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Case Report| Volume 28, P391-399, January 2021

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Hydraulic distension as a treatment for patellofemoral pain syndrome (PFPS) non-responsive to standard rehabilitation

Open AccessPublished:December 02, 2020DOI:https://doi.org/10.1016/j.knee.2020.09.016

      Abstract

      Background

      The occurrence of Patellofemoral Pain Syndrome (PFPS) is often found in daily medical care. Rehabilitation is usually applied with good results. However, patients often do not respond to standard rehabilitation, suggesting there may be some undetected factors that standard treatments cannot address.
      It is known that post-traumatic adhesive capsulitis in the knee often shows symptoms similar to those of PFPS, but idiopathic adhesive capsulitis (IAC) has seldom been mentioned as a possible cause of PFPS. Adhesive capsulitis in the shoulder joint causes frozen shoulder (FS), and hydraulic distension (HD) is often applied to FS effectively.

      Purpose

      The purpose of this study was to investigate and report on the clinical application of HD to treat PFPS non-responsive to rehabilitation treatment.

      Patients and methods

      HD was applied to 72 knees that had resisted regular conservative treatments for PFPS. Follow-up data (e.g. visual analogue scale) was collected immediately after HD, and at periods of 1, 3 and 6 months later.

      Results

      Of the 72 patients, 64 patients obtained pain relief after HD. Pain was relieved for at least 6 months for 33 of the 64 patients. No benefit was received for 8 patients.

      Conclusions

      HD could be an additional conservative option for some PFPS that resisted rehabilitation. Assuming that the mechanisms of action for HD in the knee are the same as those in FS, there is evidence to suggest that IAC might play a role in the development of PFPS for some patients.

      Keywords

      1. Introduction

      The pain of Patellofemoral Pain Syndrome (PFPS) is found retropatellar or peripatellar during activities such as running, ascending and descending stairs, squatting, and sitting with flexed knees for prolonged periods of time [
      • Page P.
      Effectiveness of elastic resistance in rehabilitation of patients with patellofemoral pains: what is the evidence?.
      ]. A large number of causes for PFPS have been suggested, with mal-tracking of the patella being a prominent example [
      • Hilyard A.
      Recent developments in the management of patellofemoral pain: the McConnell programme.
      ].
      Rehabilitation is initially applied for knees with PFPS [
      • Petersen W.
      • Ellermann A.
      • Gösele-Koppenburg A.
      • Best R.
      • Rembitzki I.V.
      • Brüggemann G.P.
      • et al.
      Patellofemoral pain syndrome.
      ,
      • Dutton R.A.
      • Khadavi M.J.
      • Fredericson M.
      Update on rehabilitation of patellofemoral pain.
      ,
      • Ismail M.M.
      • Gamaleldein M.H.
      • Hassa K.A.
      Closed kinetic chain exercises with orithout additional hip strengthening exercises in management of patellofemoral pain syndrome: a randomized controlled trial.
