HOUSTON – A personalized lifestyle coaching program focused on healthy eating increased blood pressure control by 7%, compared with usual care, among black patients with persistent hypertension.

A year after the program was instituted, the rate of blood pressure control was 69% in the intervention group, compared with 62% in the group that had the usual care offered to hypertensive patients, Mai Nguyen-Huynh, MD, said at the International Stroke Conference sponsored by the American Heart Association.

• “Shake” the salt habit.

• “Rattle” the intensity of the existing blood pressure control protocol.

• “Roll” out the results and incorporate into clinical practice.

The study was organized into three arms. Usual care was Kaiser’s typical intensified hypertension management. Patients filled out health and diet questionnaires and could voluntarily undergo a 24-hour urine sodium test.

The enhanced monitoring arm consisted of usual care, plus an in-person session with a nurse to discuss resources and possible barriers to treatment; regular blood pressure checks; intensification of pharmacotherapy, focusing on thiazides; and the addition of spironolactone for patients who had persistent hypertension despite being on three or more medications.

The lifestyle intervention arm consisted of usual care plus personalized coaching, both on the phone and in person. Participants could have up to 16 phone sessions with a specially trained counselor, with the option of bimonthly in-person group sessions.

These were accompanied by a workbook that emphasized healthy eating, from meal planning to shopping and cooking. Restaurant dining was tackled as well, including fast food and carryout. The workbook covered eight sessions. Each session ended with goal-setting for the next meeting, and opened with a review of how the prior month’s goals were accomplished.

Individualization was an important part of the lifestyle intervention program, Dr. Nguyen-Huynh said. Counselors didn’t strive to make each participant fit into a cookie-cutter solution. Instead, they worked as a team to build interventions that would work for each person.

The study group comprised 1,660 subjects. About 70% were women. Diabetes was common (about 33%), and around 10% had a history of coronary artery disease. The mean body mass index was 34 kg/m².

The primary outcome was rate of blood pressure control in the usual care vs. enhanced monitoring groups, and the usual care vs. lifestyle modification groups after 1 year.

At the end of follow-up, there was no difference in the rate of control between the usual care group and the enhanced monitoring group (62% vs. 64%). However, there was a significant difference in the rate of control between the usual care and the lifestyle modification groups (62% vs. 69%).

Again, Dr. Nguyen-Huynh said, it was tough to pinpoint any particular reason for the improvement. There was no apparent increase in compliance with antihypertensive medication. The Morisky scale, an 8-point self-reported measure of medication compliance, was not different from baseline. Participants didn’t report any big changes in salt intake or salt use in food. This was borne out in the 24-hour urine sodium screens, which were also not different from baseline. There were no significant weight changes and no changes in the use of outpatient primary care.

“What we can say is that it apparently worked,” she said. “This culturally appropriate, telephone-based lifestyle intervention, that focuses on the DASH eating plan, may be something that can help African-Americans with uncontrolled hypertension manage their condition.”

She added that Kaiser will continue to drill down in the data to discover the source of its benefit and follow the participants for at least another year to assess the longevity of the its clinical effect.

Dr. Nguyen-Huynh had no financial disclosures.

[email protected]

On Twitter @alz_gal

HOUSTON – A personalized lifestyle coaching program focused on healthy eating increased blood pressure control by 7%, compared with usual care, among black patients with persistent hypertension.

A year after the program was instituted, the rate of blood pressure control was 69% in the intervention group, compared with 62% in the group that had the usual care offered to hypertensive patients, Mai Nguyen-Huynh, MD, said at the International Stroke Conference sponsored by the American Heart Association.

• “Shake” the salt habit.

• “Rattle” the intensity of the existing blood pressure control protocol.

• “Roll” out the results and incorporate into clinical practice.

The study was organized into three arms. Usual care was Kaiser’s typical intensified hypertension management. Patients filled out health and diet questionnaires and could voluntarily undergo a 24-hour urine sodium test.

The enhanced monitoring arm consisted of usual care, plus an in-person session with a nurse to discuss resources and possible barriers to treatment; regular blood pressure checks; intensification of pharmacotherapy, focusing on thiazides; and the addition of spironolactone for patients who had persistent hypertension despite being on three or more medications.

The lifestyle intervention arm consisted of usual care plus personalized coaching, both on the phone and in person. Participants could have up to 16 phone sessions with a specially trained counselor, with the option of bimonthly in-person group sessions.

These were accompanied by a workbook that emphasized healthy eating, from meal planning to shopping and cooking. Restaurant dining was tackled as well, including fast food and carryout. The workbook covered eight sessions. Each session ended with goal-setting for the next meeting, and opened with a review of how the prior month’s goals were accomplished.

Individualization was an important part of the lifestyle intervention program, Dr. Nguyen-Huynh said. Counselors didn’t strive to make each participant fit into a cookie-cutter solution. Instead, they worked as a team to build interventions that would work for each person.

The study group comprised 1,660 subjects. About 70% were women. Diabetes was common (about 33%), and around 10% had a history of coronary artery disease. The mean body mass index was 34 kg/m².

The primary outcome was rate of blood pressure control in the usual care vs. enhanced monitoring groups, and the usual care vs. lifestyle modification groups after 1 year.

At the end of follow-up, there was no difference in the rate of control between the usual care group and the enhanced monitoring group (62% vs. 64%). However, there was a significant difference in the rate of control between the usual care and the lifestyle modification groups (62% vs. 69%).

Again, Dr. Nguyen-Huynh said, it was tough to pinpoint any particular reason for the improvement. There was no apparent increase in compliance with antihypertensive medication. The Morisky scale, an 8-point self-reported measure of medication compliance, was not different from baseline. Participants didn’t report any big changes in salt intake or salt use in food. This was borne out in the 24-hour urine sodium screens, which were also not different from baseline. There were no significant weight changes and no changes in the use of outpatient primary care.

“What we can say is that it apparently worked,” she said. “This culturally appropriate, telephone-based lifestyle intervention, that focuses on the DASH eating plan, may be something that can help African-Americans with uncontrolled hypertension manage their condition.”

She added that Kaiser will continue to drill down in the data to discover the source of its benefit and follow the participants for at least another year to assess the longevity of the its clinical effect.

Dr. Nguyen-Huynh had no financial disclosures.

[email protected]

On Twitter @alz_gal

HOUSTON – A personalized lifestyle coaching program focused on healthy eating increased blood pressure control by 7%, compared with usual care, among black patients with persistent hypertension.

A year after the program was instituted, the rate of blood pressure control was 69% in the intervention group, compared with 62% in the group that had the usual care offered to hypertensive patients, Mai Nguyen-Huynh, MD, said at the International Stroke Conference sponsored by the American Heart Association.

• “Shake” the salt habit.

• “Rattle” the intensity of the existing blood pressure control protocol.

• “Roll” out the results and incorporate into clinical practice.

The study was organized into three arms. Usual care was Kaiser’s typical intensified hypertension management. Patients filled out health and diet questionnaires and could voluntarily undergo a 24-hour urine sodium test.

The enhanced monitoring arm consisted of usual care, plus an in-person session with a nurse to discuss resources and possible barriers to treatment; regular blood pressure checks; intensification of pharmacotherapy, focusing on thiazides; and the addition of spironolactone for patients who had persistent hypertension despite being on three or more medications.

The lifestyle intervention arm consisted of usual care plus personalized coaching, both on the phone and in person. Participants could have up to 16 phone sessions with a specially trained counselor, with the option of bimonthly in-person group sessions.

These were accompanied by a workbook that emphasized healthy eating, from meal planning to shopping and cooking. Restaurant dining was tackled as well, including fast food and carryout. The workbook covered eight sessions. Each session ended with goal-setting for the next meeting, and opened with a review of how the prior month’s goals were accomplished.

Individualization was an important part of the lifestyle intervention program, Dr. Nguyen-Huynh said. Counselors didn’t strive to make each participant fit into a cookie-cutter solution. Instead, they worked as a team to build interventions that would work for each person.

The study group comprised 1,660 subjects. About 70% were women. Diabetes was common (about 33%), and around 10% had a history of coronary artery disease. The mean body mass index was 34 kg/m².

The primary outcome was rate of blood pressure control in the usual care vs. enhanced monitoring groups, and the usual care vs. lifestyle modification groups after 1 year.

At the end of follow-up, there was no difference in the rate of control between the usual care group and the enhanced monitoring group (62% vs. 64%). However, there was a significant difference in the rate of control between the usual care and the lifestyle modification groups (62% vs. 69%).

Again, Dr. Nguyen-Huynh said, it was tough to pinpoint any particular reason for the improvement. There was no apparent increase in compliance with antihypertensive medication. The Morisky scale, an 8-point self-reported measure of medication compliance, was not different from baseline. Participants didn’t report any big changes in salt intake or salt use in food. This was borne out in the 24-hour urine sodium screens, which were also not different from baseline. There were no significant weight changes and no changes in the use of outpatient primary care.

“What we can say is that it apparently worked,” she said. “This culturally appropriate, telephone-based lifestyle intervention, that focuses on the DASH eating plan, may be something that can help African-Americans with uncontrolled hypertension manage their condition.”

She added that Kaiser will continue to drill down in the data to discover the source of its benefit and follow the participants for at least another year to assess the longevity of the its clinical effect.

Dr. Nguyen-Huynh had no financial disclosures.

[email protected]

On Twitter @alz_gal

SCOTTSDALE, ARIZ. – Most psychiatrists are familiar with many of the basic tenets of psychoanalysis, but they probably aren’t relying on its therapeutic powers in practice as much as they are pharmacotherapy, according to an expert.

“There’s a great deal of discussion about whether psychoanalysis has an adequate evidence base. That’s a popular concept. It’s not so much about whether practitioners want to use it, but whether or not they can defend using it in their dialogs with insurance companies, government agencies, and other sources of support,” Robert Michels, MD, a Walsh McDermott University Professor of Medicine, and professor of psychiatry, at Cornell University, New York, said at the annual meeting of the American College of Psychiatrists. “My summary is that it has less adequate data supporting it [than pharmacologic interventions]. … There is, however, convincing evidence that all of these treatments, ranging from cognitive-behavioral therapy to [dialectical behavior therapy], to dynamic psychoanalysis, to mentalization-based treatment, do have an effect.”

[email protected]

On Twitter @whitneymcknight

SCOTTSDALE, ARIZ. – Most psychiatrists are familiar with many of the basic tenets of psychoanalysis, but they probably aren’t relying on its therapeutic powers in practice as much as they are pharmacotherapy, according to an expert.

“There’s a great deal of discussion about whether psychoanalysis has an adequate evidence base. That’s a popular concept. It’s not so much about whether practitioners want to use it, but whether or not they can defend using it in their dialogs with insurance companies, government agencies, and other sources of support,” Robert Michels, MD, a Walsh McDermott University Professor of Medicine, and professor of psychiatry, at Cornell University, New York, said at the annual meeting of the American College of Psychiatrists. “My summary is that it has less adequate data supporting it [than pharmacologic interventions]. … There is, however, convincing evidence that all of these treatments, ranging from cognitive-behavioral therapy to [dialectical behavior therapy], to dynamic psychoanalysis, to mentalization-based treatment, do have an effect.”

[email protected]

On Twitter @whitneymcknight

SCOTTSDALE, ARIZ. – Most psychiatrists are familiar with many of the basic tenets of psychoanalysis, but they probably aren’t relying on its therapeutic powers in practice as much as they are pharmacotherapy, according to an expert.

“There’s a great deal of discussion about whether psychoanalysis has an adequate evidence base. That’s a popular concept. It’s not so much about whether practitioners want to use it, but whether or not they can defend using it in their dialogs with insurance companies, government agencies, and other sources of support,” Robert Michels, MD, a Walsh McDermott University Professor of Medicine, and professor of psychiatry, at Cornell University, New York, said at the annual meeting of the American College of Psychiatrists. “My summary is that it has less adequate data supporting it [than pharmacologic interventions]. … There is, however, convincing evidence that all of these treatments, ranging from cognitive-behavioral therapy to [dialectical behavior therapy], to dynamic psychoanalysis, to mentalization-based treatment, do have an effect.”

