Fascial Hydrorelease for a Stiff Knee After Knee Replacement

Abstract

01 · Introduction

Satisfaction rates after primary total knee arthroplasty (TKA) are high; however, roughly 20% of patients are dissatisfied post-operatively, largely because of limitations in physical function.¹ Acquiring a knee flexion contracture after TKA contributes to significant stiffness. Post-operative stiffness leads to 58% of reoperations and post-operative interventions, as well as more than 25% of 90-day hospital readmissions.^2–4 Knee flexion contracture occurs in 1.4–17% of patients and is thought to increase anterior knee pain, which develops secondary to altered biomechanics that shift loading forces to the posterior tibial plateau and increase forces across the patellofemoral joint.⁵

The Knee Society defines stiffness as “limited range of motion as reported by the patient and demonstrated in a physical examination,” with extension limited to 15° short of full or flexion <90° — a multifactorial complication of primary TKA.⁶

Despite wide recognition of the posterior myofascial chain’s involvement in flexion contracture, the development and treatment of fascial adhesions after TKA has not been thoroughly described — yet it could offer a clinically meaningful path to restoring function, reducing pain, and improving satisfaction. Fascial tissues form a network intimately associated with the musculoskeletal system and contribute passively to biomechanical behavior. Post-operative adhesion development involves dynamic communication between extracellular molecules and cellular components that remodel the collagen structure. This remodeling is orchestrated by cytokines released in the extracellular matrix in response to altered load and inflammation; fibrogenic products acting through interleukin-1 (IL-1), tumor necrosis factor (TNF), and transforming growth factor beta (TGFβ-1) promote fibrosis, fibroblast proliferation, and collagen deposition.⁷ Increased matrix deposition drives fibrosis within the fascial planes and restricts motion. There is also evidence that these fibrous fascial components can actively contract, adding restrictive force on knee range of motion.⁸

Therapies targeting fascial adhesions after TKA include bedside stretching, extension orthoses, manual fascial release, manipulation under anesthesia (MUA), and botulinum toxin A injections for spastic contractures. In a double-blind randomized trial, Smith et al. found botulinum toxin A gave statistically significant range-of-motion gains at one year, though clinical significance may be limited.⁹ Because degree of extension plays a large role in reported satisfaction, there is strong interest in novel therapies to reduce flexion contracture after TKA.

Fascial hydrodissection under ultrasound guidance, as described by Courseault et al., has proven useful for releasing fascial planes scarred by chronic hamstring injury — injecting anesthetic, corticosteroid, and saline into the interfascial planes to release the fibrous tissue impeding motion and producing pain.¹⁰ Machida et al. report a similar hydrorelease for scarring after arthroscopic knee surgery in the infrapatellar fat pad.²⁹ To our knowledge, hydrorelease has not been described as a therapeutic tool for knee flexion contracture after primary TKA. This report details a successful fascial hydrorelease of a soft-tissue hamstring contracture, along with anterior knee hydrorelease, for acquired flexion deformity following primary TKA.

02 · Case Report

A 63-year-old woman with a history of hypermobility and tobacco use underwent a primary right total knee arthroplasty. She reported excellent relief of joint pain, but at her post-operative follow-up she described posterolateral tightness and sharp pain, and could extend the knee only to 155°. Standing did not improve extension, and she required a walker to ambulate. On exam her range of motion was 90–155° with no neurologic abnormalities in the lower extremity. Despite eight weeks of physical therapy, she could not achieve full extension.

Before undergoing a manipulation, she was referred to The Fascia Institute and Treatment Center for an ultrasound evaluation. She was found to have a 25° flexion contracture of the right knee. A focused neurological exam was normal. The surgical site was well healed but the scar was immobile, and she was tender along the patellar tendon, iliotibial band, and distal hamstrings.

Image A. Ultrasound (GE Logiq E, 5–13 MHz linear transducer) showing reactive hyperemia at the long and short heads of the biceps femoris, with extensive fibrotic adhesions of the semitendinosus and semimembranosus. Each area was tender to dynamic sonographic palpation.