      ]. Rehabilitation for PFPS is designed to strengthen and stretch muscles to correct the mal-tracking of the patella [
      • Pal S.
      • Draper C.E.
      • Fredericson M.
      • Gold G.E.
      • Delp S.L.
      • Beaupre G.S.
      • et al.
      Patellar maltracking correlates with vastus medialis activation delay in patellofemoral pain patients.
      ,
      • Song C.Y.
      • Lin J.J.
      • Jan M.H.
      • Lin Y.F.
      The role of patellar alignment and tracking in vivo: the potential mechanism of patellofemoral pain syndrome.
      ,
      • Mostamand J.
      • Bader D.L.
      • Hudson Z.
      The effect of patellar taping on EMG activity of vasti muscles during squatting in individuals with patellofemoral pain syndrome.
      ]. However, rehabilitation is often unsuccessful. Karlsson et al. reported that rehabilitation provided a successful outcome for PFPS in 85% of cases, while Whitelaw et al. reported a successful outcome for only 57% of patients [
      • Karlsson J.
      • Thomeé R.
      • Swärd L.
      Eleven year follow-up of patello-femoral pain syndrome.
      ,
      • Whitelaw G.P.
      • Rullo D.J.
      • Markowitz H.D.
      • Marandola M.S.
      • DeWaele M.J.
      A conservative approach to anterior knee pain.
      ]. It therefore seems that there might be other underlying causes of PFPS that cannot be addressed by rehabilitation. Unfortunately, the number of treatments for PFPS other than rehabilitation is very limited. Clearly, additional treatments are required for patients who do not respond to rehabilitation.
      Patients with PFPS also often have decreased range-of-motion (ROM) of the knee accompanying their pain. These symptoms resemble those of post-traumatic adhesive capsulitis in the knee [
      • de Abreu M.R.
      • Falcão M.
      • Sprinz C.
      • Furian R.
      • Marczyk L.R.
      Adhesive capsulitis of the knee.
      ]. To the best of our knowledge, the possibility that idiopathic adhesive capsulitis (IAC) of the knee could be a cause of PFPS has never been fully explored. Adhesive capsulitis in the shoulder joint is known to be a cause of frozen shoulder (FS) [
      • Shah N.
      • Lewis M.
      Shoulder adhesive capsulitis: systematic review of randomised trials suing multiple corticosteroid Injections.
      ], and a well-known non-surgical option for that problem is hydraulic distension (HD) [
      • Fareed D.O.
      • Gallivan W.R.
      Office management frozen shoulder syndrome. Treatment with hydraulic distention under local anesthesia.
      ,
      • van Royen B.J.
      • Pavlov P.W.
      Treatment of frozen shoulder by distension and manipulation under local anaesthesia.
      ,
      • Sharma R.K.
      • Bajekal R.A.
      • Bhan S.
      Frozen shoulder syndrome. A comparison of hydraulic distension and manipulation.
      ].
      Since the symptoms of PFPS resemble those of adhesive capsulitis and HD is quite effective in treating frozen shoulder, this study was carried out to evaluate and report on the results of applying HD to 72 knees that had resisted standard rehabilitation.