[email protected]

On Twitter @whitneymcknight

ORLANDO – Ibrutinib was associated with clinically meaningful and durable responses in patients with chronic graft-versus-host disease that did not respond to frontline systemic therapy, based on the final results of a phase II study.

Preliminary findings from that study led in 2016 to a Food and Drug Administration Breakthrough Therapy Designation for ibrutinib for chronic graft-versus-host disease (cGVHD) after the failure of one or more lines of systemic therapy, and the responses seen in this pretreated, high-risk population support the study of ibrutinib for frontline treatment of cGVHD, said David Miklos, MD, of Stanford (Calif.) University.

Sharon Worcester/Frontline Medical news

ORLANDO – Ibrutinib was associated with clinically meaningful and durable responses in patients with chronic graft-versus-host disease that did not respond to frontline systemic therapy, based on the final results of a phase II study.

Preliminary findings from that study led in 2016 to a Food and Drug Administration Breakthrough Therapy Designation for ibrutinib for chronic graft-versus-host disease (cGVHD) after the failure of one or more lines of systemic therapy, and the responses seen in this pretreated, high-risk population support the study of ibrutinib for frontline treatment of cGVHD, said David Miklos, MD, of Stanford (Calif.) University.

Sharon Worcester/Frontline Medical news

ORLANDO – Ibrutinib was associated with clinically meaningful and durable responses in patients with chronic graft-versus-host disease that did not respond to frontline systemic therapy, based on the final results of a phase II study.

Preliminary findings from that study led in 2016 to a Food and Drug Administration Breakthrough Therapy Designation for ibrutinib for chronic graft-versus-host disease (cGVHD) after the failure of one or more lines of systemic therapy, and the responses seen in this pretreated, high-risk population support the study of ibrutinib for frontline treatment of cGVHD, said David Miklos, MD, of Stanford (Calif.) University.

Sharon Worcester/Frontline Medical news

Patients with beta thalassemia major who were chelated only with oral deferasirox experienced significant improvements in liver stiffness, both from baseline and compared with patients who interrupted deferasirox therapy because of pregnancy, according to a small prospective 5-year study.

Transient elastography showed that continuous therapy with deferasirox (median dose, 35 mg per kg) yielded an 0.85 kPa average improvement in liver stiffness compared with baseline (P = .02), reported Nikolaos Sousos of Aristotle University of Thessaloniki, Greece, and his associates (Br J Haematol. 2017 Jan 20. doi: 10.1111/bjh.14509).

In contrast, interrupting therapy for a median of 16 months because of successful pregnancy led to an average increase in liver stiffness of 1.84 kPa – a significant difference between groups (P = .005) even after the researchers controlled for gender, age, ferritin levels, and T2-weighted magnetic resonance imaging (MRI) measurements of iron deposition in the liver and heart.

Patients with beta thalassemia major often develop liver fibrosis because of excessive intestinal iron absorption, iron overload from transfusions, or hepatitis C virus infection, the investigators noted. The median age of the patients in this study was 32 years (range, 20-47 years), they were HCV negative, and they received regular transfusions to maintain hemoglobin levels above 95 g/L. The seven female participants who temporarily stopped deferasirox because of pregnancy all restarted therapy at least 8 months before their follow-up transient elastography liver stiffness measurement, the investigators reported.

T2-weighted MRI measurements of liver iron concentration also had improved at follow-up, reflecting “better control of iron overload,” although the difference from baseline was not statistically significant, the investigators noted. This result reinforces previous findings (Gastroenterology. 2011;141[4]:1202-11) that long-term deferasirox therapy can significantly improve liver fibrosis in patients with beta thalassemia, regardless of liver iron concentration, the researchers added. Together, those findings suggest that “improvement in liver fibrosis, rather than liver iron concentration should be the primary effect of chelation therapy,” they suggested.

The Research Committee of Aristotle University of Thessaloniki, Novartis Hellas (Novartis AG, Basel, Switzerland), and the Greek Thalassaemia Association funded the study. The authors declared having no competing interests.

Patients with beta thalassemia major who were chelated only with oral deferasirox experienced significant improvements in liver stiffness, both from baseline and compared with patients who interrupted deferasirox therapy because of pregnancy, according to a small prospective 5-year study.

Transient elastography showed that continuous therapy with deferasirox (median dose, 35 mg per kg) yielded an 0.85 kPa average improvement in liver stiffness compared with baseline (P = .02), reported Nikolaos Sousos of Aristotle University of Thessaloniki, Greece, and his associates (Br J Haematol. 2017 Jan 20. doi: 10.1111/bjh.14509).

In contrast, interrupting therapy for a median of 16 months because of successful pregnancy led to an average increase in liver stiffness of 1.84 kPa – a significant difference between groups (P = .005) even after the researchers controlled for gender, age, ferritin levels, and T2-weighted magnetic resonance imaging (MRI) measurements of iron deposition in the liver and heart.

Patients with beta thalassemia major often develop liver fibrosis because of excessive intestinal iron absorption, iron overload from transfusions, or hepatitis C virus infection, the investigators noted. The median age of the patients in this study was 32 years (range, 20-47 years), they were HCV negative, and they received regular transfusions to maintain hemoglobin levels above 95 g/L. The seven female participants who temporarily stopped deferasirox because of pregnancy all restarted therapy at least 8 months before their follow-up transient elastography liver stiffness measurement, the investigators reported.

T2-weighted MRI measurements of liver iron concentration also had improved at follow-up, reflecting “better control of iron overload,” although the difference from baseline was not statistically significant, the investigators noted. This result reinforces previous findings (Gastroenterology. 2011;141[4]:1202-11) that long-term deferasirox therapy can significantly improve liver fibrosis in patients with beta thalassemia, regardless of liver iron concentration, the researchers added. Together, those findings suggest that “improvement in liver fibrosis, rather than liver iron concentration should be the primary effect of chelation therapy,” they suggested.

The Research Committee of Aristotle University of Thessaloniki, Novartis Hellas (Novartis AG, Basel, Switzerland), and the Greek Thalassaemia Association funded the study. The authors declared having no competing interests.

Patients with beta thalassemia major who were chelated only with oral deferasirox experienced significant improvements in liver stiffness, both from baseline and compared with patients who interrupted deferasirox therapy because of pregnancy, according to a small prospective 5-year study.

Transient elastography showed that continuous therapy with deferasirox (median dose, 35 mg per kg) yielded an 0.85 kPa average improvement in liver stiffness compared with baseline (P = .02), reported Nikolaos Sousos of Aristotle University of Thessaloniki, Greece, and his associates (Br J Haematol. 2017 Jan 20. doi: 10.1111/bjh.14509).

In contrast, interrupting therapy for a median of 16 months because of successful pregnancy led to an average increase in liver stiffness of 1.84 kPa – a significant difference between groups (P = .005) even after the researchers controlled for gender, age, ferritin levels, and T2-weighted magnetic resonance imaging (MRI) measurements of iron deposition in the liver and heart.

Patients with beta thalassemia major often develop liver fibrosis because of excessive intestinal iron absorption, iron overload from transfusions, or hepatitis C virus infection, the investigators noted. The median age of the patients in this study was 32 years (range, 20-47 years), they were HCV negative, and they received regular transfusions to maintain hemoglobin levels above 95 g/L. The seven female participants who temporarily stopped deferasirox because of pregnancy all restarted therapy at least 8 months before their follow-up transient elastography liver stiffness measurement, the investigators reported.

T2-weighted MRI measurements of liver iron concentration also had improved at follow-up, reflecting “better control of iron overload,” although the difference from baseline was not statistically significant, the investigators noted. This result reinforces previous findings (Gastroenterology. 2011;141[4]:1202-11) that long-term deferasirox therapy can significantly improve liver fibrosis in patients with beta thalassemia, regardless of liver iron concentration, the researchers added. Together, those findings suggest that “improvement in liver fibrosis, rather than liver iron concentration should be the primary effect of chelation therapy,” they suggested.

The Research Committee of Aristotle University of Thessaloniki, Novartis Hellas (Novartis AG, Basel, Switzerland), and the Greek Thalassaemia Association funded the study. The authors declared having no competing interests.

Mitoxantrone plus prednisone (MP) added to androgen deprivation therapy (ADT) does not improve outcomes in patients with clinically localized prostate cancer, according to the results of a large long-term multicenter clinical trial.

At a follow-up time of almost 11 years, outcomes were nearly the same whether patients had received chemotherapy and ADT or just ADT.

Overall survival was 87% in the cohort that received ADT only and 86% in the study arm that received ADT plus MP (HR 1.05 (CI 0.78, 1.42), P = .74). Recurrence-free survival was 84% in both groups (HR 0.98 (CI 0.78, 1.23), P = .83).

Disease free survival was 72% in both arms, and there was no statistical difference. Similarly, death without recurrence were also similar in both arms.

“Survival was greater than anticipated in both arms,” lead author L. Michael Glode, MD, of the University of Colorado, Denver, said in a press briefing held at the 2017 genitourinary cancers symposium sponsored by the American Society of Clinical Oncology, ASTRO, and the Society of Urologic Oncology. “There is no evidence that MP improves prostate cancer specific survival when added to 2 years of adjuvant ADT.”

There were 85 deaths in the ADT arm compared to 91 in the chemotherapy arm. Prostate cancer accounted for 18% of deaths among the patients receiving ADT only and 22% in the chemotherapy arm, but the incidence of other cancers was twice as common in the chemotherapy arm as in the ADT only arm.

“The predominant cancers were GI and lung,” said Dr. Glode, “And noncancer deaths were variable.”

Of note, MP increased the incidence of leukemia (one case in the ADT group vs. five in the chemotherapy group).

“This trial demonstrates the feasibility of doing adjuvant trials in prostate cancer post radical prostatectomy,” said Dr. Glode. “Survival was greater than anticipated in both arms.”

The assumptions of this trial were that 2 years of adjuvant ADT would improve overall survival and progression-free survival although definitive data were unavailable.

The rationale for doing a study using adjuvant therapy was based on published literature, in which findings had showed that while short-term neoadjuvant ADT prior to prostatectomy reduced positive margins, it had no effect on disease-free survival. In addition, research had shown that longer-term ADT improved outcomes for patients undergoing curative radiation therapy.

For chemotherapy, Dr. Glode pointed to data showing that adjuvant chemotherapy improved progression-free survival in patients who had undergone both prostatectomy and radiation therapy.

“We hypothesized that the addition of modestly active chemotherapy earlier in disease might improve overall survival and progression-free survival,” he said.

The primary objective was overall survival and the secondary endpoint was disease-free survival.

The S9921 trial enrolled 983 patients from October 1999 to January 2007 with clinically localized prostate cancer, before enrollment ceased because of the increased incidence of leukemia in the ADT plus MP arm.

Of this group, 22 patients were ineligible, and the remaining patients were assigned to goserelin acetate 10.8 mg plus bicalutamide 50 mg (n = 481) or the same ADT plus MP (n = 480).

The patients were stratified by stage (≤pT2, ≥pT3, N0 or N+), Gleason score, and intent to receive adjuvant radiation, and the presurgical PSA was 7.6 ng/mL. Radiation therapy was allowed in both arms at physician discretion, and 26% intended to receive radiation therapy.

In the ADT only arm, 402 completed the treatment, and 390 completed treatment in the ADT plus chemotherapy arm.

Grade 3 or higher adverse events were more common in the chemotherapy group (56%/30%, P less than .0001). “As for toxicities, the main difference was the presence of leukopenia in the chemotherapy arm,” said Dr. Glode.

The study was funded by Southwest Oncology Group’s Urologic Cancer Outreach Program, Eastern Cooperative Oncology Group, Cancer and Leukemia Group B, Clinical Trials Support Unit, and National Cancer Institute. None of the authors had disclosures.

Mitoxantrone plus prednisone (MP) added to androgen deprivation therapy (ADT) does not improve outcomes in patients with clinically localized prostate cancer, according to the results of a large long-term multicenter clinical trial.

At a follow-up time of almost 11 years, outcomes were nearly the same whether patients had received chemotherapy and ADT or just ADT.

