol Arthrosc. 2007;15(1):83-87.
17. Werner S, Durkan M, Jones J, Quilici S, Crawford D. Symptomatic bipartite patella: three subtypes, three representative cases. J Knee Surg. 2013;26(suppl 1):S72-S76.
18. Adachi N, Ochi M, Yamaguchi H, Uchio Y, Kuriwaka M. Vastus lateralis release for painful bipartite patella. Arthroscopy. 2002;18(4):404-411.
19. Maeno S, Hashimoto D, Otani T, Masumoto K, Hui C. The “coiling-up procedure”: a novel technique for extra-articular arthroscopy. Arthroscopy. 2010;26(11):1551-1555.
20. Ogata K. Painful bipartite patella. A new approach to operative treatment. J Bone Joint Surg Am. 1994;76(4):573-578.
21. Mori Y, Okumo H, Iketani H, Kuroki Y. Efficacy of lateral retinacular release for painful bipartite patella. Am J Sports Med. 1995;23(1):13-18.
22. Lysholm J, Gillquist J. Evaluation of knee ligament surgery results with special emphasis on use of a scoring scale. Am J Sports Med. 1982;10(3):150-154
23. Grevnerts HT, Terwee CB, Kvist J. The measurement properties of the IKDC-subjective knee form. Knee Surg Sports Traumatol Arthrosc. 2015;23(12):3698-3706.
1. Atesok K, Doral MN, Lowe J, Finsterbush A. Symptomatic bipartite patella: treatment alternatives. J Am Acad Orthop Surg. 2008;16(8):455-461.
2. Insall J. Current concepts review: patellar pain. J Bone Joint Surg Am. 1982;64(1):147-152.
3. Bourne MH, Bianco AJ Jr. Bipartite patella in the adolescent: results of surgical excision. J Pediatr Orthop. 1990;10(1):69-73.
4. Oohashi Y, Koshino T, Oohashi Y. Clinical features and classification of bipartite or tripartite patella. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1465-1469.
5. Okuno H, Sugita T, Kawamata T, Ohnuma M, Yamada N, Yoshizumi Y. Traumatic separation of a type I bipartite patella: a report of four knees. Clin Orthop Relat Res. 2004;(420):257-260.
6. Yoo JH, Kim EH, Ryu HK. Arthroscopic removal of separated bipartite patella causing snapping knee syndrome. Orthopedics. 2008;31(7):717.
7. Felli L, Fiore M, Biglieni L. Arthroscopic treatment of symptomatic bipartite patella. Knee Surg Sports Traumatol Arthrosc. 2011;19(3):398-399.
8. Green WT Jr. Painful bipartite patellae. A report of three cases. Clin Orthop Relat Res. 1975;(110):197-200.
9. Ishikawa H, Sakurai A, Hirata S, et al. Painful bipartite patella in young athletes. The diagnostic value of skyline views taken in squatting position and the results of surgical excision. Clin Orthop Relat Res. 1994;(305):223-228.
10. Stocker RL, van Laer L. Injury of a bipartite patella in a young upcoming sportsman. Arch Orthop Trauma Surg. 2011;131(1):75-78.
11. Wong CK. Bipartite patella in a young athlete. J Orthop Sports Phys Ther. 2009;39(7):560.
12. Weckström M, Parviainen M, Pihlajamäki HK. Excision of painful bipartite patella: good long-term outcome in young adults. Clin Orthop Relat Res. 2008;466(11):2848-2855.
13. Kumahashi N, Uchio Y, Iwasa J, Kawasaki K, Adachi N, Ochi M. Bone union of painful bipartite patella after treatment with low-intensity pulsed ultrasound: report of two cases. Knee. 2008;15(1):50-53.
14. Azarbod P, Agar G, Patel V. Arthroscopic excision of a painful bipartite patella fragment. Arthroscopy. 2005;21(8):1006.
15. Carney J, Thompson D, O’Daniel J, Cassidy J. Arthroscopic excision of a painful bipartite patella fragment. Am J Orthop. 2010;39(1):40-43.
16. Tauber M, Matis N, Resch H. Traumatic separation of an uncommon bipartite patella type: a case report. Knee Surg Sports Traumatol Arthrosc. 2007;15(1):83-87.
17. Werner S, Durkan M, Jones J, Quilici S, Crawford D. Symptomatic bipartite patella: three subtypes, three representative cases. J Knee Surg. 2013;26(suppl 1):S72-S76.
18. Adachi N, Ochi M, Yamaguchi H, Uchio Y, Kuriwaka M. Vastus lateralis release for painful bipartite patella. Arthroscopy. 2002;18(4):404-411.
19. Maeno S, Hashimoto D, Otani T, Masumoto K, Hui C. The “coiling-up procedure”: a novel technique for extra-articular arthroscopy. Arthroscopy. 2010;26(11):1551-1555.
20. Ogata K. Painful bipartite patella. A new approach to operative treatment. J Bone Joint Surg Am. 1994;76(4):573-578.
21. Mori Y, Okumo H, Iketani H, Kuroki Y. Efficacy of lateral retinacular release for painful bipartite patella. Am J Sports Med. 1995;23(1):13-18.
22. Lysholm J, Gillquist J. Evaluation of knee ligament surgery results with special emphasis on use of a scoring scale. Am J Sports Med. 1982;10(3):150-154
23. Grevnerts HT, Terwee CB, Kvist J. The measurement properties of the IKDC-subjective knee form. Knee Surg Sports Traumatol Arthrosc. 2015;23(12):3698-3706.
Internal Carotid Artery Dissection After Indirect Blunt Cervical Trauma in an Ice Hockey Goaltender
Take-Home Points
- ICA dissections may occur from direct or indirect trauma.
- Symptoms can be mild, including a persistent headache.
- High clinical suspicion is required for diagnosis when symptoms are mild.
- Neuroimaging is required for definitive diagnosis.
- Conservative management with serial imaging can yield successful outcomes.
Cervical artery dissection (CAD) is an uncommon but potentially life-threatening condition that accounts for a high proportion of ischemic strokes in patients under the age of 45 years.1-4 The extracranial internal carotid arteries (ICAs) and vertebral arteries are most commonly involved; dissections can occur after either direct trauma to the neck, or indirect trauma resulting in acute hyperextension or hyperflexion.4-7 ICA dissection can be difficult to diagnose because of the varying symptomatology. Clinical presentation depends on stenosis location, degree of luminal narrowing, and presence or absence of ischemic stroke. Neurologic symptoms may be delayed, and misdiagnosis of an isolated soft-tissue contusion, whiplash, can be made in the setting of indirect cervical trauma.
Although this entity is well described in the literature,2,3,5,8 there are few reported cases of injuries sustained during high-intensity athletic competition. In this case report, we describe the symptoms, physical examination findings, diagnostic imaging results, and treatment of a young male athlete who presented with delayed-onset symptoms of ICA dissection resulting from indirect cervical trauma sustained during an ice hockey game. We discuss the importance of a high level of clinical suspicion in the diagnosis of neck injuries sustained during athletic competition, as well as the need for early vascular imaging for diagnosis. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
The patient was a right-handed 32-year-old professional hockey goaltender. Four days before diagnosis, his goaltending mask and attached neck-protector were inadvertently lifted by another player’s stick just as a puck traveling at high speed struck him in the neck, to the right of the larynx, causing acute neck hyperextension. He immediately experienced discomfort and fell to the ice, saying he was “dizzy and light-headed.” Play was stopped, and medical personnel attended to him. His symptoms resolved, and he resumed play without any notable deficits. The next day, he noted discomfort at the impact site, but no additional symptoms, and received a presumptive diagnosis of cervical soft-tissue contusion. Continuing to participate in hockey that day, he did not develop any symptoms other than superficial cervical discomfort. However, the next morning, he presented complaining of severe right frontotemporal headache, which had persisted overnight. Orthopedic examination revealed palpable tenderness over the anterior cervical musculature, including the sternocleidomastoid and strap muscles. There was no appreciable hematoma in the contused area. Cervical range of motion was otherwise preserved. Cervical spine examination, including dermatomal and myotomal examination, was normal, as was cranial nerve examination. However, given the headache intensity and the recency of the injury, the potential for vascular or neurologic injury was considered. A neurology consultation was obtained, and arrangements were made for advanced cross-sectional imaging.
On further evaluation, the patient denied loss of consciousness, seizure, vomiting, amnesia, visual disturbance, language or cognitive impairment, balance or coordination difficulties, or any appreciable face or limb weakness. Review of systems was otherwise negative. Detailed neurologic examination did not reveal any cranial nerve deficits, and pupils were 3 mm, equal, and normally responsive to light and accommodation. Muscular tone and strength were symmetric and full in the upper and lower extremities. Gait, coordination, and response to vibration and temperature sensation were all preserved.
Magnetic resonance imaging of the head and neck was normal, but magnetic resonance angiography (MRA) of the neck showed a 1-cm-long region of the ICA, before piercing the petrous bone, with evidence of dissection. 
Given the normal neurologic examination, and no evidence of brain infarction or other neurovascular complications, the acute ICA dissection was managed with antiplatelet therapy using aspirin (325 mg/d). In addition, the patient was advised to refrain from strenuous physical activity and to present to the hospital immediately if symptoms worsened or any neurologic impairment developed. Follow-up and repeat MRA were planned to monitor healing progression.
Two weeks after injury, the patient returned for follow-up. His headache and neck pain had resolved. Physical examination findings were unchanged, and there were no notable neurologic deficits. Repeat MRA findings were essentially unchanged, except for slightly increased luminal stenosis, exceeding 50% (Figure 2), attributable to intramural hematoma formation. 
At 6-week follow-up, the patient had no clinical symptoms and no recurrence of headaches. 
Discussion
In cases of direct (blunt) or indirect cervical trauma, CAD should be considered, as it carries a risk of potentially debilitating ischemic stroke in otherwise healthy young patients. Fortunately, CAD is rare; its annual incidence is 1 in 100,000, occurring in 0.08% to 1.2% of blunt trauma cases.9 
As symptoms of ICA dissection can vary depending on stenosis severity, diagnosis can be challenging. The classically associated triad of symptoms includes unilateral head, facial, or neck pain accompanied by partial Horner syndrome with progression to cerebral or retinal ischemia. However, these symptoms occur in less than a third of patients with ICA dissection.2 Neck pain may occur secondary to blunt cervical trauma, consistent with a cervical soft-tissue contusion; however, it may have more severe implications and should be carefully monitored, particularly if accompanied by additional symptoms, such as headache. Headaches, which are present in 44% to 69% of patients, are often unilateral and constant. Either headache or neck pain in isolation is relatively uncommon, occurring in <10% of cases,2 though retrospective reviews of delayed-onset ICA dissection found atypical headache or neck pain in 100% of patients,11 indicating that persistent symptoms should be further evaluated.
More commonly, patients present with neurologic symptoms, particularly Horner syndrome, which is caused by the disruption of the sympathetic nerve fibers adjacent to the ICA, resulting in ipsilateral ptosis and miosis. In addition, patients may present with cranial nerve palsies, most commonly involving cranial nerve XII (the hypoglossal nerve), resulting in tongue weakness and abnormal taste. These and other neurologic findings associated with retinal or cerebral ischemia should raise clinical suspicion for the injury and prompt computed tomography or MRA evaluation.
MRA has largely replaced conventional angiography for the diagnosis of CAD. As MRA is noninvasive, it allows for improved visualization of luminal narrowing and for evaluation of the arterial wall and intramural hematoma.2 Because of the potential for devastating sequelae with missed or delayed diagnosis, several authors have become proponents of early aggressive screening for detection of these injuries.9 Postdiagnostic treatment depends on the presence of neurologic symptoms. Management is directed toward limiting neurologic deficits; anticoagulant or antiplatelet agents are used to prevent thromboembolic events. A randomized controlled trial and other studies have failed to find any appreciable difference in subsequent rates of stroke or associated complications with use of either class of medication.8,12 Conventionally, treatment is continued for 3 to 6 months, depending on clinical resolution. Endovascular or surgical intervention typically is reserved for extreme luminal narrowing, conditions that are preventing anticoagulation, an expanding area of dissection with a persistent pseudoaneurysm, and cases of failed medical management with subsequent ischemic stroke.2The literature includes several case reports involving indirect trauma in recreational athletes. First, a 31-year-old woman sustained an ICA dissection secondary to a head injury that occurred during a soccer match; she presented with headache, altered sense of taste, and objective findings of ptosis and miosis consistent with Horner syndrome.13 Second, a 39-year-old man had an ICA dissection after a snowboarding fall that caused neck hyperextension; he presented with periocular headache, ptosis, and miosis.6 Third, 3 people who participated in CrossFit training sustained ICA dissection.7 They presented with varying degrees of neurologic symptoms: ptosis and miosis; right-side upper extremity ataxia; and visual distortion and receptive aphasia. Our patient’s ICA dissection resulted from indirect trauma that caused sudden hyperextension and lateral flexion in response to contact from a hockey puck. However, his case is unique in that symptoms onset was delayed, and there were no associated neurologic findings on clinical presentation. His case should raise awareness of this potential diagnosis, even in the absence of overt neurologic findings. In addition, the patient’s return to sport at 8 weeks was facilitated by full clinical resolution of symptoms and thorough radiographic documentation of improved intramural narrowing. Finally, to our knowledge this is the first report of this injury in a professional athlete.
Conclusion
We have reported the case of a 32-year-old professional hockey goaltender who presented with isolated, persistent, worsening headache of delayed onset after ICA dissection. The ICA dissection resulted from indirect trauma, with reaction to a puck causing acute hyperextension and rotational injury. To our knowledge, this is the first report of a case of ICA dissection in an athlete, lacking neurologic examination findings that could aid in the diagnosis. The index of suspicion for CAD should be high after direct or indirect cervical trauma when patients present with unilateral neck pain or headache, even in the absence of neurologic findings, as stroke is a catastrophic but preventable complication.
Am J Orthop. 2017;46(3):E139-E143. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Mohan IV. Current optimal assessment and management of carotid and vertebral spontaneous and traumatic dissection. Angiology. 2014;65(4):274-283.
2. Patel RR, Adam R, Maldjian C, Lincoln CM, Yuen A, Arneja A. Cervical carotid artery dissection: current review of diagnosis and treatment. Cardiol Rev. 2012;20(3):145-152.
3. Biller J, Sacco RL, Albuquerque FC, et al; American Heart Association Stroke Council. Cervical arterial dissections and association with cervical manipulative therapy: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(10):3155-3174.
4. Fukunaga N, Hanaoka M, Sato K. Asymptomatic common carotid artery dissection caused by blunt injury. Emerg Med J. 2011;28(1):50.
5. Chen J, Zhou X, Li C, Cheung BM. Risk of stroke due to spontaneous cervical artery dissection. Intern Med. 2013;52(19):2237-2240.
6. Kalantzis G, Georgalas I, Chang BY, Ong C, El-Hindy N. An unusual case of traumatic internal carotid artery dissection during snowboarding. J Sports Sci Med. 2014;13(2):451-453.
