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Hoffa pad impingement syndrome, also known as Hoffa disease, fat pad impingement, and infrapatellar fat pad (IFP) syndrome, is a painful impingement of the IFP between the patella and distal femoral condyle. The diseased fat pad is characterized by inflammation, swelling, hypertrophy, and fibrosis, most often caused by trauma or prior surgery. IFP pathology is often successfully treated nonoperatively with physical therapy. If refractory to conservative management, partial arthroscopic resection of the IFP has shown favorable results. This activity outlines the evaluation and management of Hoffa pad impingement syndrome and highlights the role of the healthcare team in evaluating and treating patients with this condition. Objectives: Identify the anatomy of the infrapatellar fat pad. Evaluate the clinical examination findings and imaging of Hoffa pad impingement syndrome. Assess the nonoperative treatment for Hoffa pad impingement syndrome. Explain the operative management of Hoffa pad impingement syndrome. Access free multiple choice questions on this topic.

There are 3 primary anterior knee fat pads, such as the quadriceps suprapatellar, pre-femoral suprapatellar, and infrapatellar retro-patellar tendon (Hoffa's fat pad), all of which may experience symptomatic impingement.[1] The Hoffa pad, also known as the infrapatellar fat pad (IFP), is an extra-synovial, intracapsular structure that occupies most of the anterior knee compartment.[2]  The IFP can become 1 of many causes of anterior knee pain when it becomes inflamed, leading to impingement at the tibiofemoral joint or the lateral aspect of the patellofemoral joint, known as Hoffa pad impingement syndrome.[3] This structure is richly vascularized and innervated. Its arterial supply is from an anastomotic network of branches of the medial and lateral superior geniculate and medial and lateral inferior geniculate arteries.[4] It is innervated by the posterior articular nerve, a branch of the posterior tibial nerve that courses through the external borders of the menisci, synovium, cruciate ligaments, and the IFP.[5] A normal IFP attaches to the proximal patellar tendon, the inferior pole of the patella, anterior horns of the medial and lateral menisci, transverse meniscal ligament, and periosteum of the anterior tibia.[3] The posterior aspect of this structure is lined with synovium and extends posteriorly, connecting to the intercondylar notch and, in some structures, is continuous with the anterior cruciate ligament (ACL).[6][7]

Injury to the IFP is usually the result of a single traumatic event or repetitive microtrauma due to blunt impact, shear injury with ACL tear, dislocation of the patella, or a twisting injury at the knee.[8] Hoffa pad impingement syndrome has been well-documented as a source of anterior knee pain, commonly found in runners, cyclists, and soldiers.[9] The IFP is a potent source of pain due to its robust innervation by nociceptive Type IVa-free nerve endings and fibers targeted by substance P.[10] Substance P causes vasodilation, thereby promoting the recruitment of immune cells and potentially contributing to edema development within the tissue. This inflammatory process can cause thickening and fibrosis, leading to the loss of elastic properties of the IFP.[3] The scar tissue gradually accumulates and impinges at the intercondylar notch and trochlea, leading to a mechanical or painful block to full extension.[11] The IFP produces fibroblast growth factor, vascular endothelial growth factor, tumor necrosis factor, and interleukin-6, all of which interact to contribute to the development of inflammation, fibrosis, and pain within the IFP.[12]

The epidemiology of Hoffa pad impingement syndrome is unknown. The low documented incidence could be due to the difficulty in diagnosing the condition and its tendency to be adequately treated with conservative management.[13] It is believed that Hoffa pad impingement syndrome is underdiagnosed by imaging because it is only present in 1% of patients undergoing knee arthroscopy.[8][14]