Overall survival was 87% in the cohort that received ADT only and 86% in the study arm that received ADT plus MP (HR 1.05 (CI 0.78, 1.42), P = .74). Recurrence-free survival was 84% in both groups (HR 0.98 (CI 0.78, 1.23), P = .83).

Disease free survival was 72% in both arms, and there was no statistical difference. Similarly, death without recurrence were also similar in both arms.

“Survival was greater than anticipated in both arms,” lead author L. Michael Glode, MD, of the University of Colorado, Denver, said in a press briefing held at the 2017 genitourinary cancers symposium sponsored by the American Society of Clinical Oncology, ASTRO, and the Society of Urologic Oncology. “There is no evidence that MP improves prostate cancer specific survival when added to 2 years of adjuvant ADT.”

There were 85 deaths in the ADT arm compared to 91 in the chemotherapy arm. Prostate cancer accounted for 18% of deaths among the patients receiving ADT only and 22% in the chemotherapy arm, but the incidence of other cancers was twice as common in the chemotherapy arm as in the ADT only arm.

“The predominant cancers were GI and lung,” said Dr. Glode, “And noncancer deaths were variable.”

Of note, MP increased the incidence of leukemia (one case in the ADT group vs. five in the chemotherapy group).

“This trial demonstrates the feasibility of doing adjuvant trials in prostate cancer post radical prostatectomy,” said Dr. Glode. “Survival was greater than anticipated in both arms.”

The assumptions of this trial were that 2 years of adjuvant ADT would improve overall survival and progression-free survival although definitive data were unavailable.

The rationale for doing a study using adjuvant therapy was based on published literature, in which findings had showed that while short-term neoadjuvant ADT prior to prostatectomy reduced positive margins, it had no effect on disease-free survival. In addition, research had shown that longer-term ADT improved outcomes for patients undergoing curative radiation therapy.

For chemotherapy, Dr. Glode pointed to data showing that adjuvant chemotherapy improved progression-free survival in patients who had undergone both prostatectomy and radiation therapy.

“We hypothesized that the addition of modestly active chemotherapy earlier in disease might improve overall survival and progression-free survival,” he said.

The primary objective was overall survival and the secondary endpoint was disease-free survival.

The S9921 trial enrolled 983 patients from October 1999 to January 2007 with clinically localized prostate cancer, before enrollment ceased because of the increased incidence of leukemia in the ADT plus MP arm.

Of this group, 22 patients were ineligible, and the remaining patients were assigned to goserelin acetate 10.8 mg plus bicalutamide 50 mg (n = 481) or the same ADT plus MP (n = 480).

The patients were stratified by stage (≤pT2, ≥pT3, N0 or N+), Gleason score, and intent to receive adjuvant radiation, and the presurgical PSA was 7.6 ng/mL. Radiation therapy was allowed in both arms at physician discretion, and 26% intended to receive radiation therapy.

In the ADT only arm, 402 completed the treatment, and 390 completed treatment in the ADT plus chemotherapy arm.

Grade 3 or higher adverse events were more common in the chemotherapy group (56%/30%, P less than .0001). “As for toxicities, the main difference was the presence of leukopenia in the chemotherapy arm,” said Dr. Glode.

The study was funded by Southwest Oncology Group’s Urologic Cancer Outreach Program, Eastern Cooperative Oncology Group, Cancer and Leukemia Group B, Clinical Trials Support Unit, and National Cancer Institute. None of the authors had disclosures.

Mitoxantrone plus prednisone (MP) added to androgen deprivation therapy (ADT) does not improve outcomes in patients with clinically localized prostate cancer, according to the results of a large long-term multicenter clinical trial.

At a follow-up time of almost 11 years, outcomes were nearly the same whether patients had received chemotherapy and ADT or just ADT.

Overall survival was 87% in the cohort that received ADT only and 86% in the study arm that received ADT plus MP (HR 1.05 (CI 0.78, 1.42), P = .74). Recurrence-free survival was 84% in both groups (HR 0.98 (CI 0.78, 1.23), P = .83).

Disease free survival was 72% in both arms, and there was no statistical difference. Similarly, death without recurrence were also similar in both arms.

“Survival was greater than anticipated in both arms,” lead author L. Michael Glode, MD, of the University of Colorado, Denver, said in a press briefing held at the 2017 genitourinary cancers symposium sponsored by the American Society of Clinical Oncology, ASTRO, and the Society of Urologic Oncology. “There is no evidence that MP improves prostate cancer specific survival when added to 2 years of adjuvant ADT.”

There were 85 deaths in the ADT arm compared to 91 in the chemotherapy arm. Prostate cancer accounted for 18% of deaths among the patients receiving ADT only and 22% in the chemotherapy arm, but the incidence of other cancers was twice as common in the chemotherapy arm as in the ADT only arm.

“The predominant cancers were GI and lung,” said Dr. Glode, “And noncancer deaths were variable.”

Of note, MP increased the incidence of leukemia (one case in the ADT group vs. five in the chemotherapy group).

“This trial demonstrates the feasibility of doing adjuvant trials in prostate cancer post radical prostatectomy,” said Dr. Glode. “Survival was greater than anticipated in both arms.”

The assumptions of this trial were that 2 years of adjuvant ADT would improve overall survival and progression-free survival although definitive data were unavailable.

The rationale for doing a study using adjuvant therapy was based on published literature, in which findings had showed that while short-term neoadjuvant ADT prior to prostatectomy reduced positive margins, it had no effect on disease-free survival. In addition, research had shown that longer-term ADT improved outcomes for patients undergoing curative radiation therapy.

For chemotherapy, Dr. Glode pointed to data showing that adjuvant chemotherapy improved progression-free survival in patients who had undergone both prostatectomy and radiation therapy.

“We hypothesized that the addition of modestly active chemotherapy earlier in disease might improve overall survival and progression-free survival,” he said.

The primary objective was overall survival and the secondary endpoint was disease-free survival.

The S9921 trial enrolled 983 patients from October 1999 to January 2007 with clinically localized prostate cancer, before enrollment ceased because of the increased incidence of leukemia in the ADT plus MP arm.

Of this group, 22 patients were ineligible, and the remaining patients were assigned to goserelin acetate 10.8 mg plus bicalutamide 50 mg (n = 481) or the same ADT plus MP (n = 480).

The patients were stratified by stage (≤pT2, ≥pT3, N0 or N+), Gleason score, and intent to receive adjuvant radiation, and the presurgical PSA was 7.6 ng/mL. Radiation therapy was allowed in both arms at physician discretion, and 26% intended to receive radiation therapy.

In the ADT only arm, 402 completed the treatment, and 390 completed treatment in the ADT plus chemotherapy arm.

Grade 3 or higher adverse events were more common in the chemotherapy group (56%/30%, P less than .0001). “As for toxicities, the main difference was the presence of leukopenia in the chemotherapy arm,” said Dr. Glode.

The study was funded by Southwest Oncology Group’s Urologic Cancer Outreach Program, Eastern Cooperative Oncology Group, Cancer and Leukemia Group B, Clinical Trials Support Unit, and National Cancer Institute. None of the authors had disclosures.

A rapid point-of-care assay for acetaminophen-related liver toxicity had a sensitivity of 100% and a specificity of 86%, compared with etiologic diagnosis, based on the results of a multicenter study published in the April issue of Clinical Gastroenterology and Hepatology.

The test might help guide treatment decisions for these patients in the emergency department and intensive care unit, said Dean W. Roberts, PhD, of the University of Arkansas, Little Rock, and his associates.

About 45% of acute liver failure cases in the United States stem from acetaminophen toxicity, but the diagnosis can be hard to confirm because the drug has a short half-life and patients often cannot or will not report an overdose, which also may consist of multiple exposures, limiting the interpretability of the Rumack nonogram. High-pressure liquid chromatography with electrochemical detection (HPLC-EC) accurately detects acetaminophen-protein adducts (3-[cysteine-S-yl] acetaminophen) released by lysed hepatocytes into the peripheral circulation, but this test requires specialized equipment and skilled personnel, the researchers noted (Clin Gastroenterol Hepatol. 2016 Sep 15. doi: 10.1016/j.cgh.2016.09.007).

ironstealth/Thinkstock

Source: American Gastroenterological Association

A rapid point-of-care assay for acetaminophen-related liver toxicity had a sensitivity of 100% and a specificity of 86%, compared with etiologic diagnosis, based on the results of a multicenter study published in the April issue of Clinical Gastroenterology and Hepatology.

The test might help guide treatment decisions for these patients in the emergency department and intensive care unit, said Dean W. Roberts, PhD, of the University of Arkansas, Little Rock, and his associates.

About 45% of acute liver failure cases in the United States stem from acetaminophen toxicity, but the diagnosis can be hard to confirm because the drug has a short half-life and patients often cannot or will not report an overdose, which also may consist of multiple exposures, limiting the interpretability of the Rumack nonogram. High-pressure liquid chromatography with electrochemical detection (HPLC-EC) accurately detects acetaminophen-protein adducts (3-[cysteine-S-yl] acetaminophen) released by lysed hepatocytes into the peripheral circulation, but this test requires specialized equipment and skilled personnel, the researchers noted (Clin Gastroenterol Hepatol. 2016 Sep 15. doi: 10.1016/j.cgh.2016.09.007).

ironstealth/Thinkstock

Source: American Gastroenterological Association

A rapid point-of-care assay for acetaminophen-related liver toxicity had a sensitivity of 100% and a specificity of 86%, compared with etiologic diagnosis, based on the results of a multicenter study published in the April issue of Clinical Gastroenterology and Hepatology.

The test might help guide treatment decisions for these patients in the emergency department and intensive care unit, said Dean W. Roberts, PhD, of the University of Arkansas, Little Rock, and his associates.

About 45% of acute liver failure cases in the United States stem from acetaminophen toxicity, but the diagnosis can be hard to confirm because the drug has a short half-life and patients often cannot or will not report an overdose, which also may consist of multiple exposures, limiting the interpretability of the Rumack nonogram. High-pressure liquid chromatography with electrochemical detection (HPLC-EC) accurately detects acetaminophen-protein adducts (3-[cysteine-S-yl] acetaminophen) released by lysed hepatocytes into the peripheral circulation, but this test requires specialized equipment and skilled personnel, the researchers noted (Clin Gastroenterol Hepatol. 2016 Sep 15. doi: 10.1016/j.cgh.2016.09.007).

ironstealth/Thinkstock

Source: American Gastroenterological Association

In his first address to a joint session of Congress, President Donald Trump promised “heroic veterans will get the care they so desperately need,” that he would eliminate the defense sequester, and called for “one of the largest increases in national defense spending in American history.”

“This looks like an increase in resources for us,” VA Secretary David Shulkin, MD, is reported to have told reporters early in the day at an American Legion meeting. “I'm confident this budget is going to reflect the President’s commitment to his ability to deliver on his promises to make veterans care better and stronger.” According to reports, the White House already has approved 37,000 exemptions from the federal hiring ban to help fill the VA’s  45,000 current job vacancies.

Reports also suggest that the military will receive an additional $54 billion in funding, a 10% increase. Details of where that extra money will go have not been released. The President’s military budget is less than the $640 billion budget proposed by Senator John McCain (R- AZ) and represents a 3% increase over the budget that had been projected by President Obama.

The overall impact on federal health care remains unclear. While President Trump held to his promise to repeal and replace the Affordable Care Act, to “invest in women’s health,” and to “give our state governors the resources and flexibility they need with Medicaid to make sure no one is left out,” there were few details of how those promises would be implemented and where the funding will come from.

In the address, the President outlined 4 necessary elements of an Affordable Care Act replacement:

1.  Americans with pre-existing conditions would have access to coverage, and a stable transition for health care exchanges enrollees;
2. The use of tax credits and savings accounts for purchasing private insurance;
3. Flexibility for states to expand Medicaid coverage; and
4. Legal reforms that “protect patients and doctors from unnecessary costs that drive up the price of insurance and work to bring down the artificially high price of drugs and bring them down immediately.”