7. Lu A, Shen P, Lee P, et al. CrossFit-related cervical internal carotid artery dissection. Emerg Radiol. 2015;22(4):449-452.
8. CADISS Trial Investigators, Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015;14(4):361-367.
9. van Wessem KJ, Meijer JM, Leenen LP, van der Worp HB, Moll FL, de Borst GJ. Blunt traumatic carotid artery dissection still a pitfall? The rationale for aggressive screening. Eur J Trauma Emerg Surg. 2011;37(2):147-154.
10. Haneline M, Triano J. Cervical artery dissection. A comparison of highly dynamic mechanisms: manipulation versus motor vehicle collision. J Manipulative Physiol Ther. 2005;28(1):57-63.
11. Thomas LC, Rivett DA, Attia JR, Levi C. Risk factors and clinical presentation of cervical arterial dissection: preliminary results of a prospective case-control study. J Orthop Sports Phys Ther. 2015;45(7):503-511.
12. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev. 2010;(10):CD000255.
13. Creavin ST, Rice CM, Pollentine A, Cowburn P. Carotid artery dissection presenting with isolated headache and Horner syndrome after minor head injury. Am J Emerg Med. 2012;30(9):2103.e5-e7.
Take-Home Points
- ICA dissections may occur from direct or indirect trauma.
- Symptoms can be mild, including a persistent headache.
- High clinical suspicion is required for diagnosis when symptoms are mild.
- Neuroimaging is required for definitive diagnosis.
- Conservative management with serial imaging can yield successful outcomes.
Cervical artery dissection (CAD) is an uncommon but potentially life-threatening condition that accounts for a high proportion of ischemic strokes in patients under the age of 45 years.1-4 The extracranial internal carotid arteries (ICAs) and vertebral arteries are most commonly involved; dissections can occur after either direct trauma to the neck, or indirect trauma resulting in acute hyperextension or hyperflexion.4-7 ICA dissection can be difficult to diagnose because of the varying symptomatology. Clinical presentation depends on stenosis location, degree of luminal narrowing, and presence or absence of ischemic stroke. Neurologic symptoms may be delayed, and misdiagnosis of an isolated soft-tissue contusion, whiplash, can be made in the setting of indirect cervical trauma.
Although this entity is well described in the literature,2,3,5,8 there are few reported cases of injuries sustained during high-intensity athletic competition. In this case report, we describe the symptoms, physical examination findings, diagnostic imaging results, and treatment of a young male athlete who presented with delayed-onset symptoms of ICA dissection resulting from indirect cervical trauma sustained during an ice hockey game. We discuss the importance of a high level of clinical suspicion in the diagnosis of neck injuries sustained during athletic competition, as well as the need for early vascular imaging for diagnosis. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
The patient was a right-handed 32-year-old professional hockey goaltender. Four days before diagnosis, his goaltending mask and attached neck-protector were inadvertently lifted by another player’s stick just as a puck traveling at high speed struck him in the neck, to the right of the larynx, causing acute neck hyperextension. He immediately experienced discomfort and fell to the ice, saying he was “dizzy and light-headed.” Play was stopped, and medical personnel attended to him. His symptoms resolved, and he resumed play without any notable deficits. The next day, he noted discomfort at the impact site, but no additional symptoms, and received a presumptive diagnosis of cervical soft-tissue contusion. Continuing to participate in hockey that day, he did not develop any symptoms other than superficial cervical discomfort. However, the next morning, he presented complaining of severe right frontotemporal headache, which had persisted overnight. Orthopedic examination revealed palpable tenderness over the anterior cervical musculature, including the sternocleidomastoid and strap muscles. There was no appreciable hematoma in the contused area. Cervical range of motion was otherwise preserved. Cervical spine examination, including dermatomal and myotomal examination, was normal, as was cranial nerve examination. However, given the headache intensity and the recency of the injury, the potential for vascular or neurologic injury was considered. A neurology consultation was obtained, and arrangements were made for advanced cross-sectional imaging.
On further evaluation, the patient denied loss of consciousness, seizure, vomiting, amnesia, visual disturbance, language or cognitive impairment, balance or coordination difficulties, or any appreciable face or limb weakness. Review of systems was otherwise negative. Detailed neurologic examination did not reveal any cranial nerve deficits, and pupils were 3 mm, equal, and normally responsive to light and accommodation. Muscular tone and strength were symmetric and full in the upper and lower extremities. Gait, coordination, and response to vibration and temperature sensation were all preserved.
Magnetic resonance imaging of the head and neck was normal, but magnetic resonance angiography (MRA) of the neck showed a 1-cm-long region of the ICA, before piercing the petrous bone, with evidence of dissection.
Given the normal neurologic examination, and no evidence of brain infarction or other neurovascular complications, the acute ICA dissection was managed with antiplatelet therapy using aspirin (325 mg/d). In addition, the patient was advised to refrain from strenuous physical activity and to present to the hospital immediately if symptoms worsened or any neurologic impairment developed. Follow-up and repeat MRA were planned to monitor healing progression.
Two weeks after injury, the patient returned for follow-up. His headache and neck pain had resolved. Physical examination findings were unchanged, and there were no notable neurologic deficits. Repeat MRA findings were essentially unchanged, except for slightly increased luminal stenosis, exceeding 50% (Figure 2), attributable to intramural hematoma formation.
At 6-week follow-up, the patient had no clinical symptoms and no recurrence of headaches.
Discussion
In cases of direct (blunt) or indirect cervical trauma, CAD should be considered, as it carries a risk of potentially debilitating ischemic stroke in otherwise healthy young patients. Fortunately, CAD is rare; its annual incidence is 1 in 100,000, occurring in 0.08% to 1.2% of blunt trauma cases.9
As symptoms of ICA dissection can vary depending on stenosis severity, diagnosis can be challenging. The classically associated triad of symptoms includes unilateral head, facial, or neck pain accompanied by partial Horner syndrome with progression to cerebral or retinal ischemia. However, these symptoms occur in less than a third of patients with ICA dissection.2 Neck pain may occur secondary to blunt cervical trauma, consistent with a cervical soft-tissue contusion; however, it may have more severe implications and should be carefully monitored, particularly if accompanied by additional symptoms, such as headache. Headaches, which are present in 44% to 69% of patients, are often unilateral and constant. Either headache or neck pain in isolation is relatively uncommon, occurring in <10% of cases,2 though retrospective reviews of delayed-onset ICA dissection found atypical headache or neck pain in 100% of patients,11 indicating that persistent symptoms should be further evaluated.
More commonly, patients present with neurologic symptoms, particularly Horner syndrome, which is caused by the disruption of the sympathetic nerve fibers adjacent to the ICA, resulting in ipsilateral ptosis and miosis. In addition, patients may present with cranial nerve palsies, most commonly involving cranial nerve XII (the hypoglossal nerve), resulting in tongue weakness and abnormal taste. These and other neurologic findings associated with retinal or cerebral ischemia should raise clinical suspicion for the injury and prompt computed tomography or MRA evaluation.
MRA has largely replaced conventional angiography for the diagnosis of CAD. As MRA is noninvasive, it allows for improved visualization of luminal narrowing and for evaluation of the arterial wall and intramural hematoma.2 Because of the potential for devastating sequelae with missed or delayed diagnosis, several authors have become proponents of early aggressive screening for detection of these injuries.9 Postdiagnostic treatment depends on the presence of neurologic symptoms. Management is directed toward limiting neurologic deficits; anticoagulant or antiplatelet agents are used to prevent thromboembolic events. A randomized controlled trial and other studies have failed to find any appreciable difference in subsequent rates of stroke or associated complications with use of either class of medication.8,12 Conventionally, treatment is continued for 3 to 6 months, depending on clinical resolution. Endovascular or surgical intervention typically is reserved for extreme luminal narrowing, conditions that are preventing anticoagulation, an expanding area of dissection with a persistent pseudoaneurysm, and cases of failed medical management with subsequent ischemic stroke.2The literature includes several case reports involving indirect trauma in recreational athletes. First, a 31-year-old woman sustained an ICA dissection secondary to a head injury that occurred during a soccer match; she presented with headache, altered sense of taste, and objective findings of ptosis and miosis consistent with Horner syndrome.13 Second, a 39-year-old man had an ICA dissection after a snowboarding fall that caused neck hyperextension; he presented with periocular headache, ptosis, and miosis.6 Third, 3 people who participated in CrossFit training sustained ICA dissection.7 They presented with varying degrees of neurologic symptoms: ptosis and miosis; right-side upper extremity ataxia; and visual distortion and receptive aphasia. Our patient’s ICA dissection resulted from indirect trauma that caused sudden hyperextension and lateral flexion in response to contact from a hockey puck. However, his case is unique in that symptoms onset was delayed, and there were no associated neurologic findings on clinical presentation. His case should raise awareness of this potential diagnosis, even in the absence of overt neurologic findings. In addition, the patient’s return to sport at 8 weeks was facilitated by full clinical resolution of symptoms and thorough radiographic documentation of improved intramural narrowing. Finally, to our knowledge this is the first report of this injury in a professional athlete.
Conclusion
We have reported the case of a 32-year-old professional hockey goaltender who presented with isolated, persistent, worsening headache of delayed onset after ICA dissection. The ICA dissection resulted from indirect trauma, with reaction to a puck causing acute hyperextension and rotational injury. To our knowledge, this is the first report of a case of ICA dissection in an athlete, lacking neurologic examination findings that could aid in the diagnosis. The index of suspicion for CAD should be high after direct or indirect cervical trauma when patients present with unilateral neck pain or headache, even in the absence of neurologic findings, as stroke is a catastrophic but preventable complication.
Am J Orthop. 2017;46(3):E139-E143. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- ICA dissections may occur from direct or indirect trauma.
- Symptoms can be mild, including a persistent headache.
- High clinical suspicion is required for diagnosis when symptoms are mild.
- Neuroimaging is required for definitive diagnosis.
- Conservative management with serial imaging can yield successful outcomes.
Cervical artery dissection (CAD) is an uncommon but potentially life-threatening condition that accounts for a high proportion of ischemic strokes in patients under the age of 45 years.1-4 The extracranial internal carotid arteries (ICAs) and vertebral arteries are most commonly involved; dissections can occur after either direct trauma to the neck, or indirect trauma resulting in acute hyperextension or hyperflexion.4-7 ICA dissection can be difficult to diagnose because of the varying symptomatology. Clinical presentation depends on stenosis location, degree of luminal narrowing, and presence or absence of ischemic stroke. Neurologic symptoms may be delayed, and misdiagnosis of an isolated soft-tissue contusion, whiplash, can be made in the setting of indirect cervical trauma.
Although this entity is well described in the literature,2,3,5,8 there are few reported cases of injuries sustained during high-intensity athletic competition. In this case report, we describe the symptoms, physical examination findings, diagnostic imaging results, and treatment of a young male athlete who presented with delayed-onset symptoms of ICA dissection resulting from indirect cervical trauma sustained during an ice hockey game. We discuss the importance of a high level of clinical suspicion in the diagnosis of neck injuries sustained during athletic competition, as well as the need for early vascular imaging for diagnosis. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
The patient was a right-handed 32-year-old professional hockey goaltender. Four days before diagnosis, his goaltending mask and attached neck-protector were inadvertently lifted by another player’s stick just as a puck traveling at high speed struck him in the neck, to the right of the larynx, causing acute neck hyperextension. He immediately experienced discomfort and fell to the ice, saying he was “dizzy and light-headed.” Play was stopped, and medical personnel attended to him. His symptoms resolved, and he resumed play without any notable deficits. The next day, he noted discomfort at the impact site, but no additional symptoms, and received a presumptive diagnosis of cervical soft-tissue contusion. Continuing to participate in hockey that day, he did not develop any symptoms other than superficial cervical discomfort. However, the next morning, he presented complaining of severe right frontotemporal headache, which had persisted overnight. Orthopedic examination revealed palpable tenderness over the anterior cervical musculature, including the sternocleidomastoid and strap muscles. There was no appreciable hematoma in the contused area. Cervical range of motion was otherwise preserved. Cervical spine examination, including dermatomal and myotomal examination, was normal, as was cranial nerve examination. However, given the headache intensity and the recency of the injury, the potential for vascular or neurologic injury was considered. A neurology consultation was obtained, and arrangements were made for advanced cross-sectional imaging.
On further evaluation, the patient denied loss of consciousness, seizure, vomiting, amnesia, visual disturbance, language or cognitive impairment, balance or coordination difficulties, or any appreciable face or limb weakness. Review of systems was otherwise negative. Detailed neurologic examination did not reveal any cranial nerve deficits, and pupils were 3 mm, equal, and normally responsive to light and accommodation. Muscular tone and strength were symmetric and full in the upper and lower extremities. Gait, coordination, and response to vibration and temperature sensation were all preserved.
Magnetic resonance imaging of the head and neck was normal, but magnetic resonance angiography (MRA) of the neck showed a 1-cm-long region of the ICA, before piercing the petrous bone, with evidence of dissection.
Given the normal neurologic examination, and no evidence of brain infarction or other neurovascular complications, the acute ICA dissection was managed with antiplatelet therapy using aspirin (325 mg/d). In addition, the patient was advised to refrain from strenuous physical activity and to present to the hospital immediately if symptoms worsened or any neurologic impairment developed. Follow-up and repeat MRA were planned to monitor healing progression.
Two weeks after injury, the patient returned for follow-up. His headache and neck pain had resolved. Physical examination findings were unchanged, and there were no notable neurologic deficits. Repeat MRA findings were essentially unchanged, except for slightly increased luminal stenosis, exceeding 50% (Figure 2), attributable to intramural hematoma formation.
At 6-week follow-up, the patient had no clinical symptoms and no recurrence of headaches.
Discussion
In cases of direct (blunt) or indirect cervical trauma, CAD should be considered, as it carries a risk of potentially debilitating ischemic stroke in otherwise healthy young patients. Fortunately, CAD is rare; its annual incidence is 1 in 100,000, occurring in 0.08% to 1.2% of blunt trauma cases.9
As symptoms of ICA dissection can vary depending on stenosis severity, diagnosis can be challenging. The classically associated triad of symptoms includes unilateral head, facial, or neck pain accompanied by partial Horner syndrome with progression to cerebral or retinal ischemia. However, these symptoms occur in less than a third of patients with ICA dissection.2 Neck pain may occur secondary to blunt cervical trauma, consistent with a cervical soft-tissue contusion; however, it may have more severe implications and should be carefully monitored, particularly if accompanied by additional symptoms, such as headache. Headaches, which are present in 44% to 69% of patients, are often unilateral and constant. Either headache or neck pain in isolation is relatively uncommon, occurring in <10% of cases,2 though retrospective reviews of delayed-onset ICA dissection found atypical headache or neck pain in 100% of patients,11 indicating that persistent symptoms should be further evaluated.
More commonly, patients present with neurologic symptoms, particularly Horner syndrome, which is caused by the disruption of the sympathetic nerve fibers adjacent to the ICA, resulting in ipsilateral ptosis and miosis. In addition, patients may present with cranial nerve palsies, most commonly involving cranial nerve XII (the hypoglossal nerve), resulting in tongue weakness and abnormal taste. These and other neurologic findings associated with retinal or cerebral ischemia should raise clinical suspicion for the injury and prompt computed tomography or MRA evaluation.