      2. Materials and methods

      2.1 Participants

      Between July 2017 and August 2018, 92 patients with PFPS symptoms presented at Kouyukai Memorial Hospital. The duration of pain ranged from 3 months to 7 years prior to examination. None of the cases had a history of trauma or diseases, such as rheumatoid arthritis and gout. No obvious organic disorders were suspected after clinical evaluation. None of the knees showed manually palpable severe joint effusion, instability, a positive McMurray sign, or joint bloating. All patients had Lysholm and Gillquist scores of 80 points or more.
      The patients complained of anterior knee pain when ascending or descending stairs, squatting, or sitting with a bent knee for a long period of time. All patients complained of pain in the anterior aspect of their knee when it was bent over 90°. None of them complained of bilateral knee pain.
      All patients initially received at least 2 months of conservative therapy including physiotherapy (stretching of the quadriceps muscles, muscle strengthening, thermo-therapy, and bracing) and anti-inflammatory medication. Of the original 92 cases 20 improved, but for 72 patients the knee pain was not alleviated. Surgical treatments, including total knee arthroplasty or high tibial osteotomy, were contraindicated because of the low severity of osteoarthritis and the high Lysholm and Gillquist scores. HD was applied for the 72 non-responsive patients as an additional therapeutic method.
      Before HD, written informed consent for print and electronic publication of this report was obtained from all patients.