The FDA also drew the President’s attention. Calling the approval process “slow and burdensome,” the President charged that the FDA “keeps too many advances… from reaching those in need.” The agency is still waiting on a nomination for its commissioner position, and it is unclear how it can speed up approval while under the federal hiring freeze.

Recognizing the devastation of opioid addiction, the President also promised to “stop the drugs from pouring into our country and poisoning our youth, and we will expand treatment for those who have become so badly addicted.” The President did not specify whether treatment resources would be exempt from the hiring freeze, incorporated into the Affordable Care Act, or handled in a different manner.

In his first address to a joint session of Congress, President Donald Trump promised “heroic veterans will get the care they so desperately need,” that he would eliminate the defense sequester, and called for “one of the largest increases in national defense spending in American history.”

“This looks like an increase in resources for us,” VA Secretary David Shulkin, MD, is reported to have told reporters early in the day at an American Legion meeting. “I'm confident this budget is going to reflect the President’s commitment to his ability to deliver on his promises to make veterans care better and stronger.” According to reports, the White House already has approved 37,000 exemptions from the federal hiring ban to help fill the VA’s  45,000 current job vacancies.

Reports also suggest that the military will receive an additional $54 billion in funding, a 10% increase. Details of where that extra money will go have not been released. The President’s military budget is less than the $640 billion budget proposed by Senator John McCain (R- AZ) and represents a 3% increase over the budget that had been projected by President Obama.

The overall impact on federal health care remains unclear. While President Trump held to his promise to repeal and replace the Affordable Care Act, to “invest in women’s health,” and to “give our state governors the resources and flexibility they need with Medicaid to make sure no one is left out,” there were few details of how those promises would be implemented and where the funding will come from.

In the address, the President outlined 4 necessary elements of an Affordable Care Act replacement:

1.  Americans with pre-existing conditions would have access to coverage, and a stable transition for health care exchanges enrollees;
2. The use of tax credits and savings accounts for purchasing private insurance;
3. Flexibility for states to expand Medicaid coverage; and
4. Legal reforms that “protect patients and doctors from unnecessary costs that drive up the price of insurance and work to bring down the artificially high price of drugs and bring them down immediately.”

The FDA also drew the President’s attention. Calling the approval process “slow and burdensome,” the President charged that the FDA “keeps too many advances… from reaching those in need.” The agency is still waiting on a nomination for its commissioner position, and it is unclear how it can speed up approval while under the federal hiring freeze.

Recognizing the devastation of opioid addiction, the President also promised to “stop the drugs from pouring into our country and poisoning our youth, and we will expand treatment for those who have become so badly addicted.” The President did not specify whether treatment resources would be exempt from the hiring freeze, incorporated into the Affordable Care Act, or handled in a different manner.

In his first address to a joint session of Congress, President Donald Trump promised “heroic veterans will get the care they so desperately need,” that he would eliminate the defense sequester, and called for “one of the largest increases in national defense spending in American history.”

“This looks like an increase in resources for us,” VA Secretary David Shulkin, MD, is reported to have told reporters early in the day at an American Legion meeting. “I'm confident this budget is going to reflect the President’s commitment to his ability to deliver on his promises to make veterans care better and stronger.” According to reports, the White House already has approved 37,000 exemptions from the federal hiring ban to help fill the VA’s  45,000 current job vacancies.

Reports also suggest that the military will receive an additional $54 billion in funding, a 10% increase. Details of where that extra money will go have not been released. The President’s military budget is less than the $640 billion budget proposed by Senator John McCain (R- AZ) and represents a 3% increase over the budget that had been projected by President Obama.

The overall impact on federal health care remains unclear. While President Trump held to his promise to repeal and replace the Affordable Care Act, to “invest in women’s health,” and to “give our state governors the resources and flexibility they need with Medicaid to make sure no one is left out,” there were few details of how those promises would be implemented and where the funding will come from.

In the address, the President outlined 4 necessary elements of an Affordable Care Act replacement:

1.  Americans with pre-existing conditions would have access to coverage, and a stable transition for health care exchanges enrollees;
2. The use of tax credits and savings accounts for purchasing private insurance;
3. Flexibility for states to expand Medicaid coverage; and
4. Legal reforms that “protect patients and doctors from unnecessary costs that drive up the price of insurance and work to bring down the artificially high price of drugs and bring them down immediately.”

The FDA also drew the President’s attention. Calling the approval process “slow and burdensome,” the President charged that the FDA “keeps too many advances… from reaching those in need.” The agency is still waiting on a nomination for its commissioner position, and it is unclear how it can speed up approval while under the federal hiring freeze.

Recognizing the devastation of opioid addiction, the President also promised to “stop the drugs from pouring into our country and poisoning our youth, and we will expand treatment for those who have become so badly addicted.” The President did not specify whether treatment resources would be exempt from the hiring freeze, incorporated into the Affordable Care Act, or handled in a different manner.

Editor’s Note: One of the goals of the new AJO is to offer solutions to common problems we face as orthopedists. With that in mind, this issue tackles the patellofemoral joint and represents a collaboration between our journal and some of the key leaders of the Patellofemoral Study Group. I’m indebted to my friend and mentor, Jack Farr, for organizing this issue and a continuing patellofemoral series. I know this series will provide an invaluable look into the thought process of true orthopedic legends and find a permanent place on your shelf of orthopedic reference materials.

I’m also pleased to introduce a new feature, our online Lifestyles section. Sometimes, as orthopedists, we spend so much time taking care of others that we forget to look after ourselves and our loved ones. In an effort to make this easier, AJO has collaborated with Inspirato, the premiere luxury destination club. As a member, I’ve enjoyed truly life-changing vacations with my family and now have a way to share that opportunity with our readers. Inspirato is offering a complimentary 6-month Key membership and $250 spending credit to all AJO readers. Simply visit www.inspirato.com/orthopedics to sign up and start booking your vacations like a member. Look for future lifestyle features and special opportunities online in upcoming issues.

—Bryan T. Hanypsiak, MD

The patellofemoral compartment of the knee has been an enigma for many years. Clinicians who enjoy treating patients with knee problems have the choice of either ignoring one-third of the knee or grappling with this unique compartment. In attempting to make sense of this area of the knee, it is necessary to take into account the vast and complex overlay of multiple factors affecting this compartment. These factors span the gamut from psycho-social, to “core to floor” physiologic imbalance, to overuse, to the seemingly more “objective” elements of alignment, stability, morphology, bone, and cartilage.

Fortunately, a small merry band of international experts has made the patellofemoral compartment its “badge of courage” and continues to attempt to make sense of this small mobile sesamoid bone. We have invited a few of these stalwarts to share their experience and wisdom with us in this first of an ongoing patellofemoral series in The American Journal of Orthopedics. I appreciate the honor of assembling the works of these worldly patellofemoral gurus.

How many of us routinely order a “Merchant view”, discuss a “Fulkerson osteotomy”, or tell patients they are out of their Scott Dye “envelope of function” and they need to allow their knee to return to homeostasis through a “core to floor” rehabilitation program? We are lucky to have these living legends offer us insight into their thinking process. I purposely have begun this patellofemoral series with some of my personal mentors to set the tone: think first, understand the problem, design an evidence-based medicine approach and, above all, do no harm. To that point, Dr. Merchant, Dr. Fulkerson, Dr. Dye, and Dr. Post each detail their approach to anterior knee pain, followed by a discussion on nonoperative therapy intervention by Dr. Hiemstra. However, I understand that most readers are surgeons and, therefore I have added two articles to pique your interest: the hot topic of medial patellofemoral ligament (MPFL)—“To repair or not to repair, that is NOT the question.” The question is: “When does repair potentially benefit the patient and when is reconstruction the best approach?” Dr. Duchman and Dr. Bollier address the former, and Dr. Burrus and colleagues discuss optimizing MPFL reconstruction. I hope you enjoy learning from these authors as much as I have while producing this issue.

Am J Orthop. 2017;46(2):64. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Editor’s Note: One of the goals of the new AJO is to offer solutions to common problems we face as orthopedists. With that in mind, this issue tackles the patellofemoral joint and represents a collaboration between our journal and some of the key leaders of the Patellofemoral Study Group. I’m indebted to my friend and mentor, Jack Farr, for organizing this issue and a continuing patellofemoral series. I know this series will provide an invaluable look into the thought process of true orthopedic legends and find a permanent place on your shelf of orthopedic reference materials.

I’m also pleased to introduce a new feature, our online Lifestyles section. Sometimes, as orthopedists, we spend so much time taking care of others that we forget to look after ourselves and our loved ones. In an effort to make this easier, AJO has collaborated with Inspirato, the premiere luxury destination club. As a member, I’ve enjoyed truly life-changing vacations with my family and now have a way to share that opportunity with our readers. Inspirato is offering a complimentary 6-month Key membership and $250 spending credit to all AJO readers. Simply visit www.inspirato.com/orthopedics to sign up and start booking your vacations like a member. Look for future lifestyle features and special opportunities online in upcoming issues.

—Bryan T. Hanypsiak, MD

The patellofemoral compartment of the knee has been an enigma for many years. Clinicians who enjoy treating patients with knee problems have the choice of either ignoring one-third of the knee or grappling with this unique compartment. In attempting to make sense of this area of the knee, it is necessary to take into account the vast and complex overlay of multiple factors affecting this compartment. These factors span the gamut from psycho-social, to “core to floor” physiologic imbalance, to overuse, to the seemingly more “objective” elements of alignment, stability, morphology, bone, and cartilage.

Fortunately, a small merry band of international experts has made the patellofemoral compartment its “badge of courage” and continues to attempt to make sense of this small mobile sesamoid bone. We have invited a few of these stalwarts to share their experience and wisdom with us in this first of an ongoing patellofemoral series in The American Journal of Orthopedics. I appreciate the honor of assembling the works of these worldly patellofemoral gurus.

How many of us routinely order a “Merchant view”, discuss a “Fulkerson osteotomy”, or tell patients they are out of their Scott Dye “envelope of function” and they need to allow their knee to return to homeostasis through a “core to floor” rehabilitation program? We are lucky to have these living legends offer us insight into their thinking process. I purposely have begun this patellofemoral series with some of my personal mentors to set the tone: think first, understand the problem, design an evidence-based medicine approach and, above all, do no harm. To that point, Dr. Merchant, Dr. Fulkerson, Dr. Dye, and Dr. Post each detail their approach to anterior knee pain, followed by a discussion on nonoperative therapy intervention by Dr. Hiemstra. However, I understand that most readers are surgeons and, therefore I have added two articles to pique your interest: the hot topic of medial patellofemoral ligament (MPFL)—“To repair or not to repair, that is NOT the question.” The question is: “When does repair potentially benefit the patient and when is reconstruction the best approach?” Dr. Duchman and Dr. Bollier address the former, and Dr. Burrus and colleagues discuss optimizing MPFL reconstruction. I hope you enjoy learning from these authors as much as I have while producing this issue.

Am J Orthop. 2017;46(2):64. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Editor’s Note: One of the goals of the new AJO is to offer solutions to common problems we face as orthopedists. With that in mind, this issue tackles the patellofemoral joint and represents a collaboration between our journal and some of the key leaders of the Patellofemoral Study Group. I’m indebted to my friend and mentor, Jack Farr, for organizing this issue and a continuing patellofemoral series. I know this series will provide an invaluable look into the thought process of true orthopedic legends and find a permanent place on your shelf of orthopedic reference materials.

I’m also pleased to introduce a new feature, our online Lifestyles section. Sometimes, as orthopedists, we spend so much time taking care of others that we forget to look after ourselves and our loved ones. In an effort to make this easier, AJO has collaborated with Inspirato, the premiere luxury destination club. As a member, I’ve enjoyed truly life-changing vacations with my family and now have a way to share that opportunity with our readers. Inspirato is offering a complimentary 6-month Key membership and $250 spending credit to all AJO readers. Simply visit www.inspirato.com/orthopedics to sign up and start booking your vacations like a member. Look for future lifestyle features and special opportunities online in upcoming issues.