MRA has largely replaced conventional angiography for the diagnosis of CAD. As MRA is noninvasive, it allows for improved visualization of luminal narrowing and for evaluation of the arterial wall and intramural hematoma.2 Because of the potential for devastating sequelae with missed or delayed diagnosis, several authors have become proponents of early aggressive screening for detection of these injuries.9 Postdiagnostic treatment depends on the presence of neurologic symptoms. Management is directed toward limiting neurologic deficits; anticoagulant or antiplatelet agents are used to prevent thromboembolic events. A randomized controlled trial and other studies have failed to find any appreciable difference in subsequent rates of stroke or associated complications with use of either class of medication.8,12 Conventionally, treatment is continued for 3 to 6 months, depending on clinical resolution. Endovascular or surgical intervention typically is reserved for extreme luminal narrowing, conditions that are preventing anticoagulation, an expanding area of dissection with a persistent pseudoaneurysm, and cases of failed medical management with subsequent ischemic stroke.2The literature includes several case reports involving indirect trauma in recreational athletes. First, a 31-year-old woman sustained an ICA dissection secondary to a head injury that occurred during a soccer match; she presented with headache, altered sense of taste, and objective findings of ptosis and miosis consistent with Horner syndrome.13 Second, a 39-year-old man had an ICA dissection after a snowboarding fall that caused neck hyperextension; he presented with periocular headache, ptosis, and miosis.6 Third, 3 people who participated in CrossFit training sustained ICA dissection.7 They presented with varying degrees of neurologic symptoms: ptosis and miosis; right-side upper extremity ataxia; and visual distortion and receptive aphasia. Our patient’s ICA dissection resulted from indirect trauma that caused sudden hyperextension and lateral flexion in response to contact from a hockey puck. However, his case is unique in that symptoms onset was delayed, and there were no associated neurologic findings on clinical presentation. His case should raise awareness of this potential diagnosis, even in the absence of overt neurologic findings. In addition, the patient’s return to sport at 8 weeks was facilitated by full clinical resolution of symptoms and thorough radiographic documentation of improved intramural narrowing. Finally, to our knowledge this is the first report of this injury in a professional athlete.
Conclusion
We have reported the case of a 32-year-old professional hockey goaltender who presented with isolated, persistent, worsening headache of delayed onset after ICA dissection. The ICA dissection resulted from indirect trauma, with reaction to a puck causing acute hyperextension and rotational injury. To our knowledge, this is the first report of a case of ICA dissection in an athlete, lacking neurologic examination findings that could aid in the diagnosis. The index of suspicion for CAD should be high after direct or indirect cervical trauma when patients present with unilateral neck pain or headache, even in the absence of neurologic findings, as stroke is a catastrophic but preventable complication.
Am J Orthop. 2017;46(3):E139-E143. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Mohan IV. Current optimal assessment and management of carotid and vertebral spontaneous and traumatic dissection. Angiology. 2014;65(4):274-283.
2. Patel RR, Adam R, Maldjian C, Lincoln CM, Yuen A, Arneja A. Cervical carotid artery dissection: current review of diagnosis and treatment. Cardiol Rev. 2012;20(3):145-152.
3. Biller J, Sacco RL, Albuquerque FC, et al; American Heart Association Stroke Council. Cervical arterial dissections and association with cervical manipulative therapy: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(10):3155-3174.
4. Fukunaga N, Hanaoka M, Sato K. Asymptomatic common carotid artery dissection caused by blunt injury. Emerg Med J. 2011;28(1):50.
5. Chen J, Zhou X, Li C, Cheung BM. Risk of stroke due to spontaneous cervical artery dissection. Intern Med. 2013;52(19):2237-2240.
6. Kalantzis G, Georgalas I, Chang BY, Ong C, El-Hindy N. An unusual case of traumatic internal carotid artery dissection during snowboarding. J Sports Sci Med. 2014;13(2):451-453.
7. Lu A, Shen P, Lee P, et al. CrossFit-related cervical internal carotid artery dissection. Emerg Radiol. 2015;22(4):449-452.
8. CADISS Trial Investigators, Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015;14(4):361-367.
9. van Wessem KJ, Meijer JM, Leenen LP, van der Worp HB, Moll FL, de Borst GJ. Blunt traumatic carotid artery dissection still a pitfall? The rationale for aggressive screening. Eur J Trauma Emerg Surg. 2011;37(2):147-154.
10. Haneline M, Triano J. Cervical artery dissection. A comparison of highly dynamic mechanisms: manipulation versus motor vehicle collision. J Manipulative Physiol Ther. 2005;28(1):57-63.
11. Thomas LC, Rivett DA, Attia JR, Levi C. Risk factors and clinical presentation of cervical arterial dissection: preliminary results of a prospective case-control study. J Orthop Sports Phys Ther. 2015;45(7):503-511.
12. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev. 2010;(10):CD000255.
13. Creavin ST, Rice CM, Pollentine A, Cowburn P. Carotid artery dissection presenting with isolated headache and Horner syndrome after minor head injury. Am J Emerg Med. 2012;30(9):2103.e5-e7.
1. Mohan IV. Current optimal assessment and management of carotid and vertebral spontaneous and traumatic dissection. Angiology. 2014;65(4):274-283.
2. Patel RR, Adam R, Maldjian C, Lincoln CM, Yuen A, Arneja A. Cervical carotid artery dissection: current review of diagnosis and treatment. Cardiol Rev. 2012;20(3):145-152.
3. Biller J, Sacco RL, Albuquerque FC, et al; American Heart Association Stroke Council. Cervical arterial dissections and association with cervical manipulative therapy: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(10):3155-3174.
4. Fukunaga N, Hanaoka M, Sato K. Asymptomatic common carotid artery dissection caused by blunt injury. Emerg Med J. 2011;28(1):50.
5. Chen J, Zhou X, Li C, Cheung BM. Risk of stroke due to spontaneous cervical artery dissection. Intern Med. 2013;52(19):2237-2240.
6. Kalantzis G, Georgalas I, Chang BY, Ong C, El-Hindy N. An unusual case of traumatic internal carotid artery dissection during snowboarding. J Sports Sci Med. 2014;13(2):451-453.
7. Lu A, Shen P, Lee P, et al. CrossFit-related cervical internal carotid artery dissection. Emerg Radiol. 2015;22(4):449-452.
8. CADISS Trial Investigators, Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015;14(4):361-367.
9. van Wessem KJ, Meijer JM, Leenen LP, van der Worp HB, Moll FL, de Borst GJ. Blunt traumatic carotid artery dissection still a pitfall? The rationale for aggressive screening. Eur J Trauma Emerg Surg. 2011;37(2):147-154.
10. Haneline M, Triano J. Cervical artery dissection. A comparison of highly dynamic mechanisms: manipulation versus motor vehicle collision. J Manipulative Physiol Ther. 2005;28(1):57-63.
11. Thomas LC, Rivett DA, Attia JR, Levi C. Risk factors and clinical presentation of cervical arterial dissection: preliminary results of a prospective case-control study. J Orthop Sports Phys Ther. 2015;45(7):503-511.
12. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev. 2010;(10):CD000255.
13. Creavin ST, Rice CM, Pollentine A, Cowburn P. Carotid artery dissection presenting with isolated headache and Horner syndrome after minor head injury. Am J Emerg Med. 2012;30(9):2103.e5-e7.
Encapsulated Fat Necrosis Lesion Caused by Morel-Lavallée Lesion in a Professional Ice Hockey Player
Take-Home Points
- ML lesions usually occur with high-energy injuries and have been reported in wrestlers, football players, and other athlete populations.
- Encapsulated fat necrosis lesions are usually attributable to trauma and disruption of the blood supply in the subcutaneous area, which occurs with ML lesions.
- Encapsulated fat necrosis lesions are rare; only 65 have been reported.
- Encapsulated fat necrosis lesions are characterized by massive fat necrosis encapsulated by fibrous tissue.
- Most are small and asymptomatic; however, in some cases, athletes can develop symptoms from frequent impacts to the region where the lesions are located.
What would become known as the Morel-Lavallée (ML) lesion was first reported in 1853 by French physician Maurice Morel-Lavallée. He described a proximal thigh soft-tissue injury that resulted in a hemolymphatic collection between superficial fascial planes. Deforming forces of pressure and shear result in an internal degloving injury in which subcutaneous tissue is stripped from the fascia and replaced with a hematoma or, less commonly, necrotic fat.1-4 The injury can take several weeks to heal. Up to one-third of such injuries are initially missed because of the initial ecchymosis covering the injured area.5
ML lesions usually occur with high-energy injuries and have been reported in wrestlers,6 football players,7-9 and other athlete populations. ML lesions usually occur about the knee, the site of the sheer mechanism in these athletes’ sports. Tejwani and colleagues9 reported on 24 National Football League (NFL) players (27 knees). These elite athletes typically were able to return to practice and game play long before complete resolution of their lesions.
Nodular cystic fat necrosis was first described by Przyjemski and Schuster10 in 1977. The terms encapsulated fat necrosis lesions and mobile encapsulated lipomas11 were introduced later. Clinically, these entities usually present as lesions on the lower limbs of young men and middle-aged women and can range in size from 1 mm to 35 mm. Most of these lesions are mobile.11 They are usually attributable to trauma and disruption of the blood supply in the subcutaneous area, which occurs with ML lesions. Trauma accounts for the usual occurrence in the lower extremities, though only 40% of patients recall a precipitating event.12 Histologically, these lesions are characterized by massive fat necrosis encapsulated by fibrous tissue.13In this article, we report the case of a professional ice hockey player who presented with an ML lesion of the hip and then developed a symptomatic encapsulated fat necrosis lesion that required surgical removal. To our knowledge, this is the first reported case of an encapsulated fat necrosis lesion caused by an ML lesion in an athlete. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 21-year-old professional hockey player presented with a history of pain from a mass on his right hip. He first noticed the lesion, just lateral to the greater trochanter, about 3 years earlier. The mass appeared after he sustained a shearing-type injury to the lateral aspect of the hip. At the time, there was significant swelling along the lateral aspect, with ecchymosis that resolved over 2 months. The mass, diagnosed as an ML lesion, resolved with nonoperative treatment. However, in the area where the swelling had occurred, a hard mobile mass remained. At times, this mass became painful when direct pressure was applied, as when he hit the boards while playing hockey, or when he lay on his right side or used a roller in the training room. He rated the pain as a 4 on a 1-to-10 scale and said the mass was mobile and had not changed in size or consistency.
Physical examination revealed a palpable mass over the lateral aspect of the hip, over the greater trochanter. The mass, about 3 cm in diameter (Figure 1), was mobile in a subcutaneous pocket, consistent with an old ML lesion. 
Options discussed with the patient included use of ice, activity modification, and use of protective padded equipment. As the patient had tried these treatments before and was still intermittently having pain with direct pressure, he asked for surgical removal of the mass.
For the surgery, the patient was positioned in the lateral decubitus position with his right hip facing up. The right hip and thigh were prepared and draped in sterile fashion. An incision 4 cm in length was made directly over the mass, along the lateral aspect of the hip, over the greater trochanter. The incision was taken through skin and subcutaneous tissue down to the deep fascia. The fascia was incised longitudinally in line with the overlying skin incision. As soon as the incision was made through the fascia, the mass was easily seen. The 3-cm × 2-cm × 1-cm mass was free, not attached to any underlying soft tissue (Figure 3). 
Discussion
We have described a case of symptomatic encapsulated fat necrosis lesion caused by an ML lesion in a professional hockey player. The ML lesion had resolved with nonoperative treatment (compression), but a subcutaneous pocket remained at the lesion site. Given the patient’s lesion site and occupation as a hockey player, pain with direct pressure on this lesion was a concern.
Long-standing ML lesions have 3 common patterns on MRI.14 A central region, encapsulated partially or completely by a peripheral ring of fibrous tissue or hemosiderin, shows signal properties consistent with a seroma, a homogeneous hemorrhagic collection, or a heterogeneous hemorrhagic collection. In our patient’s case, MRI was used to characterize the mobile mass for operative planning. Although thin strands or lobules of fat have been found within ML lesions, this case was the first to demonstrate a sequestered mass of necrotic fat.
Most football players who develop ML lesions on their knees do not wear kneepads.7-9 Of the 24 NFL players in the study by Tejwani and colleagues,9 52% were successfully treated with compression wrap, cryotherapy, and motion exercises. The rest, however, were treated with aspiration, and 11% underwent doxycycline sclerodesis for recurrent fluid collection. After treatment, all of their players were able to return to football. Their outcomes are consistent with that of our patient, who was treated with compression wrap and returned to hockey without any other intervention.
After our patient’s ML lesion resolved, he developed an encapsulated fat necrosis lesion from the disruption of the blood supply in the subcutaneous pocket. Encapsulated fat necrosis lesions are rare; only 65 have been reported.13,15 Clinically, these lesions are single or multiple pale-yellow encapsulated nodes.13 Most are small and asymptomatic; however, in some cases, athletes can develop symptoms from frequent impacts to the region where the lesions are located.
The literature includes 1 report of an adolescent football player who developed multiple encapsulated fat necrosis lesions 4 months after landing on another player’s cleats.15 The patient, who was having pain with direct pressure during squatting and kneeling, elected to have the lesions surgically removed. These lesions are rare and usually asymptomatic,11 but our patient had his lesion surgically removed to address the pain induced by the direct impacts that came with playing professional hockey. Surgical removal is the treatment for symptomatic encapsulated fat necrosis lesions. Other than 1 case of recurrence after excision,16 these lesions have an excellent prognosis.
Conclusion
Our patient, a professional hockey player, underwent successful surgical removal of a symptomatic encapsulated fat necrosis lesion that had developed from an ML lesion.
Am J Orthop. 2017;46(3):E144-E147. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Aguiar RO, Viegas FC, Fernandez RY, Trudell D, Haghighi P, Resnick D. The prepatellar bursa: cadaveric investigation of regional anatomy with MRI after sonographically guided bursography. AJR Am J Roentgenol. 2007;188(4):W355-W358.
2. Hak DJ, Olson SA, Matta JM. Diagnosis and management of closed internal degloving injuries associated with pelvic and acetabular fractures: the Morel-Lavallée lesion. J Trauma. 1997;42(6):1046-1051.
3. Hudson DA, Knottenbelt JD, Krige JE. Closed degloving injuries: results following conservative surgery. Plast Reconstr Surg. 1992;89(5):853-855.
4. Mellado JM, Bencardino JT. Morel-Lavallée lesion: review with emphasis on MR imaging. Magn Reson Imaging Clin North Am. 2005;13(4):775-782.
5. Dye SF, Campagna-Pinto D, Dye CC, Shifflett S, Eiman T. Soft-tissue anatomy anterior to the human patella. J Bone Joint Surg Am. 2003;85(6):1012-1017.
6. Northam MC, Gaskin CM. Presumed prepatellar fibrosis in collegiate wrestlers: imaging findings and clinical correlation. Skeletal Radiol. 2015;44(2):271-277.