      2.2 The HD procedure

      HD was applied to the patients on an outpatient basis. Knees were sterilized with a 10% solution of povidone iodine before the procedure. Joint aspiration was performed before saline injection for every patient, and no bloody aspirate was noted. Isotonic saline (100 ml in four disposable syringes) was injected into the suprapatellar bursa (SPB) under completely aseptic conditions. For one patient, HD was carried out using 100 ml of 10-fold dilution of sodium amidotrizoate meglumine so that an arthrography could be performed during the procedure. A point was reached during saline injection when saline began to flow back into the syringe, and we recorded the volume injected before the flow-back occurred (flow-back volume, (FBV)). The patients were asked to report any significant or unusual sensations during the procedure. After injecting the saline, the clinician pushed the patella medially with both thumbs (defined as a “medial-push”, Figure 1A), and any significant or unusual observations were recorded. The injected saline was then aspirated, and the color of the aspirated fluid was reported as either clear or bloody (Figure 1B).
      Figure thumbnail gr1
      Figure 1Figures illustrating the HD method and bloody aspirates. (A, left). Photograph illustrating the “medial-push” technique. (B, right). Photograph showing two equally bloody aspirates in syringes.

      2.3 Data collection

      A single examiner (i.e. first author), performed all procedures and recorded all data.
      At their first visit to our clinic, data on patient age, gender, level of osteoarthritis according to the Kellgren-Lawrence (K/L) grading scale and femorotibial angle (FTA) was collected for each patient. The K/L grading scale and FTA were evaluated from an anterior-posterior X-ray of the knee in full extension.
      During HD, the FBV, aspirate color and any sensations with respect to changes in SPB tension were recorded.
      The level of pain was measured using the Visual Analogue Scale (VAS) both before and after HD. The bilateral difference in terminal flexion angle (BD-TFA) before HD, defined as the difference in terminal flexion angle (TFA) between the affected and non-affected knees for each patient, was also recorded.
      The VAS and TFA were monitored for a period of six months. Measurements were made before and just after HD. Follow-up measurements were also made at 1, 3 and 6 months later. The longest follow-up period was set as 6 months because patients who received pain relief were reluctant to come back to the clinic.

      2.4 Statistical analysis

      Sample size calculation was based on changes to the VAS and TFA, which are the main metrics used for assessment after HD. Assuming Student’s unpaired t-test with a significance level of 0.05, at least 52 participants were required to achieve a power of 0.8 [
      • Erdfelder E.
      • Faul F.
      • Buchner A.
      GPOWER: a general power analysis program.
      ]. The 64 patients who participated in the follow-up analysis were sufficient to achieve the desired power.
      Age, FTA, TFA, BD-TFA, VAS, and FBV data are presented as mean ± SD [95% confidence interval], and statistical comparisons were performed using Student’s unpaired t-test. Effect sizes for the VAS and TFA are reported using Hedges’ g [
      • Lakens D.
      Calculating and reporting effect sizes to facilitate cumulative science: a practical primer for t-tests and ANOVAs.
      ]. Statistical comparison for the gender, K/L grading scale, aspirate color, BD-TFA, and change to SPB tension was performed using the chi-square test, with the effect size represented using Cramer’s V [
      • Kim H.Y.
      Statistical notes for clinical researchers: chi-squared test and Fisher’s exact test.
      ].
      All statistical analyses were performed using the statistical routines in Microsoft Excel 2010. A p-value < 0.05 was considered statistically significant.

      3. Results

      3.1 Patient and clinician observations during HD

      After HD, 64 cases experienced pain relief while 8 did not. A sudden patella movement (hereafter referred to as popping), accompanied by a significant decrease in pain, was reported by 13 patients. A further 20 patients reported similar sensations with pain-relief but only after the medial-push. The remaining 31 patients reported no significant sensations other than the pain due to joint swelling during HD. However, after HD they did note improvement in the original knee pain.
      The clinician observed rapid patella popping followed by a prompt, palpable decrease in intra-articular pressure for 32 of the 33 patients who reported sudden patella movement. For one patient who experienced popping there was no decompression of the SPB. Decompression of the SPB was also noted for 16 patients who did not report popping.
      For the one patient for whom arthrography was performed, initially the medial half of the SPB was not enhanced, but after medial-push, the medial lining of the SPB appeared (Figure 2). The patient also reported popping and pain relief.
      Figure thumbnail gr2
      Figure 2Knee arthrography (anterior-posterior view). Before popping, the medial half of the suprapatellar bursa was not enhanced (left). After popping, the medial half of the suprapatellar bursa was enhanced (right, arrow).
      Hereafter, the 33 patients for which popping occurred either spontaneously or after a medial-push are classified as the pop (+) group, whereas the remaining 31 patients are in the pop (−) group.