—Bryan T. Hanypsiak, MD

The patellofemoral compartment of the knee has been an enigma for many years. Clinicians who enjoy treating patients with knee problems have the choice of either ignoring one-third of the knee or grappling with this unique compartment. In attempting to make sense of this area of the knee, it is necessary to take into account the vast and complex overlay of multiple factors affecting this compartment. These factors span the gamut from psycho-social, to “core to floor” physiologic imbalance, to overuse, to the seemingly more “objective” elements of alignment, stability, morphology, bone, and cartilage.

Fortunately, a small merry band of international experts has made the patellofemoral compartment its “badge of courage” and continues to attempt to make sense of this small mobile sesamoid bone. We have invited a few of these stalwarts to share their experience and wisdom with us in this first of an ongoing patellofemoral series in The American Journal of Orthopedics. I appreciate the honor of assembling the works of these worldly patellofemoral gurus.

How many of us routinely order a “Merchant view”, discuss a “Fulkerson osteotomy”, or tell patients they are out of their Scott Dye “envelope of function” and they need to allow their knee to return to homeostasis through a “core to floor” rehabilitation program? We are lucky to have these living legends offer us insight into their thinking process. I purposely have begun this patellofemoral series with some of my personal mentors to set the tone: think first, understand the problem, design an evidence-based medicine approach and, above all, do no harm. To that point, Dr. Merchant, Dr. Fulkerson, Dr. Dye, and Dr. Post each detail their approach to anterior knee pain, followed by a discussion on nonoperative therapy intervention by Dr. Hiemstra. However, I understand that most readers are surgeons and, therefore I have added two articles to pique your interest: the hot topic of medial patellofemoral ligament (MPFL)—“To repair or not to repair, that is NOT the question.” The question is: “When does repair potentially benefit the patient and when is reconstruction the best approach?” Dr. Duchman and Dr. Bollier address the former, and Dr. Burrus and colleagues discuss optimizing MPFL reconstruction. I hope you enjoy learning from these authors as much as I have while producing this issue.

Am J Orthop. 2017;46(2):64. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Patellofemoral disorders should be classified and diagnosed according to specific diagnostic categories (eg, lateral patellar compression syndrome) based on etiology rather than nondescriptive terminology (eg, internal derangement, patellofemoral pain syndrome).
• Patellofemoral dysplasia defines a spectrum of abnormalities ranging from the mild lateral patellar compression syndrome to the severe recurrent patellar dislocation.
• There is an inverse relationship between patient activity level and underlying patellofemoral dysplasia. This relationship determines threshold levels for each patient becoming symptomatic.
• Patients should be examined for 7 physical abnormalities, and if present, in what severity. These 7 are: vastus medialis obliquus deficiency, medial patellofemoral ligament laxity, lateral retinaculum tightness, increased quadriceps angle, hip abductor weakness, patella alta, and trochlear dysplasia.
• Advanced imaging is rarely, if ever, needed to make a diagnosis or to formulate an initial treatment plan for these common patellofemoral disorders.

To diagnose any disease or disorder implies an understanding of the condition’s cause(s), which should then lead to a logical treatment plan. For all too long, however, the diagnosis and treatment of patellofemoral disorders have been hampered by diagnoses that lack specific definitions based on etiology. A few of these are: internal derangement, chondromalacia patellae, patellar maltracking, and patellofemoral pain syndrome.

To simplify the diagnosis of patellofemoral disorders, we use a clinical classification based on etiology. This system’s defined diagnostic categories are useful in identifying probable cause(s), which can be appropriately evaluated and treated (Table).¹ In simple terms, the philosophy of this approach is to try to find out what’s wrong, and try to fix it!

This clinical classification provides a framework for common patellofemoral conditions that are more easily diagnosed, yet is intentionally incomplete omitting rare conditions (eg, tumors, metabolic bone disease, neurologic conditions).

Patellofemoral Dysplasia

Patellofemoral dysplasia (or extensor mechanism malfunction) is a cluster of physical abnormalities relating to the patellofemoral joint that vary from mild to severe and affect the normal function of that joint. As such, patellofemoral dysplasia itself should be considered on a continuum of mild to severe. To simplify the diagnosis, the clinician should systematically identify these factors and their severity. Armed with this information, the clinician can make the diagnosis and formulate a logical treatment plan for each individual patient.

This article focuses on 7 physical abnormalities that are most likely developmental and that can be identified through physical and radiologic examination. When and how each patient with patellofemoral dysplasia becomes symptomatic are determined by 2 key factors: patellofemoral dysplasia severity and activity level (sedentary to strenuous), in an inverse relationship (Figure 1).²

Seven Key Patellofemoral Physical Abnormalities

Of the 7 commonly identified physical abnormalities that affect the normal functioning of the patellofemoral joint, 5 are discovered by physical examination and 2 by radiography; CT and MRI are seldom needed in the initial evaluation. The most accurate and objective method should be used to assess the presence and severity of each abnormality.

The 7 abnormalities are vastus medialis obliquus (VMO) deficiency, medial patellofemoral ligament (MPFL) laxity, lateral retinaculum (LR) tightness, increased quadriceps (Q) angle, hip abductor weakness, patella alta, and trochlear dysplasia. We list these not in order of importance but in the order in which they are usually encountered during initial evaluation. We advocate for examining both knees including axial patellofemoral radiographs because patellofemoral disorders are frequently bilateral. It is helpful to use an abnormality checklist so none are forgotten. Also useful is a simple shorthand for findings: 0 = normal (no abnormality), 1 = mild abnormality, 2 = moderate abnormality, 3 = severe abnormality, with the right knee always recorded first (R/L). For example, severe left MPFL laxity is recorded as 0/3. Numerical values (eg, Q angles) can be directly recorded in this manner: 14°/23°.

1. Vastus Medialis Obliquus Deficiency

VMO deficiency is best seen as the sitting patient actively maintains the unsupported foot and leg at 30° knee flexion. Normally, the VMO inserts into the upper half or third of the medial edge of the patella; a deficient VMO inserts higher into the medial edge of the quadriceps tendon, or it is absent and leaves a characteristic hollow at the medial edge of the patella (Figure 2).⁴

2. Medial Patellofemoral Ligament Laxity

MPFL laxity is assessed with the lateral glide test. Again, the patient sits, but with quadriceps relaxed and foot and leg supported at 30° knee flexion. With the clinician mentally dividing the patella into vertical quadrants and pushing the patella laterally, the normal patella moves about 1 quadrant or 1 fingerbreadth. Severe MPFL laxity often elicits a positive apprehension response during the test. (Tip: Many patients are unable to relax the quadriceps while sitting; therefore, examine them supine and lift the knee into 30° flexion.) Such laxity usually means the MPFL was torn in a previous dislocation and remains elongated, leaving the patella vulnerable to repeated dislocations. The clinician should be alert to the possibility of hyperelastosis (Ehlers-Danlos syndrome) and a hyper-mobile patella. The opposite limb should be evaluated for asymmetric laxity.

3. Lateral Retinaculum Tightness

LR tightness is assessed with the medial glide test, again with the quadriceps relaxed and the knee supported at 30° flexion. With a normal LR, the patella can be pushed medially about 1 quadrant or 1 fingerbreadth. Some clinicians prefer the lateral tilt-up test, in which the lateral edge of the patella is lifted up, but this method is more difficult to quantify, is affected by the cross-sectional shape of the patella, and lacks consistency.

4. Increased Quadriceps Angle

The Q angle is one of the most important factors in the normal functioning of the patellofemoral joint. For more than a century,⁸ multiple operations have been used successfully to move the tibial tubercle (TT) and patellar ligament from a lateral position to a medial position thereby decreasing the Q angle. It is only logical to measure this angle at every knee examination to check for an abnormal increase, and the degree. The term quadriceps angle, or Q angle, was first used in 1964 by Brattström,⁷ who defined it as the “supplemental angle” to the valgus angle formed by the “quadriceps’ resultant” (line of force or vector) “+ patella + ligamentum patellae”. This might be called the dynamic Q angle. With there being no clinical method of measuring the “quadriceps line of force”, or quadriceps vector, clinicians used a line from the anterior superior iliac spine to the center of the patella, yet still called it the Q angle. By convention, this anatomical Q angle has been accepted as the Q angle.

Because the Q angle is the only clinical measurement of TT lateralization at initial evaluation, its measurement should be standardized, accurate, and simple to perform. Placing the patient supine with the lower limb in neutral rotation (patella anterior) and the knee in full extension standardizes the position. In full extension, the tibia reaches its maximum external rotation owing to the terminal “screw home” mechanism. The clinician should center the patella to the trochlear groove (TG) while measuring the Q angle, as it is the relationship of the TT to the trochlea, not to the patella, that is important. If LR tightness prevents the patella from centering, that fact should be recorded during the medial glide test for LR tightness.

5. Hip Abductor Weakness

The step-down test is easily performed in the office by having the patient stand on a short stool or stair and then slowly step down with the opposite limb to just touch the heel and slowly arise again. A positive test is indicated by the Trendelenburg sign, with the pelvis dropping down and away from the symptomatic supporting limb, the flexing knee collapsing into valgus, and the patient tending to wobble and lack stability (Figure 4).¹⁶

6. Patella Alta

Patella alta not only allows the patella to escape the confines of the trochlea earlier during active knee extension increasing the risk of patellar dislocation, but also decreases the contact footprint with the trochlea, increasing the patellofemoral joint reaction force and potentially causing patellofemoral pain and even secondary chondrosis. The simplest way to assess patellar height is with a lateral radiograph of the knee. The 3 popular methods (Insall-Salvati, Caton-Deschamps, Blackburn-Peel) all put the normal patellar height ratio at approximately 1:1, ± 20%. Berg and colleagues¹⁸ compared radiologic techniques for measuring patellar height ratio and found that Blackburn-Peel was the most accurate, reliable, and reproducible method.

7. Trochlear Dysplasia

Trochlear dysplasia, most simply a flattening of the TG, is perhaps the most important factor effecting normal patellofemoral function. However, it remains the most difficult to correctly address surgically. Senavongse and Amis¹⁹ conducted a cadaveric study demonstrating the prime importance of the TG. They found patellar stability was reduced 30% by releasing the VMO, 49% by cutting the MPFL in full knee extension, and 70% by flattening the trochlea. The most common, successful operations for correcting patellar instability depend on changing other factors that guide patellar excursion to compensate for this trochlear flattening.

The simplest way to assess trochlear dysplasia is to measure the sulcus angle on an accurate axial view radiograph of the knee at 45° flexion (Merchant view).²⁰ Dejour and colleagues²¹ popularized a technique of assessing and classifying trochlear dysplasia from a true lateral radiograph of the knee, which has the advantage of showing the trochlear at its proximal extent. Davies and colleagues²² evaluated the Dejour technique, along with patellar tilt, patellar height, and sulcus angle, to identify a rapid and reproducible radiologic feature that would indicate the need for further analysis by other imaging studies (eg, CT, MRI). They found that, if the sulcus angle was normal, analysis of other radiologic features was unlikely to reveal additional useful information. They also showed a correlation of increasing sulcus angle and severity of those other dysplasia features. Merchant and colleagues²⁰ found a mean normal sulcus angle of 138º (SD, 6º; range, 126º-150º), and Aglietti and colleagues²³ confirmed those findings with nearly identical values (mean, 137º; SD, 6º; range, 116º-151º).

Diagnosis and Initial Treatment Plan

Patellofemoral disorders generally are divided into patellofemoral pain and instability, but these 2 diagnostic categories are too broad to be useful. Patellofemoral pain is a symptom. Patellofemoral pain syndrome should never be used as a diagnosis because there is no accepted definition for the cluster of findings that customarily defines a syndrome. At initial evaluation, after the easily diagnosed causes of anterior knee pain (eg, prepatellar bursitis, TT apophysitis, patellar and quadriceps tendinitis) have been ruled out, the clinician should consider types of patellofemoral dysplasia for a presumptive diagnosis, which will then lead to a logical treatment program for each identified disorder. With a presumptive diagnosis established, almost all patients suffering from chronic anterior knee pain without history of injury are treated initially with rest, ice, and nonsteroidal anti-inflammatory drugs to restore joint homeostasis.³

Lateral Patellar Compression Syndrome

In 1975, Ficat and colleagues²⁴ described features of what they called syndrome d’hyperpression externe de la rotule. Two years later, Ficat and Hungerford²⁵ defined the syndrome as one “in which the patella is well centered in the trochlear sulcus and stable, but in which there is a functional lateralization onto a physiologically and often anatomically predominant lateral facet.” Using the tools we have described here, the clinician usually finds the cause(s) of this “functional lateralization.” Four abnormalities—VMO deficiency, LR tightness, increased standardized Q angle, and hip abductor weakness—can cause functional lateralization either alone when severe or in combination when mild or moderate.