7. Anakwenze OA, Trivedi V, Goodman AM, Ganley TJ. Concealed degloving injury (the Morel-Lavallée lesion) in childhood sports: a case report. J Bone Joint Surg Am. 2011;93(24):e148.
8. Matava MJ, Ellis E, Shah NR, Pogue D, Williams T. Morel-Lavallée lesion in a professional American football player. Am J Orthop. 2010;39(3):144-147.
9. Tejwani SG, Cohen SB, Bradley JP. Management of Morel-Lavallee lesion of the knee: twenty-seven cases in the National Football League. Am J Sports Med. 2007;35(7):1162-1167.
10. Przyjemski CJ, Schuster SR. Nodular-cystic fat necrosis. J Pediatr. 1977;91(4):605-607.
11. Kiryu H, Rikihisa W, Furue M. Encapsulated fat necrosis—a clinicopathological study of 8 cases and a literature review. J Cutan Pathol. 2000;27(1):19-23.
12. Santos-Juanes J, Coto P, Galache C, Sánchez del Rio J, Soto de Delás J. Encapsulated fat necrosis: a form of traumatic panniculitis. J Eur Acad Dermatol Venereol. 2007;21(3):405-406.
13. Sempau L, Sambucetty PS, Garcia JL, Sixto BG, Morán AG, Prieto MA. Mobile encapsulated lipoma. Int J Dermatol. 2012;51(4):448-450.
14. Mellado JM, Pérez del Palomar L, Díaz L, Ramos A, Saurí A. Long-standing Morel-Lavallée lesions of the trochanteric region and proximal thigh: MRI features in five patients. AJR Am J Roentgenol. 2004;182(5):1289-1294.
15. Sole JS, Wisniewski SJ, Dahm DL, Bond J, Smith J. Posttraumatic fat necrosis presenting as prepatellar loose bodies in an adolescent football player. PM R. 2014;6(8):749-752.
16. Felipo F, Vaquero M, del Agua C. Pseudotumoral encapsulated fat necrosis with diffuse pseudomembranous degeneration. J Cutan Pathol. 2004;31(8):565-567.
Take-Home Points
- ML lesions usually occur with high-energy injuries and have been reported in wrestlers, football players, and other athlete populations.
- Encapsulated fat necrosis lesions are usually attributable to trauma and disruption of the blood supply in the subcutaneous area, which occurs with ML lesions.
- Encapsulated fat necrosis lesions are rare; only 65 have been reported.
- Encapsulated fat necrosis lesions are characterized by massive fat necrosis encapsulated by fibrous tissue.
- Most are small and asymptomatic; however, in some cases, athletes can develop symptoms from frequent impacts to the region where the lesions are located.
What would become known as the Morel-Lavallée (ML) lesion was first reported in 1853 by French physician Maurice Morel-Lavallée. He described a proximal thigh soft-tissue injury that resulted in a hemolymphatic collection between superficial fascial planes. Deforming forces of pressure and shear result in an internal degloving injury in which subcutaneous tissue is stripped from the fascia and replaced with a hematoma or, less commonly, necrotic fat.1-4 The injury can take several weeks to heal. Up to one-third of such injuries are initially missed because of the initial ecchymosis covering the injured area.5
ML lesions usually occur with high-energy injuries and have been reported in wrestlers,6 football players,7-9 and other athlete populations. ML lesions usually occur about the knee, the site of the sheer mechanism in these athletes’ sports. Tejwani and colleagues9 reported on 24 National Football League (NFL) players (27 knees). These elite athletes typically were able to return to practice and game play long before complete resolution of their lesions.
Nodular cystic fat necrosis was first described by Przyjemski and Schuster10 in 1977. The terms encapsulated fat necrosis lesions and mobile encapsulated lipomas11 were introduced later. Clinically, these entities usually present as lesions on the lower limbs of young men and middle-aged women and can range in size from 1 mm to 35 mm. Most of these lesions are mobile.11 They are usually attributable to trauma and disruption of the blood supply in the subcutaneous area, which occurs with ML lesions. Trauma accounts for the usual occurrence in the lower extremities, though only 40% of patients recall a precipitating event.12 Histologically, these lesions are characterized by massive fat necrosis encapsulated by fibrous tissue.13In this article, we report the case of a professional ice hockey player who presented with an ML lesion of the hip and then developed a symptomatic encapsulated fat necrosis lesion that required surgical removal. To our knowledge, this is the first reported case of an encapsulated fat necrosis lesion caused by an ML lesion in an athlete. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 21-year-old professional hockey player presented with a history of pain from a mass on his right hip. He first noticed the lesion, just lateral to the greater trochanter, about 3 years earlier. The mass appeared after he sustained a shearing-type injury to the lateral aspect of the hip. At the time, there was significant swelling along the lateral aspect, with ecchymosis that resolved over 2 months. The mass, diagnosed as an ML lesion, resolved with nonoperative treatment. However, in the area where the swelling had occurred, a hard mobile mass remained. At times, this mass became painful when direct pressure was applied, as when he hit the boards while playing hockey, or when he lay on his right side or used a roller in the training room. He rated the pain as a 4 on a 1-to-10 scale and said the mass was mobile and had not changed in size or consistency.
Physical examination revealed a palpable mass over the lateral aspect of the hip, over the greater trochanter. The mass, about 3 cm in diameter (Figure 1), was mobile in a subcutaneous pocket, consistent with an old ML lesion.
Options discussed with the patient included use of ice, activity modification, and use of protective padded equipment. As the patient had tried these treatments before and was still intermittently having pain with direct pressure, he asked for surgical removal of the mass.
For the surgery, the patient was positioned in the lateral decubitus position with his right hip facing up. The right hip and thigh were prepared and draped in sterile fashion. An incision 4 cm in length was made directly over the mass, along the lateral aspect of the hip, over the greater trochanter. The incision was taken through skin and subcutaneous tissue down to the deep fascia. The fascia was incised longitudinally in line with the overlying skin incision. As soon as the incision was made through the fascia, the mass was easily seen. The 3-cm × 2-cm × 1-cm mass was free, not attached to any underlying soft tissue (Figure 3).
Discussion
We have described a case of symptomatic encapsulated fat necrosis lesion caused by an ML lesion in a professional hockey player. The ML lesion had resolved with nonoperative treatment (compression), but a subcutaneous pocket remained at the lesion site. Given the patient’s lesion site and occupation as a hockey player, pain with direct pressure on this lesion was a concern.
Long-standing ML lesions have 3 common patterns on MRI.14 A central region, encapsulated partially or completely by a peripheral ring of fibrous tissue or hemosiderin, shows signal properties consistent with a seroma, a homogeneous hemorrhagic collection, or a heterogeneous hemorrhagic collection. In our patient’s case, MRI was used to characterize the mobile mass for operative planning. Although thin strands or lobules of fat have been found within ML lesions, this case was the first to demonstrate a sequestered mass of necrotic fat.
Most football players who develop ML lesions on their knees do not wear kneepads.7-9 Of the 24 NFL players in the study by Tejwani and colleagues,9 52% were successfully treated with compression wrap, cryotherapy, and motion exercises. The rest, however, were treated with aspiration, and 11% underwent doxycycline sclerodesis for recurrent fluid collection. After treatment, all of their players were able to return to football. Their outcomes are consistent with that of our patient, who was treated with compression wrap and returned to hockey without any other intervention.
After our patient’s ML lesion resolved, he developed an encapsulated fat necrosis lesion from the disruption of the blood supply in the subcutaneous pocket. Encapsulated fat necrosis lesions are rare; only 65 have been reported.13,15 Clinically, these lesions are single or multiple pale-yellow encapsulated nodes.13 Most are small and asymptomatic; however, in some cases, athletes can develop symptoms from frequent impacts to the region where the lesions are located.
The literature includes 1 report of an adolescent football player who developed multiple encapsulated fat necrosis lesions 4 months after landing on another player’s cleats.15 The patient, who was having pain with direct pressure during squatting and kneeling, elected to have the lesions surgically removed. These lesions are rare and usually asymptomatic,11 but our patient had his lesion surgically removed to address the pain induced by the direct impacts that came with playing professional hockey. Surgical removal is the treatment for symptomatic encapsulated fat necrosis lesions. Other than 1 case of recurrence after excision,16 these lesions have an excellent prognosis.
Conclusion
Our patient, a professional hockey player, underwent successful surgical removal of a symptomatic encapsulated fat necrosis lesion that had developed from an ML lesion.
Am J Orthop. 2017;46(3):E144-E147. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- ML lesions usually occur with high-energy injuries and have been reported in wrestlers, football players, and other athlete populations.
- Encapsulated fat necrosis lesions are usually attributable to trauma and disruption of the blood supply in the subcutaneous area, which occurs with ML lesions.
- Encapsulated fat necrosis lesions are rare; only 65 have been reported.
- Encapsulated fat necrosis lesions are characterized by massive fat necrosis encapsulated by fibrous tissue.
- Most are small and asymptomatic; however, in some cases, athletes can develop symptoms from frequent impacts to the region where the lesions are located.
What would become known as the Morel-Lavallée (ML) lesion was first reported in 1853 by French physician Maurice Morel-Lavallée. He described a proximal thigh soft-tissue injury that resulted in a hemolymphatic collection between superficial fascial planes. Deforming forces of pressure and shear result in an internal degloving injury in which subcutaneous tissue is stripped from the fascia and replaced with a hematoma or, less commonly, necrotic fat.1-4 The injury can take several weeks to heal. Up to one-third of such injuries are initially missed because of the initial ecchymosis covering the injured area.5
ML lesions usually occur with high-energy injuries and have been reported in wrestlers,6 football players,7-9 and other athlete populations. ML lesions usually occur about the knee, the site of the sheer mechanism in these athletes’ sports. Tejwani and colleagues9 reported on 24 National Football League (NFL) players (27 knees). These elite athletes typically were able to return to practice and game play long before complete resolution of their lesions.
Nodular cystic fat necrosis was first described by Przyjemski and Schuster10 in 1977. The terms encapsulated fat necrosis lesions and mobile encapsulated lipomas11 were introduced later. Clinically, these entities usually present as lesions on the lower limbs of young men and middle-aged women and can range in size from 1 mm to 35 mm. Most of these lesions are mobile.11 They are usually attributable to trauma and disruption of the blood supply in the subcutaneous area, which occurs with ML lesions. Trauma accounts for the usual occurrence in the lower extremities, though only 40% of patients recall a precipitating event.12 Histologically, these lesions are characterized by massive fat necrosis encapsulated by fibrous tissue.13In this article, we report the case of a professional ice hockey player who presented with an ML lesion of the hip and then developed a symptomatic encapsulated fat necrosis lesion that required surgical removal. To our knowledge, this is the first reported case of an encapsulated fat necrosis lesion caused by an ML lesion in an athlete. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 21-year-old professional hockey player presented with a history of pain from a mass on his right hip. He first noticed the lesion, just lateral to the greater trochanter, about 3 years earlier. The mass appeared after he sustained a shearing-type injury to the lateral aspect of the hip. At the time, there was significant swelling along the lateral aspect, with ecchymosis that resolved over 2 months. The mass, diagnosed as an ML lesion, resolved with nonoperative treatment. However, in the area where the swelling had occurred, a hard mobile mass remained. At times, this mass became painful when direct pressure was applied, as when he hit the boards while playing hockey, or when he lay on his right side or used a roller in the training room. He rated the pain as a 4 on a 1-to-10 scale and said the mass was mobile and had not changed in size or consistency.
Physical examination revealed a palpable mass over the lateral aspect of the hip, over the greater trochanter. The mass, about 3 cm in diameter (Figure 1), was mobile in a subcutaneous pocket, consistent with an old ML lesion.
Options discussed with the patient included use of ice, activity modification, and use of protective padded equipment. As the patient had tried these treatments before and was still intermittently having pain with direct pressure, he asked for surgical removal of the mass.
For the surgery, the patient was positioned in the lateral decubitus position with his right hip facing up. The right hip and thigh were prepared and draped in sterile fashion. An incision 4 cm in length was made directly over the mass, along the lateral aspect of the hip, over the greater trochanter. The incision was taken through skin and subcutaneous tissue down to the deep fascia. The fascia was incised longitudinally in line with the overlying skin incision. As soon as the incision was made through the fascia, the mass was easily seen. The 3-cm × 2-cm × 1-cm mass was free, not attached to any underlying soft tissue (Figure 3).
Discussion
We have described a case of symptomatic encapsulated fat necrosis lesion caused by an ML lesion in a professional hockey player. The ML lesion had resolved with nonoperative treatment (compression), but a subcutaneous pocket remained at the lesion site. Given the patient’s lesion site and occupation as a hockey player, pain with direct pressure on this lesion was a concern.
Long-standing ML lesions have 3 common patterns on MRI.14 A central region, encapsulated partially or completely by a peripheral ring of fibrous tissue or hemosiderin, shows signal properties consistent with a seroma, a homogeneous hemorrhagic collection, or a heterogeneous hemorrhagic collection. In our patient’s case, MRI was used to characterize the mobile mass for operative planning. Although thin strands or lobules of fat have been found within ML lesions, this case was the first to demonstrate a sequestered mass of necrotic fat.
Most football players who develop ML lesions on their knees do not wear kneepads.7-9 Of the 24 NFL players in the study by Tejwani and colleagues,9 52% were successfully treated with compression wrap, cryotherapy, and motion exercises. The rest, however, were treated with aspiration, and 11% underwent doxycycline sclerodesis for recurrent fluid collection. After treatment, all of their players were able to return to football. Their outcomes are consistent with that of our patient, who was treated with compression wrap and returned to hockey without any other intervention.
After our patient’s ML lesion resolved, he developed an encapsulated fat necrosis lesion from the disruption of the blood supply in the subcutaneous pocket. Encapsulated fat necrosis lesions are rare; only 65 have been reported.13,15 Clinically, these lesions are single or multiple pale-yellow encapsulated nodes.13 Most are small and asymptomatic; however, in some cases, athletes can develop symptoms from frequent impacts to the region where the lesions are located.
The literature includes 1 report of an adolescent football player who developed multiple encapsulated fat necrosis lesions 4 months after landing on another player’s cleats.15 The patient, who was having pain with direct pressure during squatting and kneeling, elected to have the lesions surgically removed. These lesions are rare and usually asymptomatic,11 but our patient had his lesion surgically removed to address the pain induced by the direct impacts that came with playing professional hockey. Surgical removal is the treatment for symptomatic encapsulated fat necrosis lesions. Other than 1 case of recurrence after excision,16 these lesions have an excellent prognosis.
Conclusion
Our patient, a professional hockey player, underwent successful surgical removal of a symptomatic encapsulated fat necrosis lesion that had developed from an ML lesion.
Am J Orthop. 2017;46(3):E144-E147. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Aguiar RO, Viegas FC, Fernandez RY, Trudell D, Haghighi P, Resnick D. The prepatellar bursa: cadaveric investigation of regional anatomy with MRI after sonographically guided bursography. AJR Am J Roentgenol. 2007;188(4):W355-W358.