      3.2 Patient data for the two groups before HD

      Osteoarthritis grade according to the K/L system is in Table 1. The number of K/L grade one and two patients in the pop (+) and pop (−) groups was not statistically different (Table 1).
      Table 1Kellgren-Lawrence (K/L) grading scale.
      GroupK/L grade 1K/L grade 2TotalComparison between pop (+)/(−)
      Pop (+)82533
      Pop (−)112031
      Total194564p = 0.25 (chi-square test)
      Cramer’s V = 0.12
      Table 2 contains information about the gender of the patients. There was no significant difference in gender between the pop (+) and pop (−) groups (Table 2).
      Table 2Gender difference.
      GroupMaleFemaleTotalComparison between pop (+)/(−)
      Pop (+)122133
      Pop (−)151631
      Total273764p = 0.33 (chi-square test)
      Cramer’s V = 0.12
      Table 3 contains further data for the two groups before HD. For convenience, the FBV data is also included in Table 3. Comparison of the data for the pop (+) and pop (−) groups prior to HD indicates, with one exception, that there was no significant difference between the groups. The exception was the BD-TFA (Table 3).
      Table 3Patient data before HD.
      Overall
      Data presented as mean ± SD [95% confidence interval].
      (64 patients)
      Pop
      Data presented as mean ± SD [95% confidence interval].
      (+) group (33 patients)
      Pop
      Data presented as mean ± SD [95% confidence interval].
      (−) group (31 patients)
      Comparison between Pop (+)/Pop (−)
      p-value (unpaired t-test)Effect size (Hedges' g)
      Age67.9 ± 13.9

      [64.4, 71.3]
      68.4 ± 13.2

      [63.9, 72.9]
      67.2 ± 14.7

      [62.0, 72.4]
      p = 0.74g = 0.09
      Femorotibial angle (FTA)176.8 ± 2.3

      [176.3, 177.4]
      176.9 ± 2.6

      [176.0, 177.8]
      176.8 ± 2.0

      [176.1, 177.5]
      p = 0.90g = 0.04
      Terminal flexion angle (TFA)131.0 ± 12.2

      [128.0, 134.0]
      129.4 ± 13.8

      [124.7, 134.1]
      132.7 ± 10.1

      [129.1, 136.3]
      p = 0.27g = 0.27
      Bilateral difference in TFA (BD-TFA)15.8 ± 9.5

      [13.4, 18.2]
      18.1 ± 10.7

      [14.5, 21.8]
      13.3 ± 7.5

      [10.7, 15.9]
      p = 0.046g = 0.52
      Visual analogue scale (VAS)51.3 ± 19.2

      [46.5, 56.1]
      52.7 ± 19.4

      [46.1, 59.3]
      49.8 ± 19.3

      [43.0, 56.6]
      p = 0.56g = 0.15
      Flow back volume (FBV)41.0 ± 20.4

      [35.9, 46.1]
      40.0 ± 19.3

      [33.4, 46.6]
      42.2 ± 21.8

      [34.5, 49.9]
      p = 0.68g = 0.09
      * Data presented as mean ± SD [95% confidence interval].
      Both the pop (+) and (−) groups were further divided into two sub-groups according to the value of the BD-TFA; that is, those with BD-TFA values over 15° or under 10°. The number of patients with a BD-TFA over 15° was significantly different to the number under 10° between the two groups (Table 4).
      Table 4Bilateral difference in terminal flexion angle (BD-TFA).
      GroupOver 15°Under 10°TotalComparison between Pop (+)/(−)
      Pop (+)24933
      Pop (−)151631
      Total392564p = 0.046 (chi-square test)
      Cramer’s V = 0.25