For a presumptive diagnosis of LPCS, initial treatment is nonoperative, and successful in about 90% of patients. It should be obvious that most patients with chronic anterior knee pain have quadriceps atrophy. Physical therapy should be specifically focused on quadriceps strengthening, with absolutely no stress placed on the patellofemoral joint in flexion initially, and on hip abductor strengthening. Progressive resistive isometric quadriceps exercises can be performed with a weight-bench technique (Figures 5A-5D).²⁶

Chronic Subluxation of Patella

With the use of axial patellofemoral radiographs (Merchant views),²⁰ the clinician can determine if the “patella is well centered in the trochlear sulcus and stable” (an important part of the definition of LPCS). If the patient has no symptoms of recurrent instability or patellar dislocation, and these radiographs show a laterally subluxed patella (one not well centered in the trochlea), the diagnosis is most likely CSP, a moderate form of patellofemoral dysplasia (section II of the Table). In addition to the 4 abnormalities used in the diagnosis of LPCS (mentioned earlier), trochlear dysplasia also comes into play in the diagnosis of CSP. Just as the other abnormalities can vary from mild to severe, trochlear dysplasia can vary from mild (slightly shallow sulcus angle) to severe (flat or even convex sulcus angle). As the sulcus becomes shallower, the patella slides more laterally, increasing the likelihood of patellar dislocation.

As the patient with CSP gives no history of episodic patellar instability, treatment for CSP is almost identical to that for LPCS, with the primary focus on isometric quadriceps strengthening (DeHaven isometric exercises)²⁷ and hip abductor muscle strengthening. In the presence of CSP radiographically, it is important to use McConnell taping and/or patellar bracing during muscular strengthening. A patient who achieves 20-lb isometric quadriceps strength, demonstrates a normal step-down test, and is assumed to be asymptomatic can be allowed to return to sports activities with use of a patellar brace. The patient should be counseled that there is an increased risk for patellar dislocation because of this chronic subluxation and the shallower sulcus.

As in LPCS, CSP symptoms that persist after dynamic strength is regained may require surgical intervention. The severity of identified abnormal factors (tight LR, increased Q angle, trochlear dysplasia) guides the surgeon in selecting appropriate corrective technique(s).

Recurrent Dislocation of Patella

Admittedly, given the number and subtlety of abnormal factors, the diagnosis of LPCS as a cause of patellofemoral pain can be challenging. However, RDP is at the opposite end of the spectrum. A history of prior patellar dislocation(s) almost always makes the diagnosis of RDP easier. The patient occasionally complains of a recurrent symptom, the knee “going out” or “giving way,” indicating that the diagnosis might be RDP. By carefully asking what the patient was doing and what happened when the knee “went out”, the clinician may be able to determine if the injury stemmed from sudden patellar pain causing reflex inhibition of the quadriceps or was a true dislocation. Both may be described as “going out” or “giving way”.

Assessment for the same 7 abnormalities helps establish the diagnosis, a logical treatment plan, and a guide for indicated surgery. The diagnostic focus is MPFL laxity and trochlear dysplasia. Prior lateral dislocation of the patella almost always requires rupture of the normal MPFL. The infrequent exception is a patient with hyper-elasticity of the skin and multiple joints (Ehlers-Danlos syndrome). Trochlear dysplasia is a significant risk factor for patellar dislocation. If the trochlea is normal and there is no MPFL laxity, the diagnosis of RDP should be questioned.

If surgery is indicated, the surgeon uses a list of the patient’s abnormalities and their severity as a guide in selecting reconstructive techniques. The more abnormalities found and the greater the severity of each, the more techniques are needed to achieve success. Preoperative exercises help speed postoperative recovery by addressing quadriceps and hip abductor weakness. In addition, an active exercise program gives the surgeon insight into the patient’s desire for and commitment to recovery. Other physical abnormalities to be considered in preoperative planning include MPFL laxity, LR tightness, increased Q angle, patella alta, and trochlear dysplasia.

Surgical tips: 1. When releasing the LR, never cut the vastus lateralis tendon, as this has a high likelihood of causing iatrogenic medial patellar subluxation.²⁹ 2. When medializing the TT, consider compensating for a shallow trochlea by “over-correcting” the Q angle to 5° to 10° measured with a surgical goniometer intraoperatively.

Summary

Basing clinical classification of disorders on etiology is a simple and effective way to diagnose common patellofemoral conditions. Identifying and rating the severity of patellofemoral dysplasia, using 7 commonly found physical abnormalities, guide the physician to a proper diagnosis and down logical treatment pathways. These principles should be incorporated into the routine evaluation of patellofemoral disorders to optimize diagnosis, formulate a treatment plan, and improve patient outcomes. After all, this is what our patients are asking us to do: Try to find what’s wrong, and then try to fix it!

Am J Orthop. 2017;46(2):68-75. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Patellofemoral disorders should be classified and diagnosed according to specific diagnostic categories (eg, lateral patellar compression syndrome) based on etiology rather than nondescriptive terminology (eg, internal derangement, patellofemoral pain syndrome).
• Patellofemoral dysplasia defines a spectrum of abnormalities ranging from the mild lateral patellar compression syndrome to the severe recurrent patellar dislocation.
• There is an inverse relationship between patient activity level and underlying patellofemoral dysplasia. This relationship determines threshold levels for each patient becoming symptomatic.
• Patients should be examined for 7 physical abnormalities, and if present, in what severity. These 7 are: vastus medialis obliquus deficiency, medial patellofemoral ligament laxity, lateral retinaculum tightness, increased quadriceps angle, hip abductor weakness, patella alta, and trochlear dysplasia.
• Advanced imaging is rarely, if ever, needed to make a diagnosis or to formulate an initial treatment plan for these common patellofemoral disorders.

To diagnose any disease or disorder implies an understanding of the condition’s cause(s), which should then lead to a logical treatment plan. For all too long, however, the diagnosis and treatment of patellofemoral disorders have been hampered by diagnoses that lack specific definitions based on etiology. A few of these are: internal derangement, chondromalacia patellae, patellar maltracking, and patellofemoral pain syndrome.

To simplify the diagnosis of patellofemoral disorders, we use a clinical classification based on etiology. This system’s defined diagnostic categories are useful in identifying probable cause(s), which can be appropriately evaluated and treated (Table).¹ In simple terms, the philosophy of this approach is to try to find out what’s wrong, and try to fix it!

This clinical classification provides a framework for common patellofemoral conditions that are more easily diagnosed, yet is intentionally incomplete omitting rare conditions (eg, tumors, metabolic bone disease, neurologic conditions).

Patellofemoral Dysplasia

Patellofemoral dysplasia (or extensor mechanism malfunction) is a cluster of physical abnormalities relating to the patellofemoral joint that vary from mild to severe and affect the normal function of that joint. As such, patellofemoral dysplasia itself should be considered on a continuum of mild to severe. To simplify the diagnosis, the clinician should systematically identify these factors and their severity. Armed with this information, the clinician can make the diagnosis and formulate a logical treatment plan for each individual patient.

This article focuses on 7 physical abnormalities that are most likely developmental and that can be identified through physical and radiologic examination. When and how each patient with patellofemoral dysplasia becomes symptomatic are determined by 2 key factors: patellofemoral dysplasia severity and activity level (sedentary to strenuous), in an inverse relationship (Figure 1).²

Seven Key Patellofemoral Physical Abnormalities

Of the 7 commonly identified physical abnormalities that affect the normal functioning of the patellofemoral joint, 5 are discovered by physical examination and 2 by radiography; CT and MRI are seldom needed in the initial evaluation. The most accurate and objective method should be used to assess the presence and severity of each abnormality.

The 7 abnormalities are vastus medialis obliquus (VMO) deficiency, medial patellofemoral ligament (MPFL) laxity, lateral retinaculum (LR) tightness, increased quadriceps (Q) angle, hip abductor weakness, patella alta, and trochlear dysplasia. We list these not in order of importance but in the order in which they are usually encountered during initial evaluation. We advocate for examining both knees including axial patellofemoral radiographs because patellofemoral disorders are frequently bilateral. It is helpful to use an abnormality checklist so none are forgotten. Also useful is a simple shorthand for findings: 0 = normal (no abnormality), 1 = mild abnormality, 2 = moderate abnormality, 3 = severe abnormality, with the right knee always recorded first (R/L). For example, severe left MPFL laxity is recorded as 0/3. Numerical values (eg, Q angles) can be directly recorded in this manner: 14°/23°.

1. Vastus Medialis Obliquus Deficiency

VMO deficiency is best seen as the sitting patient actively maintains the unsupported foot and leg at 30° knee flexion. Normally, the VMO inserts into the upper half or third of the medial edge of the patella; a deficient VMO inserts higher into the medial edge of the quadriceps tendon, or it is absent and leaves a characteristic hollow at the medial edge of the patella (Figure 2).⁴

2. Medial Patellofemoral Ligament Laxity

MPFL laxity is assessed with the lateral glide test. Again, the patient sits, but with quadriceps relaxed and foot and leg supported at 30° knee flexion. With the clinician mentally dividing the patella into vertical quadrants and pushing the patella laterally, the normal patella moves about 1 quadrant or 1 fingerbreadth. Severe MPFL laxity often elicits a positive apprehension response during the test. (Tip: Many patients are unable to relax the quadriceps while sitting; therefore, examine them supine and lift the knee into 30° flexion.) Such laxity usually means the MPFL was torn in a previous dislocation and remains elongated, leaving the patella vulnerable to repeated dislocations. The clinician should be alert to the possibility of hyperelastosis (Ehlers-Danlos syndrome) and a hyper-mobile patella. The opposite limb should be evaluated for asymmetric laxity.

3. Lateral Retinaculum Tightness

LR tightness is assessed with the medial glide test, again with the quadriceps relaxed and the knee supported at 30° flexion. With a normal LR, the patella can be pushed medially about 1 quadrant or 1 fingerbreadth. Some clinicians prefer the lateral tilt-up test, in which the lateral edge of the patella is lifted up, but this method is more difficult to quantify, is affected by the cross-sectional shape of the patella, and lacks consistency.

4. Increased Quadriceps Angle

The Q angle is one of the most important factors in the normal functioning of the patellofemoral joint. For more than a century,⁸ multiple operations have been used successfully to move the tibial tubercle (TT) and patellar ligament from a lateral position to a medial position thereby decreasing the Q angle. It is only logical to measure this angle at every knee examination to check for an abnormal increase, and the degree. The term quadriceps angle, or Q angle, was first used in 1964 by Brattström,⁷ who defined it as the “supplemental angle” to the valgus angle formed by the “quadriceps’ resultant” (line of force or vector) “+ patella + ligamentum patellae”. This might be called the dynamic Q angle. With there being no clinical method of measuring the “quadriceps line of force”, or quadriceps vector, clinicians used a line from the anterior superior iliac spine to the center of the patella, yet still called it the Q angle. By convention, this anatomical Q angle has been accepted as the Q angle.

Because the Q angle is the only clinical measurement of TT lateralization at initial evaluation, its measurement should be standardized, accurate, and simple to perform. Placing the patient supine with the lower limb in neutral rotation (patella anterior) and the knee in full extension standardizes the position. In full extension, the tibia reaches its maximum external rotation owing to the terminal “screw home” mechanism. The clinician should center the patella to the trochlear groove (TG) while measuring the Q angle, as it is the relationship of the TT to the trochlea, not to the patella, that is important. If LR tightness prevents the patella from centering, that fact should be recorded during the medial glide test for LR tightness.