2. Hak DJ, Olson SA, Matta JM. Diagnosis and management of closed internal degloving injuries associated with pelvic and acetabular fractures: the Morel-Lavallée lesion. J Trauma. 1997;42(6):1046-1051.
3. Hudson DA, Knottenbelt JD, Krige JE. Closed degloving injuries: results following conservative surgery. Plast Reconstr Surg. 1992;89(5):853-855.
4. Mellado JM, Bencardino JT. Morel-Lavallée lesion: review with emphasis on MR imaging. Magn Reson Imaging Clin North Am. 2005;13(4):775-782.
5. Dye SF, Campagna-Pinto D, Dye CC, Shifflett S, Eiman T. Soft-tissue anatomy anterior to the human patella. J Bone Joint Surg Am. 2003;85(6):1012-1017.
6. Northam MC, Gaskin CM. Presumed prepatellar fibrosis in collegiate wrestlers: imaging findings and clinical correlation. Skeletal Radiol. 2015;44(2):271-277.
7. Anakwenze OA, Trivedi V, Goodman AM, Ganley TJ. Concealed degloving injury (the Morel-Lavallée lesion) in childhood sports: a case report. J Bone Joint Surg Am. 2011;93(24):e148.
8. Matava MJ, Ellis E, Shah NR, Pogue D, Williams T. Morel-Lavallée lesion in a professional American football player. Am J Orthop. 2010;39(3):144-147.
9. Tejwani SG, Cohen SB, Bradley JP. Management of Morel-Lavallee lesion of the knee: twenty-seven cases in the National Football League. Am J Sports Med. 2007;35(7):1162-1167.
10. Przyjemski CJ, Schuster SR. Nodular-cystic fat necrosis. J Pediatr. 1977;91(4):605-607.
11. Kiryu H, Rikihisa W, Furue M. Encapsulated fat necrosis—a clinicopathological study of 8 cases and a literature review. J Cutan Pathol. 2000;27(1):19-23.
12. Santos-Juanes J, Coto P, Galache C, Sánchez del Rio J, Soto de Delás J. Encapsulated fat necrosis: a form of traumatic panniculitis. J Eur Acad Dermatol Venereol. 2007;21(3):405-406.
13. Sempau L, Sambucetty PS, Garcia JL, Sixto BG, Morán AG, Prieto MA. Mobile encapsulated lipoma. Int J Dermatol. 2012;51(4):448-450.
14. Mellado JM, Pérez del Palomar L, Díaz L, Ramos A, Saurí A. Long-standing Morel-Lavallée lesions of the trochanteric region and proximal thigh: MRI features in five patients. AJR Am J Roentgenol. 2004;182(5):1289-1294.
15. Sole JS, Wisniewski SJ, Dahm DL, Bond J, Smith J. Posttraumatic fat necrosis presenting as prepatellar loose bodies in an adolescent football player. PM R. 2014;6(8):749-752.
16. Felipo F, Vaquero M, del Agua C. Pseudotumoral encapsulated fat necrosis with diffuse pseudomembranous degeneration. J Cutan Pathol. 2004;31(8):565-567.
1. Aguiar RO, Viegas FC, Fernandez RY, Trudell D, Haghighi P, Resnick D. The prepatellar bursa: cadaveric investigation of regional anatomy with MRI after sonographically guided bursography. AJR Am J Roentgenol. 2007;188(4):W355-W358.
2. Hak DJ, Olson SA, Matta JM. Diagnosis and management of closed internal degloving injuries associated with pelvic and acetabular fractures: the Morel-Lavallée lesion. J Trauma. 1997;42(6):1046-1051.
3. Hudson DA, Knottenbelt JD, Krige JE. Closed degloving injuries: results following conservative surgery. Plast Reconstr Surg. 1992;89(5):853-855.
4. Mellado JM, Bencardino JT. Morel-Lavallée lesion: review with emphasis on MR imaging. Magn Reson Imaging Clin North Am. 2005;13(4):775-782.
5. Dye SF, Campagna-Pinto D, Dye CC, Shifflett S, Eiman T. Soft-tissue anatomy anterior to the human patella. J Bone Joint Surg Am. 2003;85(6):1012-1017.
6. Northam MC, Gaskin CM. Presumed prepatellar fibrosis in collegiate wrestlers: imaging findings and clinical correlation. Skeletal Radiol. 2015;44(2):271-277.
7. Anakwenze OA, Trivedi V, Goodman AM, Ganley TJ. Concealed degloving injury (the Morel-Lavallée lesion) in childhood sports: a case report. J Bone Joint Surg Am. 2011;93(24):e148.
8. Matava MJ, Ellis E, Shah NR, Pogue D, Williams T. Morel-Lavallée lesion in a professional American football player. Am J Orthop. 2010;39(3):144-147.
9. Tejwani SG, Cohen SB, Bradley JP. Management of Morel-Lavallee lesion of the knee: twenty-seven cases in the National Football League. Am J Sports Med. 2007;35(7):1162-1167.
10. Przyjemski CJ, Schuster SR. Nodular-cystic fat necrosis. J Pediatr. 1977;91(4):605-607.
11. Kiryu H, Rikihisa W, Furue M. Encapsulated fat necrosis—a clinicopathological study of 8 cases and a literature review. J Cutan Pathol. 2000;27(1):19-23.
12. Santos-Juanes J, Coto P, Galache C, Sánchez del Rio J, Soto de Delás J. Encapsulated fat necrosis: a form of traumatic panniculitis. J Eur Acad Dermatol Venereol. 2007;21(3):405-406.
13. Sempau L, Sambucetty PS, Garcia JL, Sixto BG, Morán AG, Prieto MA. Mobile encapsulated lipoma. Int J Dermatol. 2012;51(4):448-450.
14. Mellado JM, Pérez del Palomar L, Díaz L, Ramos A, Saurí A. Long-standing Morel-Lavallée lesions of the trochanteric region and proximal thigh: MRI features in five patients. AJR Am J Roentgenol. 2004;182(5):1289-1294.
15. Sole JS, Wisniewski SJ, Dahm DL, Bond J, Smith J. Posttraumatic fat necrosis presenting as prepatellar loose bodies in an adolescent football player. PM R. 2014;6(8):749-752.
16. Felipo F, Vaquero M, del Agua C. Pseudotumoral encapsulated fat necrosis with diffuse pseudomembranous degeneration. J Cutan Pathol. 2004;31(8):565-567.
Joint-Preserving Osteotomies for Isolated Patellofemoral Osteoarthritis: Alternatives to Arthroplasty
Take-Home Points
- Patellofemoral osteotomies can provide excellent and reliable symptomatic relief for many patients with symptomatic isolated PFOA.
- PLPF of 1 cm to 1.5 cm of lateral bone can provide excellent pain relief in patients with isolated lateral facet arthritis and overhanging osteophytes without diffuse chondromalacia or hypermobility.
- At 5-year follow-up, >80% of partial lateral facetectomy patients have symptomatic relief.
- Tibial tubercle AMZ (Fulkerson procedure) can provide excellent results in patients with distal and lateral patella chondropathy.
- Avoidance of overmedialization, early range of motion, and limited weight-bearing can help avoid complications associated with tibial tubercle AMZ.
Isolated patellofemoral osteoarthritis (PFOA) is a relatively common disorder. Based on radiological evidence, its prevalence is 24% in women and 11% in men aged over 55 years.1 However, the presence of PFOA on radiographic images does not always correlate with clinical symptoms. PFOA is symptomatic in only 8% of women and 2% of men aged over 55 years,1 and a mismatch often occurs between the symptoms and radiological severity (Figures 1A-1E). 
PFOA surgery may be considered when nonsurgical treatment is ineffective and pain becomes disabling. However, which surgical treatment for isolated PFOA is optimal remains controversial. The largest setback in weighing nonarthroplasty surgical options for isolated PFOA is that few studies have been published. Furthermore, published studies offer little scientific evidence; they include case series with few patients and retrospective analyses with limited follow-up and no control group for comparison.
This article focuses on osteotomies, which are described in only 15 articles found through PubMed. The small number is logical given that the prevalence of symptomatic isolated PFOA is low1 and that the majority of patients do not need surgical treatment. A complicating factor is that osteotomy is often associated with other surgical procedures, such as lateral retinaculum release. In descriptions of these cases, it is not clear if the outcome for PFOA is attributable to the osteotomy, is secondary to the associated procedure, or both.
Several alternatives to patellofemoral arthroplasty—partial lateral patellar facetectomy (PLPF), patella-thinning osteotomy (PTO), anteromedialization (AMZ), and sulcus-deepening trochleoplasty (SDT)—are available for the management of isolated PFOA. In this article, we analyze the value of each of these techniques in preserving the patellofemoral joint in the presence of PFOA. These techniques combine the US and European perspectives. The ultimate objective with these surgical techniques is to delay arthroplasty as long as possible.
Partial Lateral Patellar Facetectomy
PLPF is a relatively simple and effective surgical treatment for isolated PFOA in active middle-aged to elderly patients who want to maintain their activity level.3-6 Using an oscillating saw to resect 1 cm to 1.5 cm of the lateral facet of the patella reduces lateral retinaculum tension and thereby decreases lateral patellofemoral contact pressures (Figures 2A, 2B). 
PLPF improves pain and function over the long-term and delays the need for major surgery. Wetzels and Bellemans5 evaluated 155 consecutive patients (168 knees) with mean post-PLPF follow-up of 10.9 years. By final follow-up, 62 knees (36.9%) had failed and been revised to total knee arthroplasty (TKA) (60 knees), patellofemoral arthroplasty (1 knee), or total patellectomy (1 knee). Mean time to reoperation was 8 years. Kaplan-Meier survival rates with reoperation as the endpoint were 85% at 5 years, 67.2% at 10 years, and 46.7% at 20 years. At final follow-up, 79 (74.5%) of the 106 knees that had not been revised were rated good or fair, which accounts for 47% of the original group of 168 knees. The key finding is that the effects of PLPF lasted through the 10-year follow-up in half of the patients.5 Paulos and colleagues4 found 5 years of symptomatic relief in more than 80% of carefully selected patients who did not have significant (grade IV) arthritis in the medial or lateral knee compartments.
PLPF is a safe, low-cost, and relatively minor surgery with a low morbidity rate and fast recovery. Also, it does not close the door on other surgery and can easily be converted to TKA. Wetzels and Bellemans5 found that 36.9% of reoperations were TKAs, and López-Franco and colleagues3 found that 30% of knees required secondary TKA.
Patella-Thinning Osteotomy
In patients who are under 65 years old and have disabling anterior knee pain recalcitrant to conservative treatment, PTO may be considered for isolated PFOA with any type of chondral lesion (including severe diffuse chondropathy with exposed bone) (Figures 3A-3C), patellofemoral joint space reduced by more than 50% on skyline view, patellar thickness of 20 mm or more, and normal TT-TG distance.7 
Vaquero and colleagues7 analyzed PTO outcomes in 31 patients (35 knees) with mean follow-up of 9 years and noted significant improvements in functional scores and radiologic parameters. All patients except 1 were satisfied with the operation. Radiologic progression of PFOA was slowed, but radiologic femorotibial osteoarthritis progressed in 23 cases (65%), and 4 required TKA. The authors found satisfactory clinical and radiologic outcomes—only 4 patients (12.5%) required TKA—and good functional outcomes.7
PTO, a low-morbidity surgery with good functional outcomes, does not close the door on other surgery, such as TKA.7
Tibial Tubercle Anteromedialization Osteotomy
Whereas PLPF and PTO are indicated in knees with normal TT-TG distance, Fulkerson AMZ osteotomy must be considered in isolated PFOA with articular cartilage lesions at the distal or lateral patellar facets resulting from long-standing malalignment with increased TT-TG distance (Figures 4A, 4B). 
AMZ unloads the distal and lateral facets of the patella while improving the extensor mechanism.11,12 A successful AMZ outcome requires preservation of some of the medial and proximal articular cartilage of the patella. In 1983, Fulkerson13 described use of tibial tubercle AMZ osteotomy to address patellofemoral pain associated with patellofemoral chondrosis in conjunction with patellofemoral tilt and/or chronic patellar subluxation. This technique is indicated when the patella needs to be realigned for relief of elevated contact stress and centralization. Currently the technique is used not only in patients with isolated PFOA but in patients with chronic lateral patellar instability. Fulkerson osteotomy combines the benefits of the Maquet technique (unloading) and the Elmslie-Trillat technique (tracking improvement) in a single osteotomy, with no distraction of the osteotomy site with bone graft and without the complication rate of Maquet tibial tubercle elevation. Before surgery, computed tomography (CT) or magnetic resonance imaging (MRI) is routinely used to measure TT-TG distance to determine the tibial tubercle medialization required in the Fulkerson osteotomy. However, TT-TG distance must be used with caution, as it cannot be determined in cases with trochlear dysplasia. Consequently, physical examination and arthroscopic examination for evaluation of patellofemoral tracking and location of chondral defects should be performed before the Fulkerson osteotomy.
Rationale; Indications and Contraindications; Preoperative Planning
As already noted, AMZ unloads the distal and lateral facets of the patella. Beck and colleagues14 suggested AMZ is appropriate for unloading the lateral trochlea. However, it is not useful for central chondral defects and may actually increase the load in patients with medial chondral defects. As AMZ shifts contact force to the medial trochlea, Fulkerson osteotomy is appropriate when distal and lateral chondral lesions must be unloaded. Because this procedure moves the tibial tubercle medially and anteriorly, loads are transferred to the proximal and medial facets of the patella. Therefore, the procedure is contraindicated when diffuse, proximal, or medial chondral lesions are present. Moreover, AMZ is contraindicated in patients with normal TT-TG distance because there is the risk that overmedialization will cause symptomatic medial subluxation. Grade III or IV central trochlear cartilage lesions are also less likely to have successful AMZ outcomes. Therefore, before Fulkerson osteotomy is performed, MRI should be obtained to evaluate the patellofemoral articular surface and TT-TG distance. MRI provides information that is useful for preoperative planning because it allows assessment of articular cartilage lesions, including their location and severity. Moreover, because the osseous and cartilaginous contours of the patella differ, MRI gives a more accurate picture of the patellofemoral congruence than CT does. Last, before the open surgery is performed, the patellofemoral joint should be arthroscopically examined to determine the location of chondral lesions. Cartilage lesion mapping is important because Fulkerson osteotomy outcomes depend on chondral lesion location. Pidoriano and colleagues15 correlated AMZ outcomes with articular lesion location and noted optimal outcomes in patients with distal and lateral patellar articular lesions and intact trochlear cartilage (87% good and excellent outcomes). Patients with medial lesions and proximal or diffuse lesions generally did poorly (55% good and excellent outcomes in medial lesions vs 20% good and excellent outcomes in proximal and diffuse lesions). Central trochlear lesions were associated with medial patellar lesions, and all patients with central trochlear lesions had poor outcomes. Interestingly, Outerbridge grading of patellar lesions was not significantly correlated with overall outcomes.15 Even in cases of severe chondropathy, including bone-on-bone arthritis, AMZ has had reliable outcomes and may be superior to arthroplasty because of joint preservation, duration up to 8 years, and restoration of patellofemoral tracking. It should be noted that a resurfacing technique such as patellofemoral arthroplasty is not a substitute for patella realignment. Any patellofemoral maltracking must be corrected before patellofemoral arthroplasty. Fulkerson osteotomy does not preclude subsequent surgery (eg, TKA). Furthermore, AMZ may prevent the natural progression of PFOA related to chronic lateral tracking.