      3.3 Group data after HD

      For both groups, the post-HD VASs were significantly different from the pre-HD scores at all time points. However, with time, the mean VAS of the pop (−) group appeared to be returning to the pre- HD level more quickly than for the pop (+) group. Note that comparison of the VAS between the two groups at each time point shows that they are not significantly different, except for at 6 months (Table 5 and Figure 3). None of the patients experienced a worsening of their pain or any of the objective metrics after HD.
      Table 5Visual Analogue Scale (VAS) for both groups over time.
      Pop (+) groupPop (−) group
      VAS
      Data presented as mean ± SD [95% confidence interval].
      score
      Comparison between pre-HD and each post-HD scoreVAS
      Data presented as mean ± SD [95% confidence interval].
      score
      Comparison between pre-HD and each post-HD scoreComparison between Pop (+)/(−) scores at each follow-up period
      p-value
      Calculated using Student's unpaired t-test.
      Effect size
      Effect size presented using Hedges' g.
      p-value
      Calculated using Student's unpaired t-test.
      Effect size
      Effect size presented using Hedges' g.
      p-value
      Calculated using Student's unpaired t-test.
      Effect size
      Effect size presented using Hedges' g.
      Pre-HD52.7 ± 19.4N/AN/A49.8 ± 19.3N/AN/Ap = 0.56g = 0.15
      [46.1, 59.3][43.0, 56.6]
      Just after HD9.4 ± 7.4p < 0.001g = 2.9511.8 ± 10.8p < 0.001g = 2.43p = 0.30g = 0.26
      [6.9, 11.9][8.0, 15.6]
      1 month after HD9.8 ± 12.1p < 0.001g = 2.6315.2 ± 14.3p < 0.001g = 2.03p = 0.13g = 0.41
      [5.5, 14.1][10.0, 20.4]
      3 months after HD8.2 ± 12.6p < 0.001g = 2.5915.0 ± 16.6p < 0.001g = 1.90p = 0.13g = 0.46
      [2.7, 13.7][7.5, 22.5]
      6 months after HD6.7 ± 8.4p < 0.001g = 2.6622.3 ± 21.3p < 0.001g = 1.37p = 0.02g = 0.90
      [2.0, 11.4][12.2, 32.4]
      * Data presented as mean ± SD [95% confidence interval].
      ** Calculated using Student's unpaired t-test.
      *** Effect size presented using Hedges' g.
      Figure thumbnail gr3
      Figure 3Bar chart showing the visual analogue scale (VAS) for the pop (+) and pop (−) groups over the period of six months before and after HD. The p-value was calculated using Student’s unpaired t-test. The error bars denote standard deviation.
      All cases showed an increase of the TFA after HD. Comparison with the pre-HD TFA for the pop (+) group found that there was a significant difference in TFA post-HD at all time points. On the other hand, a similar comparison for the pop (−) group found there was a significant difference only for the measurements immediately and 3 months after HD. Comparison of the TFA for each group was also made at each time point. Between the two groups there were significant differences for the TFA between the value recorded pre-HD and the recordings at 3 and 6 months (Table 6 and Figure 4).
      Table 6Terminal flexion angle (TFA) for both groups over time.
      Pop (+) groupPop (−) group
      TFA
      Data presented as mean ± SD [95% confidence interval].
      Comparison between pre-HD and each post-HD scoreTFA
      Data presented as mean ± SD [95% confidence interval].
      Comparison between pre-HD and each post-HD scoreComparison between Pop (+)/(−) scores at each follow-up period
      p-value
      Calculated using Student's unpaired t-test.
      Effect size
      Effect size presented using Hedges' g.
      p-value
      Calculated using Student's unpaired t-test.
      Effect size
      Effect size presented using Hedges' g.
      p-value
      Calculated using Student's unpaired t-test.
      Effect size
      Effect size presented using Hedges' g.
      Pre-HD129.4 ± 13.8N/AN/A132.7 ± 10.1N/AN/Ap = 0.27g = 0.27
      [124.7, 134.1][129.1, 136.3]
      Just after HD143.3 ± 8.1p < 0.001g = 1.23141.0 ± 9.2p = 0.0013g = 0.86p = 0.28g = 0.27
      [140.5, 146.1][137.8, 144.2]
      1 month after HD141.0 ± 7.1p < 0.001g = 1.04137.9 ± 10.3p = 0.053g = 0.51p = 0.19g = 0.35
      [138.5, 143.5][134.2, 141.6]
      3 months after HD137.5 ± 8.1p = 0.016g = 0.68138.3 ± 8.4p = 0.03g = 0.59p = 0.74g = 0.10
      [134.0, 141.1][134.5, 142.1]
      6 months after HD139.2 ± 6.3p = 0.023g = 0.80136.8 ± 7.3p = 0.15g = 0.44p = 0.37g = 0.34
      [135.6, 142.8][133.3, 140.3]
      * Data presented as mean ± SD [95% confidence interval].
      ** Calculated using Student's unpaired t-test.
      *** Effect size presented using Hedges' g.
      Figure thumbnail gr4
      Figure 4Bar chart showing the terminal flexion angle (TFA) in degrees for the pop (+) and pop (−) groups. We calculated the p-value using Student’s unpaired t-test. The error bars denote standard deviation.
      Aspirate color after HD differed significantly between the pop (+) and pop (−) groups (Table 7).
      Table 7Aspirate color.
      GroupBloodyClearTotalComparison between Pop (+)/(−)
      Pop (+)231033
      Pop (−)52631
      283664p < 0.001 (chi-square test)
      Cramer's V = 0.54
      The number of patients who experienced a decrease of SPB tension after HD was statistically significant between the two groups (Table 8).
      Table 8Decrease in Suprapatellar bursa tension.
      GroupDecreaseNo decreaseTotalComparison between Pop (+)/(−)
      Pop (+)32133
      Pop (−)161531
      Total481664p < 0.001 (chi-square test)
      Cramer’s V = 0.52