5. Hip Abductor Weakness

The step-down test is easily performed in the office by having the patient stand on a short stool or stair and then slowly step down with the opposite limb to just touch the heel and slowly arise again. A positive test is indicated by the Trendelenburg sign, with the pelvis dropping down and away from the symptomatic supporting limb, the flexing knee collapsing into valgus, and the patient tending to wobble and lack stability (Figure 4).¹⁶

6. Patella Alta

Patella alta not only allows the patella to escape the confines of the trochlea earlier during active knee extension increasing the risk of patellar dislocation, but also decreases the contact footprint with the trochlea, increasing the patellofemoral joint reaction force and potentially causing patellofemoral pain and even secondary chondrosis. The simplest way to assess patellar height is with a lateral radiograph of the knee. The 3 popular methods (Insall-Salvati, Caton-Deschamps, Blackburn-Peel) all put the normal patellar height ratio at approximately 1:1, ± 20%. Berg and colleagues¹⁸ compared radiologic techniques for measuring patellar height ratio and found that Blackburn-Peel was the most accurate, reliable, and reproducible method.

7. Trochlear Dysplasia

Trochlear dysplasia, most simply a flattening of the TG, is perhaps the most important factor effecting normal patellofemoral function. However, it remains the most difficult to correctly address surgically. Senavongse and Amis¹⁹ conducted a cadaveric study demonstrating the prime importance of the TG. They found patellar stability was reduced 30% by releasing the VMO, 49% by cutting the MPFL in full knee extension, and 70% by flattening the trochlea. The most common, successful operations for correcting patellar instability depend on changing other factors that guide patellar excursion to compensate for this trochlear flattening.

The simplest way to assess trochlear dysplasia is to measure the sulcus angle on an accurate axial view radiograph of the knee at 45° flexion (Merchant view).²⁰ Dejour and colleagues²¹ popularized a technique of assessing and classifying trochlear dysplasia from a true lateral radiograph of the knee, which has the advantage of showing the trochlear at its proximal extent. Davies and colleagues²² evaluated the Dejour technique, along with patellar tilt, patellar height, and sulcus angle, to identify a rapid and reproducible radiologic feature that would indicate the need for further analysis by other imaging studies (eg, CT, MRI). They found that, if the sulcus angle was normal, analysis of other radiologic features was unlikely to reveal additional useful information. They also showed a correlation of increasing sulcus angle and severity of those other dysplasia features. Merchant and colleagues²⁰ found a mean normal sulcus angle of 138º (SD, 6º; range, 126º-150º), and Aglietti and colleagues²³ confirmed those findings with nearly identical values (mean, 137º; SD, 6º; range, 116º-151º).

Diagnosis and Initial Treatment Plan

Patellofemoral disorders generally are divided into patellofemoral pain and instability, but these 2 diagnostic categories are too broad to be useful. Patellofemoral pain is a symptom. Patellofemoral pain syndrome should never be used as a diagnosis because there is no accepted definition for the cluster of findings that customarily defines a syndrome. At initial evaluation, after the easily diagnosed causes of anterior knee pain (eg, prepatellar bursitis, TT apophysitis, patellar and quadriceps tendinitis) have been ruled out, the clinician should consider types of patellofemoral dysplasia for a presumptive diagnosis, which will then lead to a logical treatment program for each identified disorder. With a presumptive diagnosis established, almost all patients suffering from chronic anterior knee pain without history of injury are treated initially with rest, ice, and nonsteroidal anti-inflammatory drugs to restore joint homeostasis.³

Lateral Patellar Compression Syndrome

In 1975, Ficat and colleagues²⁴ described features of what they called syndrome d’hyperpression externe de la rotule. Two years later, Ficat and Hungerford²⁵ defined the syndrome as one “in which the patella is well centered in the trochlear sulcus and stable, but in which there is a functional lateralization onto a physiologically and often anatomically predominant lateral facet.” Using the tools we have described here, the clinician usually finds the cause(s) of this “functional lateralization.” Four abnormalities—VMO deficiency, LR tightness, increased standardized Q angle, and hip abductor weakness—can cause functional lateralization either alone when severe or in combination when mild or moderate.

For a presumptive diagnosis of LPCS, initial treatment is nonoperative, and successful in about 90% of patients. It should be obvious that most patients with chronic anterior knee pain have quadriceps atrophy. Physical therapy should be specifically focused on quadriceps strengthening, with absolutely no stress placed on the patellofemoral joint in flexion initially, and on hip abductor strengthening. Progressive resistive isometric quadriceps exercises can be performed with a weight-bench technique (Figures 5A-5D).²⁶

Chronic Subluxation of Patella

With the use of axial patellofemoral radiographs (Merchant views),²⁰ the clinician can determine if the “patella is well centered in the trochlear sulcus and stable” (an important part of the definition of LPCS). If the patient has no symptoms of recurrent instability or patellar dislocation, and these radiographs show a laterally subluxed patella (one not well centered in the trochlea), the diagnosis is most likely CSP, a moderate form of patellofemoral dysplasia (section II of the Table). In addition to the 4 abnormalities used in the diagnosis of LPCS (mentioned earlier), trochlear dysplasia also comes into play in the diagnosis of CSP. Just as the other abnormalities can vary from mild to severe, trochlear dysplasia can vary from mild (slightly shallow sulcus angle) to severe (flat or even convex sulcus angle). As the sulcus becomes shallower, the patella slides more laterally, increasing the likelihood of patellar dislocation.

As the patient with CSP gives no history of episodic patellar instability, treatment for CSP is almost identical to that for LPCS, with the primary focus on isometric quadriceps strengthening (DeHaven isometric exercises)²⁷ and hip abductor muscle strengthening. In the presence of CSP radiographically, it is important to use McConnell taping and/or patellar bracing during muscular strengthening. A patient who achieves 20-lb isometric quadriceps strength, demonstrates a normal step-down test, and is assumed to be asymptomatic can be allowed to return to sports activities with use of a patellar brace. The patient should be counseled that there is an increased risk for patellar dislocation because of this chronic subluxation and the shallower sulcus.

As in LPCS, CSP symptoms that persist after dynamic strength is regained may require surgical intervention. The severity of identified abnormal factors (tight LR, increased Q angle, trochlear dysplasia) guides the surgeon in selecting appropriate corrective technique(s).

Recurrent Dislocation of Patella

Admittedly, given the number and subtlety of abnormal factors, the diagnosis of LPCS as a cause of patellofemoral pain can be challenging. However, RDP is at the opposite end of the spectrum. A history of prior patellar dislocation(s) almost always makes the diagnosis of RDP easier. The patient occasionally complains of a recurrent symptom, the knee “going out” or “giving way,” indicating that the diagnosis might be RDP. By carefully asking what the patient was doing and what happened when the knee “went out”, the clinician may be able to determine if the injury stemmed from sudden patellar pain causing reflex inhibition of the quadriceps or was a true dislocation. Both may be described as “going out” or “giving way”.

Assessment for the same 7 abnormalities helps establish the diagnosis, a logical treatment plan, and a guide for indicated surgery. The diagnostic focus is MPFL laxity and trochlear dysplasia. Prior lateral dislocation of the patella almost always requires rupture of the normal MPFL. The infrequent exception is a patient with hyper-elasticity of the skin and multiple joints (Ehlers-Danlos syndrome). Trochlear dysplasia is a significant risk factor for patellar dislocation. If the trochlea is normal and there is no MPFL laxity, the diagnosis of RDP should be questioned.

If surgery is indicated, the surgeon uses a list of the patient’s abnormalities and their severity as a guide in selecting reconstructive techniques. The more abnormalities found and the greater the severity of each, the more techniques are needed to achieve success. Preoperative exercises help speed postoperative recovery by addressing quadriceps and hip abductor weakness. In addition, an active exercise program gives the surgeon insight into the patient’s desire for and commitment to recovery. Other physical abnormalities to be considered in preoperative planning include MPFL laxity, LR tightness, increased Q angle, patella alta, and trochlear dysplasia.

Surgical tips: 1. When releasing the LR, never cut the vastus lateralis tendon, as this has a high likelihood of causing iatrogenic medial patellar subluxation.²⁹ 2. When medializing the TT, consider compensating for a shallow trochlea by “over-correcting” the Q angle to 5° to 10° measured with a surgical goniometer intraoperatively.

Summary

Basing clinical classification of disorders on etiology is a simple and effective way to diagnose common patellofemoral conditions. Identifying and rating the severity of patellofemoral dysplasia, using 7 commonly found physical abnormalities, guide the physician to a proper diagnosis and down logical treatment pathways. These principles should be incorporated into the routine evaluation of patellofemoral disorders to optimize diagnosis, formulate a treatment plan, and improve patient outcomes. After all, this is what our patients are asking us to do: Try to find what’s wrong, and then try to fix it!

Am J Orthop. 2017;46(2):68-75. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Patellofemoral disorders should be classified and diagnosed according to specific diagnostic categories (eg, lateral patellar compression syndrome) based on etiology rather than nondescriptive terminology (eg, internal derangement, patellofemoral pain syndrome).
• Patellofemoral dysplasia defines a spectrum of abnormalities ranging from the mild lateral patellar compression syndrome to the severe recurrent patellar dislocation.
• There is an inverse relationship between patient activity level and underlying patellofemoral dysplasia. This relationship determines threshold levels for each patient becoming symptomatic.
• Patients should be examined for 7 physical abnormalities, and if present, in what severity. These 7 are: vastus medialis obliquus deficiency, medial patellofemoral ligament laxity, lateral retinaculum tightness, increased quadriceps angle, hip abductor weakness, patella alta, and trochlear dysplasia.
• Advanced imaging is rarely, if ever, needed to make a diagnosis or to formulate an initial treatment plan for these common patellofemoral disorders.

To diagnose any disease or disorder implies an understanding of the condition’s cause(s), which should then lead to a logical treatment plan. For all too long, however, the diagnosis and treatment of patellofemoral disorders have been hampered by diagnoses that lack specific definitions based on etiology. A few of these are: internal derangement, chondromalacia patellae, patellar maltracking, and patellofemoral pain syndrome.

To simplify the diagnosis of patellofemoral disorders, we use a clinical classification based on etiology. This system’s defined diagnostic categories are useful in identifying probable cause(s), which can be appropriately evaluated and treated (Table).¹ In simple terms, the philosophy of this approach is to try to find out what’s wrong, and try to fix it!

This clinical classification provides a framework for common patellofemoral conditions that are more easily diagnosed, yet is intentionally incomplete omitting rare conditions (eg, tumors, metabolic bone disease, neurologic conditions).

Patellofemoral Dysplasia

Patellofemoral dysplasia (or extensor mechanism malfunction) is a cluster of physical abnormalities relating to the patellofemoral joint that vary from mild to severe and affect the normal function of that joint. As such, patellofemoral dysplasia itself should be considered on a continuum of mild to severe. To simplify the diagnosis, the clinician should systematically identify these factors and their severity. Armed with this information, the clinician can make the diagnosis and formulate a logical treatment plan for each individual patient.

This article focuses on 7 physical abnormalities that are most likely developmental and that can be identified through physical and radiologic examination. When and how each patient with patellofemoral dysplasia becomes symptomatic are determined by 2 key factors: patellofemoral dysplasia severity and activity level (sedentary to strenuous), in an inverse relationship (Figure 1).²

Seven Key Patellofemoral Physical Abnormalities

Of the 7 commonly identified physical abnormalities that affect the normal functioning of the patellofemoral joint, 5 are discovered by physical examination and 2 by radiography; CT and MRI are seldom needed in the initial evaluation. The most accurate and objective method should be used to assess the presence and severity of each abnormality.

The 7 abnormalities are vastus medialis obliquus (VMO) deficiency, medial patellofemoral ligament (MPFL) laxity, lateral retinaculum (LR) tightness, increased quadriceps (Q) angle, hip abductor weakness, patella alta, and trochlear dysplasia. We list these not in order of importance but in the order in which they are usually encountered during initial evaluation. We advocate for examining both knees including axial patellofemoral radiographs because patellofemoral disorders are frequently bilateral. It is helpful to use an abnormality checklist so none are forgotten. Also useful is a simple shorthand for findings: 0 = normal (no abnormality), 1 = mild abnormality, 2 = moderate abnormality, 3 = severe abnormality, with the right knee always recorded first (R/L). For example, severe left MPFL laxity is recorded as 0/3. Numerical values (eg, Q angles) can be directly recorded in this manner: 14°/23°.