AMZ osteotomy can be adjusted for the specific indication and for the location of chondral defects. If the primary goal is unloading a lateral lesion, or lateral maltracking, then a flatter osteotomy may be performed to increase the relative medialization of the tubercle; however, if the primary goal is unloading a distal lesion, then a relatively more oblique or vertical osteotomy may be performed to transfer the load more proximally. This is the technique preferred by authors in most cases in which more anteriorization is desired.
When TT-TG distance is used to guide surgical realignment, patellofemoral chondrosis associated with normal TT-TG distance can be addressed with directly anterior displacement of the tibial tubercle. Anteriorization of the tibial tubercle can be obtained by inserting a bone block between the tubercle and the tibial cut (Figure 5A).16 The medialization can be neutralized by making this block as thick as the measured medialization.16 
Surgical Outcomes of Anteromedialization in Patellofemoral Osteoarthritis
Fulkerson and colleagues10 followed 30 patients for more than 2 years after they underwent AMZ of the tibial tubercle for persistent patellofemoral pain associated with patellar articular degeneration. Of these 30 patients, 12 were followed for more than 5 years. The authors reported 93% good and excellent subjective outcomes and 89% good and excellent objective outcomes. Quality of improvement was sustained for all 12 patients reevaluated more than 5 years after surgery. When examined separately, 75% of patients with advanced PFOA had a good outcome, but none had an excellent outcome. Carofino and Fulkerson17 retrospectively evaluated tibial tubercle AMZ for isolated PFOA in 22 knees (17 active patients older than 50 years at time of surgery; mean age, 55 years) with minimum follow-up of 2 years (mean, 77 months). Mean postoperative Lysholm score was 83. According to Lysholm scores, outcomes were good to excellent in 12 cases, fair in 6, and poor in 1. The authors concluded that tibial tubercle AMZ is a definitive treatment option for isolated PFOA in active older patients. Morshuis and colleagues18 retrospectively evaluated 22 patients (25 knees) who underwent Fulkerson osteotomy for patellofemoral pain. Outcomes were evaluated a mean of 12 and 30 months after surgery. At the first evaluation, 84% of patients had satisfactory outcomes, and, at the second (≤38 months after surgery), 70%. Only in relatively young patients without signs of PFOA did outcomes remain satisfactory in all cases. At the later evaluation, 60% of patients with PFOA and/or lateralization had satisfactory outcomes.
Tips and Tricks to Avoid Complications
For some patients, AMZ performed technically correctly produced unhappiness—an outcome that may arise from incorrect patient selection or failure to meet patient expectations. It is important to discuss objectives and expectations with the patient before surgery. With correct patient selection and meticulous surgical technique (with customization of osteotomy angle and translation based on underlying lesion), surgeons have obtained excellent outcomes with infrequent complications (Table). 
Intraoperative complications may involve neurovascular structures. The anterior tibial artery and the peroneal nerve are at risk during Fulkerson osteotomy. Decreased anterior sensation related to the infrapatellar branch of the saphenous nerve is not uncommon. Reducing the risk of neurovascular injury requires use of retractors and keeping the saw blade visible at all times. Another potential devastating complication is injury of the posterior vascular structures during bicortical tibial drilling for screw placement. According to Kline and colleagues,19 bicortical drilling may occur precariously near the posterior vascular structures of the knee. They advised extreme caution in drilling the posterior cortex during this procedure. To avoid the risk of compartment syndrome, surgeons can leave the anterior compartment fascia open or pie crust it by making multiple small perforations to decrease tension. Tibial fracture is another potential complication with this osteotomy. Reducing the risk of fracture involves tapering the distal cut anteriorly and avoiding a “notched” osteotomy (Figures 6A-6C). 
Postoperative complications, which are similar to those associated with any knee surgery, include infection, arthrofibrosis, complex regional pain syndrome, thromboembolism, nonunion, fixation failure, and fracture. Arthrofibrosis has many causes, but the problem decreases with secure osteotomy fixation, early knee motion, and patellar mobilization. Overmedialization can result in medial patella instability, typically subluxation rather than complete dislocation. The instability can be relatively subtle or can cause pain and weakness. Lateralization of the tibial tubercle might be appropiate.23
Sulcus-Deepening Trochleoplasty
High-grade trochlear dysplasia with a prominence, frequently present in lateral patellar instability, is thought to correlate with PFOA because it produces an anti-Maquet effect.24 The dysplasia provokes an increment of the patellofemoral joint pressure that could explain patellofemoral chondropathy and ultimately PFOA. In fact, 33% of patients with isolated PFOA have a history of objective patellar dislocation.24 In these cases, SDT could be considered. Several studies have examined use of this technique in the treatment of instability, but not PFOA.25 After SDT, pain resolves despite the chondral lesions being left alone (Figures 7A, 7B). 
Conclusion
Patellofemoral joint replacement is an option for patellofemoral pain only in very select cases. Preserving the joint is always a primary goal. As not all PFOA cases are equal, joint-preserving surgery must be tailored to the patient. The keys to success are good indication, precise surgery, proper rehabilitation, and, above all, doing only what is needed.
Am J Orthop. 2017;46(3):139-145. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. McAlindon TE, Snow S, Cooper C, Dieppe PA. Radiographic patterns of osteoarthritis of the knee joint in the community: the importance of the patellofemoral joint. Ann Rheum Dis. 1992;51(7):844-849.
2. Iwano T, Kurosawa H, Tokuyama H, Hoshikawa Y. Roentgenographic and clinical findings of patellofemoral osteoarthrosis. With special reference to its relationship to femorotibial osteoarthrosis and etiologic factors. Clin Orthop Relat Res. 1990;(252):190-197.
3. López-Franco M, Murciano-Antón MA, Fernández-Aceñero MJ, De Lucas-Villarrubia JC, López-Martín N, Gómez-Barrena E. Evaluation of a minimally aggressive method of patellofemoral osteoarthritis treatment at 10 years minimum follow-up. Knee. 2013;20(6):476-481.
4. Paulos LE, O’Connor DL, Karistinos A. Partial lateral patellar facetectomy for treatment of arthritis due to lateral patellar compression syndrome. Arthroscopy. 2008;24(5):547-553.
5. Wetzels T, Bellemans J. Patellofemoral osteoarthritis treated by partial lateral facetectomy: results at long-term follow up. Knee. 2012;19(4):411-415.
6. Yercan HS, Ait Si Selmi T, Neyret P. The treatment of patellofemoral osteoarthritis with partial lateral facetectomy. Clin Orthop Relat Res. 2005;(436):14-19.
7. Vaquero J, Calvo JA, Chana F, Perez-Mañanes R. The patellar thinning osteotomy in patellofemoral arthritis: four to 18 years’ follow-up. J Bone Joint Surg Br. 2010;92(10):1385-1391.
8. Vaquero J, Arriaza R. The patella thinning osteotomy. An experimental study of a new technique for reducing patellofemoral pressure. Int Orthop. 1992;16(4):372-376.
9. Fulkerson JP. Disorders of the Patellofemoral Joint. 3rd ed. Baltimore, MD: Williams & Wilkins; 1997.
10. Fulkerson JP, Becker GJ, Meaney JA, Miranda M, Folcik MA. Anteromedial tibial tubercle transfer without bone graft. Am J Sports Med. 1990;18(5):490-496.
11. Fulkerson JP. Patellofemoral pain disorders: evaluation and management. J Am Acad Orthop Surg. 1994;2(2):124-132.
12. Fulkerson JP. Diagnosis and treatment of patients with patellofemoral pain. Am J Sports Med. 2002;30(3):447-456.
13. Fulkerson JP. Anteromedialization of the tibial tuberosity for patellofemoral malalignment. Clin Orthop Relat Res. 1983;(177):176-181.
14. Beck PR, Thomas AL, Farr J, Lewis PB, Cole BJ. Trochlear contact pressures after anteromedialization of the tibial tubercle. Am J Sports Med. 2005;33(11):1710-1715.
15. Pidoriano AJ, Weinstein RN, Buuck DA, Fulkerson JP. Correlation of patellar articular lesions with results from anteromedial tibial tubercle transfer. Am J Sports Med. 1997;25(4):533-537.
16. Farr J. Tibial tubercle osteotomy. Tech Knee Surg. 2003;2:28-42.
17. Carofino BC, Fulkerson JP. Anteromedialization of the tibial tubercle for patellofemoral arthritis in patients > 50 years. J Knee Surg. 2008;21(2):101-105.
18. Morshuis WJ, Pavlov PW, de Rooy KP. Anteromedialization of the tibial tuberosity in the treatment of patellofemoral pain and malalignment. Clin Orthop Relat Res. 1990;(255):242-250.
19. Kline AJ, Gonzales J, Beach WR, Miller MD. Vascular risk associated with bicortical tibial drilling during anteromedial tibial tubercle transfer. Am J Orthop. 2006;35(1):30-32.
20. Stetson WB, Friedman MJ, Fulkerson JP, Cheng M, Buuck D. Fracture of the proximal tibia with immediate weightbearing after a Fulkerson osteotomy. Am J Sports Med. 1997;25(4):570-574.
21. Fulkerson JP. Fracture of the proximal tibia after Fulkerson anteromedial tibial tubercle transfer. A report of four cases. Am J Sports Med. 1999;27(2):265.
22. Cosgarea AJ, Freedman JA, McFarland EG. Nonunion of the tibial tubercle shingle following Fulkerson osteotomy. Am J Knee Surg. 2001;14(1):51-54.
23. Fulkerson JP. Anterolateralization of the tibial tubercle. Tech Orthop. 1997;12:165-169.
24. Grelsamer RP, Dejour D, Gould J. The pathophysiology of patellofemoral arthritis. Orthop Clin North Am. 2008;39(3):269-274.
25. Ntagiopoulos PG, Byn P, Dejour D. Midterm results of comprehensive surgical reconstruction including sulcus-deepening trochleoplasty in recurrent patellar dislocations with high-grade trochlear dysplasia. Am J Sports Med. 2013;41(5):998-1004.
26. Oberlander MA, Baker CL, Morgan BE. Patellofemoral arthrosis: the treatment options. Am J Orthop. 1998;27(4):263-270.
27. Scuderi GR. The Patella. New York, NY: Springer-Verlag; 1995.
28. Buuck D, Fulkerson JP. Anteromedialization of the tibial tubercle: a 4 to 12 year follow up. Oper Tech Sports Med. 2000;8:131-137.
Take-Home Points
- Patellofemoral osteotomies can provide excellent and reliable symptomatic relief for many patients with symptomatic isolated PFOA.
- PLPF of 1 cm to 1.5 cm of lateral bone can provide excellent pain relief in patients with isolated lateral facet arthritis and overhanging osteophytes without diffuse chondromalacia or hypermobility.
- At 5-year follow-up, >80% of partial lateral facetectomy patients have symptomatic relief.
- Tibial tubercle AMZ (Fulkerson procedure) can provide excellent results in patients with distal and lateral patella chondropathy.
- Avoidance of overmedialization, early range of motion, and limited weight-bearing can help avoid complications associated with tibial tubercle AMZ.
Isolated patellofemoral osteoarthritis (PFOA) is a relatively common disorder. Based on radiological evidence, its prevalence is 24% in women and 11% in men aged over 55 years.1 However, the presence of PFOA on radiographic images does not always correlate with clinical symptoms. PFOA is symptomatic in only 8% of women and 2% of men aged over 55 years,1 and a mismatch often occurs between the symptoms and radiological severity (Figures 1A-1E).
PFOA surgery may be considered when nonsurgical treatment is ineffective and pain becomes disabling. However, which surgical treatment for isolated PFOA is optimal remains controversial. The largest setback in weighing nonarthroplasty surgical options for isolated PFOA is that few studies have been published. Furthermore, published studies offer little scientific evidence; they include case series with few patients and retrospective analyses with limited follow-up and no control group for comparison.
This article focuses on osteotomies, which are described in only 15 articles found through PubMed. The small number is logical given that the prevalence of symptomatic isolated PFOA is low1 and that the majority of patients do not need surgical treatment. A complicating factor is that osteotomy is often associated with other surgical procedures, such as lateral retinaculum release. In descriptions of these cases, it is not clear if the outcome for PFOA is attributable to the osteotomy, is secondary to the associated procedure, or both.
Several alternatives to patellofemoral arthroplasty—partial lateral patellar facetectomy (PLPF), patella-thinning osteotomy (PTO), anteromedialization (AMZ), and sulcus-deepening trochleoplasty (SDT)—are available for the management of isolated PFOA. In this article, we analyze the value of each of these techniques in preserving the patellofemoral joint in the presence of PFOA. These techniques combine the US and European perspectives. The ultimate objective with these surgical techniques is to delay arthroplasty as long as possible.
Partial Lateral Patellar Facetectomy
PLPF is a relatively simple and effective surgical treatment for isolated PFOA in active middle-aged to elderly patients who want to maintain their activity level.3-6 Using an oscillating saw to resect 1 cm to 1.5 cm of the lateral facet of the patella reduces lateral retinaculum tension and thereby decreases lateral patellofemoral contact pressures (Figures 2A, 2B).
PLPF improves pain and function over the long-term and delays the need for major surgery. Wetzels and Bellemans5 evaluated 155 consecutive patients (168 knees) with mean post-PLPF follow-up of 10.9 years. By final follow-up, 62 knees (36.9%) had failed and been revised to total knee arthroplasty (TKA) (60 knees), patellofemoral arthroplasty (1 knee), or total patellectomy (1 knee). Mean time to reoperation was 8 years. Kaplan-Meier survival rates with reoperation as the endpoint were 85% at 5 years, 67.2% at 10 years, and 46.7% at 20 years. At final follow-up, 79 (74.5%) of the 106 knees that had not been revised were rated good or fair, which accounts for 47% of the original group of 168 knees. The key finding is that the effects of PLPF lasted through the 10-year follow-up in half of the patients.5 Paulos and colleagues4 found 5 years of symptomatic relief in more than 80% of carefully selected patients who did not have significant (grade IV) arthritis in the medial or lateral knee compartments.
PLPF is a safe, low-cost, and relatively minor surgery with a low morbidity rate and fast recovery. Also, it does not close the door on other surgery and can easily be converted to TKA. Wetzels and Bellemans5 found that 36.9% of reoperations were TKAs, and López-Franco and colleagues3 found that 30% of knees required secondary TKA.