      3.4 Treatment for the patients non-responsive to HD

      Of the 8 patients who did not benefit from HD, four later underwent a magnetic resonance imaging (MRI) exam and two of those showed a bucket-handle tear of the lateral meniscus. Arthroscopic meniscal suture relieved their symptoms. The other two MRI patients showed inflammation of the pes anserinus, and intra-tendon sheath injection of local anesthetic was applied effectively. The remaining four patients moved to other hospitals asking for second opinions, so no follow-up was possible.

      4. Discussion

      The most important finding of the study was that HD provided some level of pain relief for 64 of 72 patients that had resisted standard rehabilitation. Of the 72 patients, 33 experienced pain relief after a clear popping sensation. A further 31 patients also noted some pain relief but did not experience any significant sensations. The final 8 patients received no benefit from the procedure. After organizing the patients who reported some form of pain relief into pop (+) and pop (−) groups, analysis of the metrics used to monitor progress after HD found significant differences between the two groups.
      The etiology of PFPS has been controversial. In 2004, Whittingham et al. reported that PFPS develops due to poor muscular control, patella malalignment, reduced flexibility of the hamstrings, gastrocnemius, iliotibial band, tensor fasciae latae, and biomechanical changes in the lower extremity [
      • Whittingham M.
      • Palmer S.
      • Macmillan F.
      Effects of taping on pain and function in patellofemoral pain syndrome: a randomized controlled trial.
      ]. In 2013, Halabchi et al. suggested that the causes of PFPS are weak quadriceps, muscle tightness, lower leg length discrepancy and patellar malalignment [
      • Halabchi F.
      • Mazaheri R.
      • Seif-Barghi T.
      Patellofemoral pain syndrome and modifiable intrinsic risk factors; How to assess and address? Asian.
      ]. It has also been suggested that anatomical disorders such as an abnormal Q-angle or anteversion of the hip, and incongruence between the patellar surface and patellar groove leads to malalignment of the patellofemoral (PF) joint bringing about PFPS [
      • Waryasz G.R.
      • McDermott A.Y.
      Patellofemoral pain syndrome (PFPS): a systematic review of anatomy and potential risk factors.
      ,
      • Bazett-Jones D.M.
      • Cobb S.C.
      • Huddleston W.E.
      • O'Connor K.M.
      • Armstrong B.S.R.
      • Earl-Boehm J.E.
      Effect of patellofemoral pain on strength and mechanics after an exhaustive run.
      ,
      • Souza R.B.
      • Powers C.M.
      Predictors of hip internal rotation during running: an evaluation of hip strength and femoral structure in women with and without patellofemoral pain.
      ]. However, not every knee with the factors mentioned above develops PFPS [
      • Almeida G.P.L.
      • Silva A.P.
      • França F.J.R.
      • Magalhães M.O.
      • Burke T.N.
      • Marques A.P.
      Q-angle in patellofemoral pain: relationship with dynamic knee valgus, hip abductor torque, pain and function.
      ].
      In 2015, Islam et al. emphasized that the development of PFPS is related to increased PF joint stress [
      • Islam K.
      • Duke K.
      • Mustafy T.
      • Adeeb S.M.
      • Ronsky J.L.
      • El-Rich M.
      A geometric approach to study the contact mechanisms in the patellofemoral joint of normal versus patellofemoral pain syndrome subjects.
      ], and there are some reports about what the causes of excessive PF joint stress might be. In particular, Ahmad et al. reported that post-traumatic adhesion in the knee causes higher PF joint stress than usual, leading to knee pain and limited motion of joints [
      • Ahmad C.S.
      • Kwak S.D.
      • Ateshian G.A.
      • Warden W.H.
      • Steadman J.R.
      • Mow V.C.
      Effects of patellar tendon adhesion to the anterior tibia on knee mechanics.
      ]. Mikula et al. also found that PF contact stress was significantly increased by adhesions in the SPB [
      • Mikula J.D.
      • Slette E.L.
      • Dahl K.D.
      • Montgomery S.R.
      • Dornan G.J.
      • O’Brien L.
      • et al.
      Intraarticular arthrofibrosis of the knee alters patellofemoral contact biomechanics.
      ].
      Intra-articular adhesion is known to be a cause of FS. HD is often successfully applied to treat FS. It is also reported that excessive scar tissue is observed in FS, which causes joint stiffness and pain [
      • Le H.V.
      • Lee S.J.
      • Nazarian A.
      • Rodriguez E.K.
      Adhesive capsulitis of the shoulder: review of pathophysiology and current clinical treatments.
      ]. The mechanisms of action for HD in FS are said to be: (1) Expansion of the stiff joint capsule; (2) Joint rupture; and (3) Peeling of an adhesion [
      • Kim K.
      • Lee K.J.
      • Kim H.C.
      • Lee K.J.
      • Kim D.K.
      • Chung S.G.
      Capsule preservation improves short-term outcome of hydraulic distension in painful stiff shoulder.
      ,
      • Lee J.H.
      • Kim S.B.
      • Lee K.W.
      • Lee S.J.
      • Lee J.U.
      Effect of hypertonic saline in intra-articular hydraulic distension for adhesive capsulitis.
      ,
      • Rizk T.E.
      • Gavant M.L.
      • Pinals R.S.