1. Vastus Medialis Obliquus Deficiency

VMO deficiency is best seen as the sitting patient actively maintains the unsupported foot and leg at 30° knee flexion. Normally, the VMO inserts into the upper half or third of the medial edge of the patella; a deficient VMO inserts higher into the medial edge of the quadriceps tendon, or it is absent and leaves a characteristic hollow at the medial edge of the patella (Figure 2).⁴

2. Medial Patellofemoral Ligament Laxity

MPFL laxity is assessed with the lateral glide test. Again, the patient sits, but with quadriceps relaxed and foot and leg supported at 30° knee flexion. With the clinician mentally dividing the patella into vertical quadrants and pushing the patella laterally, the normal patella moves about 1 quadrant or 1 fingerbreadth. Severe MPFL laxity often elicits a positive apprehension response during the test. (Tip: Many patients are unable to relax the quadriceps while sitting; therefore, examine them supine and lift the knee into 30° flexion.) Such laxity usually means the MPFL was torn in a previous dislocation and remains elongated, leaving the patella vulnerable to repeated dislocations. The clinician should be alert to the possibility of hyperelastosis (Ehlers-Danlos syndrome) and a hyper-mobile patella. The opposite limb should be evaluated for asymmetric laxity.

3. Lateral Retinaculum Tightness

LR tightness is assessed with the medial glide test, again with the quadriceps relaxed and the knee supported at 30° flexion. With a normal LR, the patella can be pushed medially about 1 quadrant or 1 fingerbreadth. Some clinicians prefer the lateral tilt-up test, in which the lateral edge of the patella is lifted up, but this method is more difficult to quantify, is affected by the cross-sectional shape of the patella, and lacks consistency.

4. Increased Quadriceps Angle

The Q angle is one of the most important factors in the normal functioning of the patellofemoral joint. For more than a century,⁸ multiple operations have been used successfully to move the tibial tubercle (TT) and patellar ligament from a lateral position to a medial position thereby decreasing the Q angle. It is only logical to measure this angle at every knee examination to check for an abnormal increase, and the degree. The term quadriceps angle, or Q angle, was first used in 1964 by Brattström,⁷ who defined it as the “supplemental angle” to the valgus angle formed by the “quadriceps’ resultant” (line of force or vector) “+ patella + ligamentum patellae”. This might be called the dynamic Q angle. With there being no clinical method of measuring the “quadriceps line of force”, or quadriceps vector, clinicians used a line from the anterior superior iliac spine to the center of the patella, yet still called it the Q angle. By convention, this anatomical Q angle has been accepted as the Q angle.

Because the Q angle is the only clinical measurement of TT lateralization at initial evaluation, its measurement should be standardized, accurate, and simple to perform. Placing the patient supine with the lower limb in neutral rotation (patella anterior) and the knee in full extension standardizes the position. In full extension, the tibia reaches its maximum external rotation owing to the terminal “screw home” mechanism. The clinician should center the patella to the trochlear groove (TG) while measuring the Q angle, as it is the relationship of the TT to the trochlea, not to the patella, that is important. If LR tightness prevents the patella from centering, that fact should be recorded during the medial glide test for LR tightness.

5. Hip Abductor Weakness

The step-down test is easily performed in the office by having the patient stand on a short stool or stair and then slowly step down with the opposite limb to just touch the heel and slowly arise again. A positive test is indicated by the Trendelenburg sign, with the pelvis dropping down and away from the symptomatic supporting limb, the flexing knee collapsing into valgus, and the patient tending to wobble and lack stability (Figure 4).¹⁶

6. Patella Alta

Patella alta not only allows the patella to escape the confines of the trochlea earlier during active knee extension increasing the risk of patellar dislocation, but also decreases the contact footprint with the trochlea, increasing the patellofemoral joint reaction force and potentially causing patellofemoral pain and even secondary chondrosis. The simplest way to assess patellar height is with a lateral radiograph of the knee. The 3 popular methods (Insall-Salvati, Caton-Deschamps, Blackburn-Peel) all put the normal patellar height ratio at approximately 1:1, ± 20%. Berg and colleagues¹⁸ compared radiologic techniques for measuring patellar height ratio and found that Blackburn-Peel was the most accurate, reliable, and reproducible method.

7. Trochlear Dysplasia

Trochlear dysplasia, most simply a flattening of the TG, is perhaps the most important factor effecting normal patellofemoral function. However, it remains the most difficult to correctly address surgically. Senavongse and Amis¹⁹ conducted a cadaveric study demonstrating the prime importance of the TG. They found patellar stability was reduced 30% by releasing the VMO, 49% by cutting the MPFL in full knee extension, and 70% by flattening the trochlea. The most common, successful operations for correcting patellar instability depend on changing other factors that guide patellar excursion to compensate for this trochlear flattening.

The simplest way to assess trochlear dysplasia is to measure the sulcus angle on an accurate axial view radiograph of the knee at 45° flexion (Merchant view).²⁰ Dejour and colleagues²¹ popularized a technique of assessing and classifying trochlear dysplasia from a true lateral radiograph of the knee, which has the advantage of showing the trochlear at its proximal extent. Davies and colleagues²² evaluated the Dejour technique, along with patellar tilt, patellar height, and sulcus angle, to identify a rapid and reproducible radiologic feature that would indicate the need for further analysis by other imaging studies (eg, CT, MRI). They found that, if the sulcus angle was normal, analysis of other radiologic features was unlikely to reveal additional useful information. They also showed a correlation of increasing sulcus angle and severity of those other dysplasia features. Merchant and colleagues²⁰ found a mean normal sulcus angle of 138º (SD, 6º; range, 126º-150º), and Aglietti and colleagues²³ confirmed those findings with nearly identical values (mean, 137º; SD, 6º; range, 116º-151º).

Diagnosis and Initial Treatment Plan

Patellofemoral disorders generally are divided into patellofemoral pain and instability, but these 2 diagnostic categories are too broad to be useful. Patellofemoral pain is a symptom. Patellofemoral pain syndrome should never be used as a diagnosis because there is no accepted definition for the cluster of findings that customarily defines a syndrome. At initial evaluation, after the easily diagnosed causes of anterior knee pain (eg, prepatellar bursitis, TT apophysitis, patellar and quadriceps tendinitis) have been ruled out, the clinician should consider types of patellofemoral dysplasia for a presumptive diagnosis, which will then lead to a logical treatment program for each identified disorder. With a presumptive diagnosis established, almost all patients suffering from chronic anterior knee pain without history of injury are treated initially with rest, ice, and nonsteroidal anti-inflammatory drugs to restore joint homeostasis.³

Lateral Patellar Compression Syndrome

In 1975, Ficat and colleagues²⁴ described features of what they called syndrome d’hyperpression externe de la rotule. Two years later, Ficat and Hungerford²⁵ defined the syndrome as one “in which the patella is well centered in the trochlear sulcus and stable, but in which there is a functional lateralization onto a physiologically and often anatomically predominant lateral facet.” Using the tools we have described here, the clinician usually finds the cause(s) of this “functional lateralization.” Four abnormalities—VMO deficiency, LR tightness, increased standardized Q angle, and hip abductor weakness—can cause functional lateralization either alone when severe or in combination when mild or moderate.

For a presumptive diagnosis of LPCS, initial treatment is nonoperative, and successful in about 90% of patients. It should be obvious that most patients with chronic anterior knee pain have quadriceps atrophy. Physical therapy should be specifically focused on quadriceps strengthening, with absolutely no stress placed on the patellofemoral joint in flexion initially, and on hip abductor strengthening. Progressive resistive isometric quadriceps exercises can be performed with a weight-bench technique (Figures 5A-5D).²⁶

Chronic Subluxation of Patella

With the use of axial patellofemoral radiographs (Merchant views),²⁰ the clinician can determine if the “patella is well centered in the trochlear sulcus and stable” (an important part of the definition of LPCS). If the patient has no symptoms of recurrent instability or patellar dislocation, and these radiographs show a laterally subluxed patella (one not well centered in the trochlea), the diagnosis is most likely CSP, a moderate form of patellofemoral dysplasia (section II of the Table). In addition to the 4 abnormalities used in the diagnosis of LPCS (mentioned earlier), trochlear dysplasia also comes into play in the diagnosis of CSP. Just as the other abnormalities can vary from mild to severe, trochlear dysplasia can vary from mild (slightly shallow sulcus angle) to severe (flat or even convex sulcus angle). As the sulcus becomes shallower, the patella slides more laterally, increasing the likelihood of patellar dislocation.

As the patient with CSP gives no history of episodic patellar instability, treatment for CSP is almost identical to that for LPCS, with the primary focus on isometric quadriceps strengthening (DeHaven isometric exercises)²⁷ and hip abductor muscle strengthening. In the presence of CSP radiographically, it is important to use McConnell taping and/or patellar bracing during muscular strengthening. A patient who achieves 20-lb isometric quadriceps strength, demonstrates a normal step-down test, and is assumed to be asymptomatic can be allowed to return to sports activities with use of a patellar brace. The patient should be counseled that there is an increased risk for patellar dislocation because of this chronic subluxation and the shallower sulcus.

As in LPCS, CSP symptoms that persist after dynamic strength is regained may require surgical intervention. The severity of identified abnormal factors (tight LR, increased Q angle, trochlear dysplasia) guides the surgeon in selecting appropriate corrective technique(s).

Recurrent Dislocation of Patella

Admittedly, given the number and subtlety of abnormal factors, the diagnosis of LPCS as a cause of patellofemoral pain can be challenging. However, RDP is at the opposite end of the spectrum. A history of prior patellar dislocation(s) almost always makes the diagnosis of RDP easier. The patient occasionally complains of a recurrent symptom, the knee “going out” or “giving way,” indicating that the diagnosis might be RDP. By carefully asking what the patient was doing and what happened when the knee “went out”, the clinician may be able to determine if the injury stemmed from sudden patellar pain causing reflex inhibition of the quadriceps or was a true dislocation. Both may be described as “going out” or “giving way”.

Assessment for the same 7 abnormalities helps establish the diagnosis, a logical treatment plan, and a guide for indicated surgery. The diagnostic focus is MPFL laxity and trochlear dysplasia. Prior lateral dislocation of the patella almost always requires rupture of the normal MPFL. The infrequent exception is a patient with hyper-elasticity of the skin and multiple joints (Ehlers-Danlos syndrome). Trochlear dysplasia is a significant risk factor for patellar dislocation. If the trochlea is normal and there is no MPFL laxity, the diagnosis of RDP should be questioned.

If surgery is indicated, the surgeon uses a list of the patient’s abnormalities and their severity as a guide in selecting reconstructive techniques. The more abnormalities found and the greater the severity of each, the more techniques are needed to achieve success. Preoperative exercises help speed postoperative recovery by addressing quadriceps and hip abductor weakness. In addition, an active exercise program gives the surgeon insight into the patient’s desire for and commitment to recovery. Other physical abnormalities to be considered in preoperative planning include MPFL laxity, LR tightness, increased Q angle, patella alta, and trochlear dysplasia.

Surgical tips: 1. When releasing the LR, never cut the vastus lateralis tendon, as this has a high likelihood of causing iatrogenic medial patellar subluxation.²⁹ 2. When medializing the TT, consider compensating for a shallow trochlea by “over-correcting” the Q angle to 5° to 10° measured with a surgical goniometer intraoperatively.

Summary

Basing clinical classification of disorders on etiology is a simple and effective way to diagnose common patellofemoral conditions. Identifying and rating the severity of patellofemoral dysplasia, using 7 commonly found physical abnormalities, guide the physician to a proper diagnosis and down logical treatment pathways. These principles should be incorporated into the routine evaluation of patellofemoral disorders to optimize diagnosis, formulate a treatment plan, and improve patient outcomes. After all, this is what our patients are asking us to do: Try to find what’s wrong, and then try to fix it!

Am J Orthop. 2017;46(2):68-75. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.