Patella-Thinning Osteotomy
In patients who are under 65 years old and have disabling anterior knee pain recalcitrant to conservative treatment, PTO may be considered for isolated PFOA with any type of chondral lesion (including severe diffuse chondropathy with exposed bone) (Figures 3A-3C), patellofemoral joint space reduced by more than 50% on skyline view, patellar thickness of 20 mm or more, and normal TT-TG distance.7
Vaquero and colleagues7 analyzed PTO outcomes in 31 patients (35 knees) with mean follow-up of 9 years and noted significant improvements in functional scores and radiologic parameters. All patients except 1 were satisfied with the operation. Radiologic progression of PFOA was slowed, but radiologic femorotibial osteoarthritis progressed in 23 cases (65%), and 4 required TKA. The authors found satisfactory clinical and radiologic outcomes—only 4 patients (12.5%) required TKA—and good functional outcomes.7
PTO, a low-morbidity surgery with good functional outcomes, does not close the door on other surgery, such as TKA.7
Tibial Tubercle Anteromedialization Osteotomy
Whereas PLPF and PTO are indicated in knees with normal TT-TG distance, Fulkerson AMZ osteotomy must be considered in isolated PFOA with articular cartilage lesions at the distal or lateral patellar facets resulting from long-standing malalignment with increased TT-TG distance (Figures 4A, 4B).
AMZ unloads the distal and lateral facets of the patella while improving the extensor mechanism.11,12 A successful AMZ outcome requires preservation of some of the medial and proximal articular cartilage of the patella. In 1983, Fulkerson13 described use of tibial tubercle AMZ osteotomy to address patellofemoral pain associated with patellofemoral chondrosis in conjunction with patellofemoral tilt and/or chronic patellar subluxation. This technique is indicated when the patella needs to be realigned for relief of elevated contact stress and centralization. Currently the technique is used not only in patients with isolated PFOA but in patients with chronic lateral patellar instability. Fulkerson osteotomy combines the benefits of the Maquet technique (unloading) and the Elmslie-Trillat technique (tracking improvement) in a single osteotomy, with no distraction of the osteotomy site with bone graft and without the complication rate of Maquet tibial tubercle elevation. Before surgery, computed tomography (CT) or magnetic resonance imaging (MRI) is routinely used to measure TT-TG distance to determine the tibial tubercle medialization required in the Fulkerson osteotomy. However, TT-TG distance must be used with caution, as it cannot be determined in cases with trochlear dysplasia. Consequently, physical examination and arthroscopic examination for evaluation of patellofemoral tracking and location of chondral defects should be performed before the Fulkerson osteotomy.
Rationale; Indications and Contraindications; Preoperative Planning
As already noted, AMZ unloads the distal and lateral facets of the patella. Beck and colleagues14 suggested AMZ is appropriate for unloading the lateral trochlea. However, it is not useful for central chondral defects and may actually increase the load in patients with medial chondral defects. As AMZ shifts contact force to the medial trochlea, Fulkerson osteotomy is appropriate when distal and lateral chondral lesions must be unloaded. Because this procedure moves the tibial tubercle medially and anteriorly, loads are transferred to the proximal and medial facets of the patella. Therefore, the procedure is contraindicated when diffuse, proximal, or medial chondral lesions are present. Moreover, AMZ is contraindicated in patients with normal TT-TG distance because there is the risk that overmedialization will cause symptomatic medial subluxation. Grade III or IV central trochlear cartilage lesions are also less likely to have successful AMZ outcomes. Therefore, before Fulkerson osteotomy is performed, MRI should be obtained to evaluate the patellofemoral articular surface and TT-TG distance. MRI provides information that is useful for preoperative planning because it allows assessment of articular cartilage lesions, including their location and severity. Moreover, because the osseous and cartilaginous contours of the patella differ, MRI gives a more accurate picture of the patellofemoral congruence than CT does. Last, before the open surgery is performed, the patellofemoral joint should be arthroscopically examined to determine the location of chondral lesions. Cartilage lesion mapping is important because Fulkerson osteotomy outcomes depend on chondral lesion location. Pidoriano and colleagues15 correlated AMZ outcomes with articular lesion location and noted optimal outcomes in patients with distal and lateral patellar articular lesions and intact trochlear cartilage (87% good and excellent outcomes). Patients with medial lesions and proximal or diffuse lesions generally did poorly (55% good and excellent outcomes in medial lesions vs 20% good and excellent outcomes in proximal and diffuse lesions). Central trochlear lesions were associated with medial patellar lesions, and all patients with central trochlear lesions had poor outcomes. Interestingly, Outerbridge grading of patellar lesions was not significantly correlated with overall outcomes.15 Even in cases of severe chondropathy, including bone-on-bone arthritis, AMZ has had reliable outcomes and may be superior to arthroplasty because of joint preservation, duration up to 8 years, and restoration of patellofemoral tracking. It should be noted that a resurfacing technique such as patellofemoral arthroplasty is not a substitute for patella realignment. Any patellofemoral maltracking must be corrected before patellofemoral arthroplasty. Fulkerson osteotomy does not preclude subsequent surgery (eg, TKA). Furthermore, AMZ may prevent the natural progression of PFOA related to chronic lateral tracking.
AMZ osteotomy can be adjusted for the specific indication and for the location of chondral defects. If the primary goal is unloading a lateral lesion, or lateral maltracking, then a flatter osteotomy may be performed to increase the relative medialization of the tubercle; however, if the primary goal is unloading a distal lesion, then a relatively more oblique or vertical osteotomy may be performed to transfer the load more proximally. This is the technique preferred by authors in most cases in which more anteriorization is desired.
When TT-TG distance is used to guide surgical realignment, patellofemoral chondrosis associated with normal TT-TG distance can be addressed with directly anterior displacement of the tibial tubercle. Anteriorization of the tibial tubercle can be obtained by inserting a bone block between the tubercle and the tibial cut (Figure 5A).16 The medialization can be neutralized by making this block as thick as the measured medialization.16
Surgical Outcomes of Anteromedialization in Patellofemoral Osteoarthritis
Fulkerson and colleagues10 followed 30 patients for more than 2 years after they underwent AMZ of the tibial tubercle for persistent patellofemoral pain associated with patellar articular degeneration. Of these 30 patients, 12 were followed for more than 5 years. The authors reported 93% good and excellent subjective outcomes and 89% good and excellent objective outcomes. Quality of improvement was sustained for all 12 patients reevaluated more than 5 years after surgery. When examined separately, 75% of patients with advanced PFOA had a good outcome, but none had an excellent outcome. Carofino and Fulkerson17 retrospectively evaluated tibial tubercle AMZ for isolated PFOA in 22 knees (17 active patients older than 50 years at time of surgery; mean age, 55 years) with minimum follow-up of 2 years (mean, 77 months). Mean postoperative Lysholm score was 83. According to Lysholm scores, outcomes were good to excellent in 12 cases, fair in 6, and poor in 1. The authors concluded that tibial tubercle AMZ is a definitive treatment option for isolated PFOA in active older patients. Morshuis and colleagues18 retrospectively evaluated 22 patients (25 knees) who underwent Fulkerson osteotomy for patellofemoral pain. Outcomes were evaluated a mean of 12 and 30 months after surgery. At the first evaluation, 84% of patients had satisfactory outcomes, and, at the second (≤38 months after surgery), 70%. Only in relatively young patients without signs of PFOA did outcomes remain satisfactory in all cases. At the later evaluation, 60% of patients with PFOA and/or lateralization had satisfactory outcomes.
Tips and Tricks to Avoid Complications
For some patients, AMZ performed technically correctly produced unhappiness—an outcome that may arise from incorrect patient selection or failure to meet patient expectations. It is important to discuss objectives and expectations with the patient before surgery. With correct patient selection and meticulous surgical technique (with customization of osteotomy angle and translation based on underlying lesion), surgeons have obtained excellent outcomes with infrequent complications (Table).
Intraoperative complications may involve neurovascular structures. The anterior tibial artery and the peroneal nerve are at risk during Fulkerson osteotomy. Decreased anterior sensation related to the infrapatellar branch of the saphenous nerve is not uncommon. Reducing the risk of neurovascular injury requires use of retractors and keeping the saw blade visible at all times. Another potential devastating complication is injury of the posterior vascular structures during bicortical tibial drilling for screw placement. According to Kline and colleagues,19 bicortical drilling may occur precariously near the posterior vascular structures of the knee. They advised extreme caution in drilling the posterior cortex during this procedure. To avoid the risk of compartment syndrome, surgeons can leave the anterior compartment fascia open or pie crust it by making multiple small perforations to decrease tension. Tibial fracture is another potential complication with this osteotomy. Reducing the risk of fracture involves tapering the distal cut anteriorly and avoiding a “notched” osteotomy (Figures 6A-6C).
Postoperative complications, which are similar to those associated with any knee surgery, include infection, arthrofibrosis, complex regional pain syndrome, thromboembolism, nonunion, fixation failure, and fracture. Arthrofibrosis has many causes, but the problem decreases with secure osteotomy fixation, early knee motion, and patellar mobilization. Overmedialization can result in medial patella instability, typically subluxation rather than complete dislocation. The instability can be relatively subtle or can cause pain and weakness. Lateralization of the tibial tubercle might be appropiate.23
Sulcus-Deepening Trochleoplasty
High-grade trochlear dysplasia with a prominence, frequently present in lateral patellar instability, is thought to correlate with PFOA because it produces an anti-Maquet effect.24 The dysplasia provokes an increment of the patellofemoral joint pressure that could explain patellofemoral chondropathy and ultimately PFOA. In fact, 33% of patients with isolated PFOA have a history of objective patellar dislocation.24 In these cases, SDT could be considered. Several studies have examined use of this technique in the treatment of instability, but not PFOA.25 After SDT, pain resolves despite the chondral lesions being left alone (Figures 7A, 7B).
Conclusion
Patellofemoral joint replacement is an option for patellofemoral pain only in very select cases. Preserving the joint is always a primary goal. As not all PFOA cases are equal, joint-preserving surgery must be tailored to the patient. The keys to success are good indication, precise surgery, proper rehabilitation, and, above all, doing only what is needed.
Am J Orthop. 2017;46(3):139-145. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- Patellofemoral osteotomies can provide excellent and reliable symptomatic relief for many patients with symptomatic isolated PFOA.
- PLPF of 1 cm to 1.5 cm of lateral bone can provide excellent pain relief in patients with isolated lateral facet arthritis and overhanging osteophytes without diffuse chondromalacia or hypermobility.
- At 5-year follow-up, >80% of partial lateral facetectomy patients have symptomatic relief.
- Tibial tubercle AMZ (Fulkerson procedure) can provide excellent results in patients with distal and lateral patella chondropathy.
- Avoidance of overmedialization, early range of motion, and limited weight-bearing can help avoid complications associated with tibial tubercle AMZ.
Isolated patellofemoral osteoarthritis (PFOA) is a relatively common disorder. Based on radiological evidence, its prevalence is 24% in women and 11% in men aged over 55 years.1 However, the presence of PFOA on radiographic images does not always correlate with clinical symptoms. PFOA is symptomatic in only 8% of women and 2% of men aged over 55 years,1 and a mismatch often occurs between the symptoms and radiological severity (Figures 1A-1E).
PFOA surgery may be considered when nonsurgical treatment is ineffective and pain becomes disabling. However, which surgical treatment for isolated PFOA is optimal remains controversial. The largest setback in weighing nonarthroplasty surgical options for isolated PFOA is that few studies have been published. Furthermore, published studies offer little scientific evidence; they include case series with few patients and retrospective analyses with limited follow-up and no control group for comparison.
This article focuses on osteotomies, which are described in only 15 articles found through PubMed. The small number is logical given that the prevalence of symptomatic isolated PFOA is low1 and that the majority of patients do not need surgical treatment. A complicating factor is that osteotomy is often associated with other surgical procedures, such as lateral retinaculum release. In descriptions of these cases, it is not clear if the outcome for PFOA is attributable to the osteotomy, is secondary to the associated procedure, or both.
Several alternatives to patellofemoral arthroplasty—partial lateral patellar facetectomy (PLPF), patella-thinning osteotomy (PTO), anteromedialization (AMZ), and sulcus-deepening trochleoplasty (SDT)—are available for the management of isolated PFOA. In this article, we analyze the value of each of these techniques in preserving the patellofemoral joint in the presence of PFOA. These techniques combine the US and European perspectives. The ultimate objective with these surgical techniques is to delay arthroplasty as long as possible.
Partial Lateral Patellar Facetectomy
PLPF is a relatively simple and effective surgical treatment for isolated PFOA in active middle-aged to elderly patients who want to maintain their activity level.3-6 Using an oscillating saw to resect 1 cm to 1.5 cm of the lateral facet of the patella reduces lateral retinaculum tension and thereby decreases lateral patellofemoral contact pressures (Figures 2A, 2B).
PLPF improves pain and function over the long-term and delays the need for major surgery. Wetzels and Bellemans5 evaluated 155 consecutive patients (168 knees) with mean post-PLPF follow-up of 10.9 years. By final follow-up, 62 knees (36.9%) had failed and been revised to total knee arthroplasty (TKA) (60 knees), patellofemoral arthroplasty (1 knee), or total patellectomy (1 knee). Mean time to reoperation was 8 years. Kaplan-Meier survival rates with reoperation as the endpoint were 85% at 5 years, 67.2% at 10 years, and 46.7% at 20 years. At final follow-up, 79 (74.5%) of the 106 knees that had not been revised were rated good or fair, which accounts for 47% of the original group of 168 knees. The key finding is that the effects of PLPF lasted through the 10-year follow-up in half of the patients.5 Paulos and colleagues4 found 5 years of symptomatic relief in more than 80% of carefully selected patients who did not have significant (grade IV) arthritis in the medial or lateral knee compartments.
PLPF is a safe, low-cost, and relatively minor surgery with a low morbidity rate and fast recovery. Also, it does not close the door on other surgery and can easily be converted to TKA. Wetzels and Bellemans5 found that 36.9% of reoperations were TKAs, and López-Franco and colleagues3 found that 30% of knees required secondary TKA.
Patella-Thinning Osteotomy
In patients who are under 65 years old and have disabling anterior knee pain recalcitrant to conservative treatment, PTO may be considered for isolated PFOA with any type of chondral lesion (including severe diffuse chondropathy with exposed bone) (Figures 3A-3C), patellofemoral joint space reduced by more than 50% on skyline view, patellar thickness of 20 mm or more, and normal TT-TG distance.7
Vaquero and colleagues7 analyzed PTO outcomes in 31 patients (35 knees) with mean follow-up of 9 years and noted significant improvements in functional scores and radiologic parameters. All patients except 1 were satisfied with the operation. Radiologic progression of PFOA was slowed, but radiologic femorotibial osteoarthritis progressed in 23 cases (65%), and 4 required TKA. The authors found satisfactory clinical and radiologic outcomes—only 4 patients (12.5%) required TKA—and good functional outcomes.7
PTO, a low-morbidity surgery with good functional outcomes, does not close the door on other surgery, such as TKA.7
Tibial Tubercle Anteromedialization Osteotomy
Whereas PLPF and PTO are indicated in knees with normal TT-TG distance, Fulkerson AMZ osteotomy must be considered in isolated PFOA with articular cartilage lesions at the distal or lateral patellar facets resulting from long-standing malalignment with increased TT-TG distance (Figures 4A, 4B).