      Treatment of adhesive capsulitis (frozen shoulder) with arthrographic capsular distension and rupture.
      ,
      • Rymaruk S.
      • Peach C.
      Indications for hydrodilatation for frozen shoulder.
      ]. The results of this study can be discussed under the assumption that the same mechanisms are active in the knee.
      Deliwala et al. reported that a rupture might occur at the apex of the SPB, after which the patient will experience localized pain, swelling and erythema, which look like symptoms of deep vein thrombosis [
      • Deliwala U.H.
      • Jadeja H.R.
      • Rathod C.L.
      • Loya N.
      The Suprapatellar pouch of the knee and its disorders.
      ]. None of the cases in this study showed these symptoms, so it is likely that joint rupture can be eliminated as the mechanism of action after HD in this study.
      It has been reported by Matziolis et al. that the mean volume in normal knees is 135 ± 53 ml [
      • Matziolis G.
      • Roehner E.
      • Windische C.
      • Wagner T.A.
      The volume of the human knee joint.
      ]. If it is assumed that the FBV reflects the volume of the affected knees, our FBV measurements (Table 3) indicate that the joint volume of the knees involved in this study was reduced prior to HD for both the pop (+) and (−) groups. Also, all joints were aspirated before saline injection, but no bloody fluid was noted. After HD, however, bloody aspirate indicating intra-articular bleeding was noted more frequently for the pop (+) group than for the pop (−) group. The arthrography performed on one patient who experienced popping showed that the affected SPB was expanded via HD. These results suggest that popping of the patella occurred when an intra-articular structure that partitioned the SPB, such as an adhesion or something similar, was torn rapidly with bleeding [
      • Yamamoto Z.
      • Fujita A.
      • Minami G.
      • Ishida R.
      • Abe M.
      Atraumatic hemarthrosis caused by a large mediopatellar plica.
      ], after which the PF joint stress decreased to relieve the symptoms of PFPS for at least 6 months. Although there is no direct evidence that IAC was present prior to HD, our observations are consistent with the action of HD in FS when peeling of an adhesion occurs [
      • Enad J.G.
      Arthroscopic lysis of adhesions for the stiff total knee arthroplasty.
      ,
      • Stiefel E.C.
      • McIntyre L.
      Arthroscopic lysis of adhesions for treatment of post-traumatic arthrofibrosis of the knee joint.
      ,
      • Kukreja M.
      • Kang J.
      • Curry E.J.
      • Li X.
      Arthroscopic lysis of adhesions and anterior interval release with manipulation under anesthesia for severe post-traumatic knee stiffness: A simple and reproducible step-by-step guide.
      ,
      • Simpson J.K.
      • Budge R.
      Treatment of frozen shoulder using distension arthrography (hydrodilatation): a case series.
      ,
      • D'Orsi G.M.
      • Via A.G.
      • Antonio Frizziero A.
      • Oliva F.
      Treatment of adhesive capsulitis: a review.
      ]. Therefore, under the assumption that the mechanisms of action for HD in the knee are the same as those in FS, it seems that IAC could have played a role in the development of PFPS for the pop (+) group.
      On the other hand, there was no popping of the patella or intra-articular bleeding after HD for the members of the pop (−) group. Nor was decompression of the SPB experienced for 15 out of the 31 patients in the group (Table 8). Nevertheless, although the improvement did not last for as long as the pop (+) group, all cases received pain relief. Assuming again that the mechanisms of action for FS are also applicable in the knee, these results provide no evidence that the pop (−) group received pain relief from peeling of an adhesion. Rather, it is possible to argue for the pop (−) group that excessive scar formation, or something similar, had shrunk and stiffened the joint capsule. After joint expansion via HD, the return of symptoms may be due to gradual re-shrinking of the joint capsule with time.
      As a note of caution for applying HD, the technique requires joint puncture that may cause pain and/or anxiety for some patients. In that case some other treatment may be more suitable.
      Finally, it should be mentioned that PFPS is most often found among young and active people. However, the age of the patients in this study was relatively high (67.9 ± 13.9 years). This is probably because data were collected at one hospital and by one clinician, which might bias the results. A further study on a group with a more diverse range of ages would be beneficial.

      5. Conclusions

      If the symptoms of PFPS are caused by an adhesion or similar intra-articular structure, then it can be expected that standard rehabilitation will fail. The data collected in this study indicates that HD provided pain relief for 64 of 72 knees that resisted traditional rehabilitation, indicating that HD might be an effective option for PFPS when additional therapy is required. Under the assumption that the mechanisms of action for HD in the knee are the same as those in FS, it has been argued that IAC might play a role in the development of PFPS for some cases. An initial BD-TFA of over 15° might be a good indicator that the patient will respond well to HD.

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