Hydrodissection

Because the patient had completed aggressive physical therapy without achieving full range of motion, the next step was a fascial hydrorelease of the distal hamstring fibrotic fascia. After reviewing risks and benefits, she agreed to the procedure. After identifying the sciatic nerve and popliteal vessels, an ultrasound-guided hamstring fascial hydrodissection (3.5-inch 25-G Tuohy needle) was performed with a mixture of 5 cc 1% lidocaine, 10 cc normal saline, and 1 cc 40 mg/mL methylprednisolone. Strength and sensation were normal afterward. Immediately following the injection, her posterolateral knee pain decreased and she gained an additional 7° of extension. She could ambulate without her walker but still had difficulty with full heel contact.

At her one-month follow-up she was satisfied with her progress in extension and ambulation and had weaned off the walker, with decreased hamstring tightness — but still could not fully extend the knee. She continued to report anterior knee pain over the patellar tendon, IT band, and pes anserine tendons. Ultrasound showed slight reactive hyperemia of the patellar tendon and an adhesion at the patellar fat pad. A second hydrorelease was directed to the patellar fat pad, iliotibial band, vastus lateralis, vastus medialis, pes anserine, and the saphenous and genicular nerves, using 20 cc 1% lidocaine with 20 cc 50% dextrose (35 cc total, 5 cc per site under ultrasound guidance). The patellar tendon, IT band, and hamstring adhesions were released; the pes anserine insertion was injected; and the saphenous and genicular nerves received perineural hydrorelease.

The patient underwent 3 additional hydrorelease treatments at 4-week intervals, noting continued improvement at each session. Ultrasound demonstrated a progressive decrease in hamstring, iliotibial band, and posterior patellar fibrotic tissue, with a significant reduction in reactive hyperemia around the knee. She continued physical therapy throughout treatment.

Post-procedure course

Twelve months after her primary TKA, the patient reported 100% improvement in pain. She had achieved full knee extension and no longer required a cane. She also reported losing 10 pounds owing to her increased activity. She continued to note occasional anterior knee pain, though much reduced from presentation. Because she had bilateral flexible pes planus with overpronation, her residual anterior knee pain was attributed to altered gait mechanics loading the anterior knees; stability shoes with medial arch support were recommended, and the added support decreased her pain.

03 · Discussion

Fixed flexion deformity (FFD) after primary TKA may arise from many contributing factors. A pre-operative FFD is a positive predictor of a post-operative FFD, though contractures also occur without one.^11,12 The most common cause of immediate stiffness is pain and effusion, both of which resolve over time.^13,14 Intrinsic technical factors include overstuffing the patellofemoral joint, flexion/extension gap mismatch, inaccurate ligament balancing, femoral or tibial malrotation, joint-line elevation, and excessive tightening of the extensor mechanism.^15–19 Importantly, some patients may be biologically predisposed to FFD.²⁰

Multiple treatments exist, with variable success. McGrath et al. developed a custom-molded knee device as an adjunct to therapy; 27 of 29 primary-TKA patients achieved full extension after nine months.²¹ Finger et al. reported a post-TKA patient who improved from 20° to 12° over 28 therapy sessions, then to full extension after eight weeks of nightly dynamic splinting.²² These non-operative strategies avoid additional surgery and anesthesia but require considerable time.

Because our patient had completed three months of therapy without improvement, we elected fascial hydrorelease — a safe technique for separating tissue along anatomical planes, in which fluid is injected under pressure into the fascial planes with ultrasound guidance.^23,24 Its reported uses include dissecting intra-abdominal adhesions in re-operative surgery and preserving perforating arteries in breast reconstruction.^23,24 Courseault et al. reported its utility in chronic hamstring injuries, with immediate pain reduction and return to competition,¹⁰ and Machida et al. described a similar procedure for infrapatellar fat-pad scarring after arthroscopy.²⁹ In our case, hydrorelease was used to release fascial adhesions detected on ultrasound that were presumed to cause the contracture.

Our patient underwent five hydrorelease treatments and, twelve months after surgery, achieved full extension of her knee. Ultrasound-guided fascial hydrorelease for FFD is a novel procedure, and this case demonstrates its capacity to offer a successful outcome. Growing interest in ultrasound evaluation and hydrorelease for post-TKA FFD highlights the need for larger studies to further investigate the success and safety of these procedures, and to determine which injectate provides optimal results.

References

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This case report is provided for education and professional reference; it describes a single patient’s experience, is not medical advice, and does not create a physician–patient relationship. Individual results vary. Fascial hydrorelease is a procedure performed under ultrasound guidance by qualified clinicians. The Fascia Institute and Treatment Center® · 2520 Harvard Ave, Ste 2B, Metairie, LA 70001 · (504) 704-1254.