AMZ unloads the distal and lateral facets of the patella while improving the extensor mechanism.11,12 A successful AMZ outcome requires preservation of some of the medial and proximal articular cartilage of the patella. In 1983, Fulkerson13 described use of tibial tubercle AMZ osteotomy to address patellofemoral pain associated with patellofemoral chondrosis in conjunction with patellofemoral tilt and/or chronic patellar subluxation. This technique is indicated when the patella needs to be realigned for relief of elevated contact stress and centralization. Currently the technique is used not only in patients with isolated PFOA but in patients with chronic lateral patellar instability. Fulkerson osteotomy combines the benefits of the Maquet technique (unloading) and the Elmslie-Trillat technique (tracking improvement) in a single osteotomy, with no distraction of the osteotomy site with bone graft and without the complication rate of Maquet tibial tubercle elevation. Before surgery, computed tomography (CT) or magnetic resonance imaging (MRI) is routinely used to measure TT-TG distance to determine the tibial tubercle medialization required in the Fulkerson osteotomy. However, TT-TG distance must be used with caution, as it cannot be determined in cases with trochlear dysplasia. Consequently, physical examination and arthroscopic examination for evaluation of patellofemoral tracking and location of chondral defects should be performed before the Fulkerson osteotomy.
Rationale; Indications and Contraindications; Preoperative Planning
As already noted, AMZ unloads the distal and lateral facets of the patella. Beck and colleagues14 suggested AMZ is appropriate for unloading the lateral trochlea. However, it is not useful for central chondral defects and may actually increase the load in patients with medial chondral defects. As AMZ shifts contact force to the medial trochlea, Fulkerson osteotomy is appropriate when distal and lateral chondral lesions must be unloaded. Because this procedure moves the tibial tubercle medially and anteriorly, loads are transferred to the proximal and medial facets of the patella. Therefore, the procedure is contraindicated when diffuse, proximal, or medial chondral lesions are present. Moreover, AMZ is contraindicated in patients with normal TT-TG distance because there is the risk that overmedialization will cause symptomatic medial subluxation. Grade III or IV central trochlear cartilage lesions are also less likely to have successful AMZ outcomes. Therefore, before Fulkerson osteotomy is performed, MRI should be obtained to evaluate the patellofemoral articular surface and TT-TG distance. MRI provides information that is useful for preoperative planning because it allows assessment of articular cartilage lesions, including their location and severity. Moreover, because the osseous and cartilaginous contours of the patella differ, MRI gives a more accurate picture of the patellofemoral congruence than CT does. Last, before the open surgery is performed, the patellofemoral joint should be arthroscopically examined to determine the location of chondral lesions. Cartilage lesion mapping is important because Fulkerson osteotomy outcomes depend on chondral lesion location. Pidoriano and colleagues15 correlated AMZ outcomes with articular lesion location and noted optimal outcomes in patients with distal and lateral patellar articular lesions and intact trochlear cartilage (87% good and excellent outcomes). Patients with medial lesions and proximal or diffuse lesions generally did poorly (55% good and excellent outcomes in medial lesions vs 20% good and excellent outcomes in proximal and diffuse lesions). Central trochlear lesions were associated with medial patellar lesions, and all patients with central trochlear lesions had poor outcomes. Interestingly, Outerbridge grading of patellar lesions was not significantly correlated with overall outcomes.15 Even in cases of severe chondropathy, including bone-on-bone arthritis, AMZ has had reliable outcomes and may be superior to arthroplasty because of joint preservation, duration up to 8 years, and restoration of patellofemoral tracking. It should be noted that a resurfacing technique such as patellofemoral arthroplasty is not a substitute for patella realignment. Any patellofemoral maltracking must be corrected before patellofemoral arthroplasty. Fulkerson osteotomy does not preclude subsequent surgery (eg, TKA). Furthermore, AMZ may prevent the natural progression of PFOA related to chronic lateral tracking.
AMZ osteotomy can be adjusted for the specific indication and for the location of chondral defects. If the primary goal is unloading a lateral lesion, or lateral maltracking, then a flatter osteotomy may be performed to increase the relative medialization of the tubercle; however, if the primary goal is unloading a distal lesion, then a relatively more oblique or vertical osteotomy may be performed to transfer the load more proximally. This is the technique preferred by authors in most cases in which more anteriorization is desired.
When TT-TG distance is used to guide surgical realignment, patellofemoral chondrosis associated with normal TT-TG distance can be addressed with directly anterior displacement of the tibial tubercle. Anteriorization of the tibial tubercle can be obtained by inserting a bone block between the tubercle and the tibial cut (Figure 5A).16 The medialization can be neutralized by making this block as thick as the measured medialization.16
Surgical Outcomes of Anteromedialization in Patellofemoral Osteoarthritis
Fulkerson and colleagues10 followed 30 patients for more than 2 years after they underwent AMZ of the tibial tubercle for persistent patellofemoral pain associated with patellar articular degeneration. Of these 30 patients, 12 were followed for more than 5 years. The authors reported 93% good and excellent subjective outcomes and 89% good and excellent objective outcomes. Quality of improvement was sustained for all 12 patients reevaluated more than 5 years after surgery. When examined separately, 75% of patients with advanced PFOA had a good outcome, but none had an excellent outcome. Carofino and Fulkerson17 retrospectively evaluated tibial tubercle AMZ for isolated PFOA in 22 knees (17 active patients older than 50 years at time of surgery; mean age, 55 years) with minimum follow-up of 2 years (mean, 77 months). Mean postoperative Lysholm score was 83. According to Lysholm scores, outcomes were good to excellent in 12 cases, fair in 6, and poor in 1. The authors concluded that tibial tubercle AMZ is a definitive treatment option for isolated PFOA in active older patients. Morshuis and colleagues18 retrospectively evaluated 22 patients (25 knees) who underwent Fulkerson osteotomy for patellofemoral pain. Outcomes were evaluated a mean of 12 and 30 months after surgery. At the first evaluation, 84% of patients had satisfactory outcomes, and, at the second (≤38 months after surgery), 70%. Only in relatively young patients without signs of PFOA did outcomes remain satisfactory in all cases. At the later evaluation, 60% of patients with PFOA and/or lateralization had satisfactory outcomes.
Tips and Tricks to Avoid Complications
For some patients, AMZ performed technically correctly produced unhappiness—an outcome that may arise from incorrect patient selection or failure to meet patient expectations. It is important to discuss objectives and expectations with the patient before surgery. With correct patient selection and meticulous surgical technique (with customization of osteotomy angle and translation based on underlying lesion), surgeons have obtained excellent outcomes with infrequent complications (Table).
Intraoperative complications may involve neurovascular structures. The anterior tibial artery and the peroneal nerve are at risk during Fulkerson osteotomy. Decreased anterior sensation related to the infrapatellar branch of the saphenous nerve is not uncommon. Reducing the risk of neurovascular injury requires use of retractors and keeping the saw blade visible at all times. Another potential devastating complication is injury of the posterior vascular structures during bicortical tibial drilling for screw placement. According to Kline and colleagues,19 bicortical drilling may occur precariously near the posterior vascular structures of the knee. They advised extreme caution in drilling the posterior cortex during this procedure. To avoid the risk of compartment syndrome, surgeons can leave the anterior compartment fascia open or pie crust it by making multiple small perforations to decrease tension. Tibial fracture is another potential complication with this osteotomy. Reducing the risk of fracture involves tapering the distal cut anteriorly and avoiding a “notched” osteotomy (Figures 6A-6C).
Postoperative complications, which are similar to those associated with any knee surgery, include infection, arthrofibrosis, complex regional pain syndrome, thromboembolism, nonunion, fixation failure, and fracture. Arthrofibrosis has many causes, but the problem decreases with secure osteotomy fixation, early knee motion, and patellar mobilization. Overmedialization can result in medial patella instability, typically subluxation rather than complete dislocation. The instability can be relatively subtle or can cause pain and weakness. Lateralization of the tibial tubercle might be appropiate.23
Sulcus-Deepening Trochleoplasty
High-grade trochlear dysplasia with a prominence, frequently present in lateral patellar instability, is thought to correlate with PFOA because it produces an anti-Maquet effect.24 The dysplasia provokes an increment of the patellofemoral joint pressure that could explain patellofemoral chondropathy and ultimately PFOA. In fact, 33% of patients with isolated PFOA have a history of objective patellar dislocation.24 In these cases, SDT could be considered. Several studies have examined use of this technique in the treatment of instability, but not PFOA.25 After SDT, pain resolves despite the chondral lesions being left alone (Figures 7A, 7B).
Conclusion
Patellofemoral joint replacement is an option for patellofemoral pain only in very select cases. Preserving the joint is always a primary goal. As not all PFOA cases are equal, joint-preserving surgery must be tailored to the patient. The keys to success are good indication, precise surgery, proper rehabilitation, and, above all, doing only what is needed.
Am J Orthop. 2017;46(3):139-145. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. McAlindon TE, Snow S, Cooper C, Dieppe PA. Radiographic patterns of osteoarthritis of the knee joint in the community: the importance of the patellofemoral joint. Ann Rheum Dis. 1992;51(7):844-849.
2. Iwano T, Kurosawa H, Tokuyama H, Hoshikawa Y. Roentgenographic and clinical findings of patellofemoral osteoarthrosis. With special reference to its relationship to femorotibial osteoarthrosis and etiologic factors. Clin Orthop Relat Res. 1990;(252):190-197.
3. López-Franco M, Murciano-Antón MA, Fernández-Aceñero MJ, De Lucas-Villarrubia JC, López-Martín N, Gómez-Barrena E. Evaluation of a minimally aggressive method of patellofemoral osteoarthritis treatment at 10 years minimum follow-up. Knee. 2013;20(6):476-481.
4. Paulos LE, O’Connor DL, Karistinos A. Partial lateral patellar facetectomy for treatment of arthritis due to lateral patellar compression syndrome. Arthroscopy. 2008;24(5):547-553.
5. Wetzels T, Bellemans J. Patellofemoral osteoarthritis treated by partial lateral facetectomy: results at long-term follow up. Knee. 2012;19(4):411-415.
6. Yercan HS, Ait Si Selmi T, Neyret P. The treatment of patellofemoral osteoarthritis with partial lateral facetectomy. Clin Orthop Relat Res. 2005;(436):14-19.
7. Vaquero J, Calvo JA, Chana F, Perez-Mañanes R. The patellar thinning osteotomy in patellofemoral arthritis: four to 18 years’ follow-up. J Bone Joint Surg Br. 2010;92(10):1385-1391.
8. Vaquero J, Arriaza R. The patella thinning osteotomy. An experimental study of a new technique for reducing patellofemoral pressure. Int Orthop. 1992;16(4):372-376.
9. Fulkerson JP. Disorders of the Patellofemoral Joint. 3rd ed. Baltimore, MD: Williams & Wilkins; 1997.
10. Fulkerson JP, Becker GJ, Meaney JA, Miranda M, Folcik MA. Anteromedial tibial tubercle transfer without bone graft. Am J Sports Med. 1990;18(5):490-496.
11. Fulkerson JP. Patellofemoral pain disorders: evaluation and management. J Am Acad Orthop Surg. 1994;2(2):124-132.
12. Fulkerson JP. Diagnosis and treatment of patients with patellofemoral pain. Am J Sports Med. 2002;30(3):447-456.
13. Fulkerson JP. Anteromedialization of the tibial tuberosity for patellofemoral malalignment. Clin Orthop Relat Res. 1983;(177):176-181.
14. Beck PR, Thomas AL, Farr J, Lewis PB, Cole BJ. Trochlear contact pressures after anteromedialization of the tibial tubercle. Am J Sports Med. 2005;33(11):1710-1715.
15. Pidoriano AJ, Weinstein RN, Buuck DA, Fulkerson JP. Correlation of patellar articular lesions with results from anteromedial tibial tubercle transfer. Am J Sports Med. 1997;25(4):533-537.
16. Farr J. Tibial tubercle osteotomy. Tech Knee Surg. 2003;2:28-42.
17. Carofino BC, Fulkerson JP. Anteromedialization of the tibial tubercle for patellofemoral arthritis in patients > 50 years. J Knee Surg. 2008;21(2):101-105.
18. Morshuis WJ, Pavlov PW, de Rooy KP. Anteromedialization of the tibial tuberosity in the treatment of patellofemoral pain and malalignment. Clin Orthop Relat Res. 1990;(255):242-250.
19. Kline AJ, Gonzales J, Beach WR, Miller MD. Vascular risk associated with bicortical tibial drilling during anteromedial tibial tubercle transfer. Am J Orthop. 2006;35(1):30-32.
20. Stetson WB, Friedman MJ, Fulkerson JP, Cheng M, Buuck D. Fracture of the proximal tibia with immediate weightbearing after a Fulkerson osteotomy. Am J Sports Med. 1997;25(4):570-574.
21. Fulkerson JP. Fracture of the proximal tibia after Fulkerson anteromedial tibial tubercle transfer. A report of four cases. Am J Sports Med. 1999;27(2):265.
22. Cosgarea AJ, Freedman JA, McFarland EG. Nonunion of the tibial tubercle shingle following Fulkerson osteotomy. Am J Knee Surg. 2001;14(1):51-54.
23. Fulkerson JP. Anterolateralization of the tibial tubercle. Tech Orthop. 1997;12:165-169.
24. Grelsamer RP, Dejour D, Gould J. The pathophysiology of patellofemoral arthritis. Orthop Clin North Am. 2008;39(3):269-274.
25. Ntagiopoulos PG, Byn P, Dejour D. Midterm results of comprehensive surgical reconstruction including sulcus-deepening trochleoplasty in recurrent patellar dislocations with high-grade trochlear dysplasia. Am J Sports Med. 2013;41(5):998-1004.
26. Oberlander MA, Baker CL, Morgan BE. Patellofemoral arthrosis: the treatment options. Am J Orthop. 1998;27(4):263-270.
27. Scuderi GR. The Patella. New York, NY: Springer-Verlag; 1995.
28. Buuck D, Fulkerson JP. Anteromedialization of the tibial tubercle: a 4 to 12 year follow up. Oper Tech Sports Med. 2000;8:131-137.
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23. Fulkerson JP. Anterolateralization of the tibial tubercle. Tech Orthop. 1997;12:165-169.
24. Grelsamer RP, Dejour D, Gould J. The pathophysiology of patellofemoral arthritis. Orthop Clin North Am. 2008;39(3):269-274.
25. Ntagiopoulos PG, Byn P, Dejour D. Midterm results of comprehensive surgical reconstruction including sulcus-deepening trochleoplasty in recurrent patellar dislocations with high-grade trochlear dysplasia. Am J Sports Med. 2013;41(5):998-1004.
26. Oberlander MA, Baker CL, Morgan BE. Patellofemoral arthrosis: the treatment options. Am J Orthop. 1998;27(4):263-270.
27. Scuderi GR. The Patella. New York, NY: Springer-Verlag; 1995.
28. Buuck D, Fulkerson JP. Anteromedialization of the tibial tubercle: a 4 to 12 year follow up. Oper Tech Sports Med. 2000;8:131-137.