Hoffa first described the most accepted etiology of Hoffa pad impingement syndrome in 1904, which entailed IFP injury followed by associated bleeding, inflammation, hypertrophy, and eventual fibrosis.[15] Acute injury, repetitive microtrauma, and iatrogenic injury can lead to the initial cascade of events ending in fibrosis. Iatrogenic causes of IFP pathology include fibrosis due to arthroscopy portals, bone-patella tendon-bone autograft harvest during ACL reconstruction, or fat pad resection.[16] The clinical manifestations of other lesions inside IFP are comparable and often include swelling, knee discomfort, restricted range of motion, and an occasional palpable lump. Synovial lipomas, pigmented villonodular synovitis, glomus tumors, synovial chondromatosis, synovial haemangiomas, and ganglion cysts are among the possible causes.[17][18] It results from repeated pinching of the exterior part of the fat pad between the cartilage of the lateral facet of the trochlea and the lateral patellofemoral ligament. Any pathology that reduces the space between these 2 structures might encourage local impingement. HFP impingement is also linked to a higher patella position (patella alta).[19]

On MRI, IFP appears similar to subcutaneous adipose tissue and has fibrous structures dispersed throughout the adipocytes.[20] Histologically, non-diseased tissue resembles visceral adipose tissue.[21] Inflamed IFP demonstrates fibro-fatty tissue and degenerative change, consistent with chronic injury and inflammation.[3] The dense fibrous tissue gradually replaces lipocytes and occasionally transforms into cartilaginous tissue with ossifications.[22] Obvious visible fibrotic changes or calcifications of the diseased IFP are rare, although when present, they are specific for Hoffa pad impingement.[22] The synovial lining of the inferior patellar fat pad has type IVa free nerve terminals, which are the primary source of anterior knee discomfort.[23]

Patients with Hoffa pad impingement syndrome report a "burning" or "aching" sensation to the anterior knee localized deep to and on either side of the patellar tendon adjacent to the inferior pole of the patella. This most commonly occurs with the knee at full extension, dynamic extension, or prolonged flexion. The pain usually occurs over a prolonged period and may be associated with a previous knee injury or idiopathic. Physical examination reveals discomfort and tenderness around the patellar tendon, typically located close to the inferior pole of the patella. All patients have some degree of range of motion restriction, and 1 study reported severe limiting at 20 degrees of flexion. Pain at the end of the extension is also common in patients with fat pad impingement.[3] The patient's symptoms can be reproduced with the Hoffa test, which is performed by applying firm pressure with the thumb inferior to the patella just outside the margin of the patellar tendon with the knee in 30 degrees of flexion. With steady pressure, the knee is fully extended. Increased pain with this maneuver is a positive test. The test is then repeated on the medial or lateral side of the tendon.[15] Care must be taken to differentiate this anterior knee pain from joint line pain secondary to anterior meniscal pathology.[24] Pain may also be reproduced with isometric quadriceps contraction with the knee in full extension. The diseased IFP may be enlarged, firm, or tender to palpation. IFP pathology is also associated with an extension block and decreased patellar mobility.[25] The arthroscopic release has been devised for anterior interval release followed by rehabilitation, which focuses on preventing re-scarring with extension exercises and patellar mobilization.[15] An "infrapatellar plica" is the term used to describe the thickening and fibrosis of the ligamentum mucosum. Nonspecific symptoms such as continuous agonizing knee discomfort made worse by movement, sporadic popping, snapping, and effusion have been reported in patients with symptomatic infrapatellar plica.[26]

Sagittal MRI is the gold standard imaging modality for assessing IFP pathology. On T1-weighted MRI of the normal IFP, the appearance is similar to surrounding subcutaneous fat except for the foci of lower signal intensity representing the interposed fibrous septae (see Image. Hoffa Pad Impingement Syndrome, MRI).[25] Hypointense vertical clefts are present in the proximal aspect of the fat pad, and horizontal clefts are present in its posterior aspect. The hypointense signal on T1 adjacent to the anterior horns of the medial and lateral menisci represents the transverse meniscal ligament.[27] T2 fat saturation MRI portrays the IFP as isointense to muscle.[28] The posterior continuation of the Hoffa fat pad synovium, also known as ligamentum mucosum, can occasionally be appreciated as a T2 hyper-intense band anterior to the ACL and inserted within the intercondylar notch. Blood vessels are also visualized on T2 MRI, taking a vertical course in the medial and lateral aspects of the IFP.[28] In Hoffa pad impingement syndrome, an increased signal on T1 or hypo-intense T2 signal within the IFP indicates fibrosis. Intra-fat pad ossification can be differentiated from fibrosis using an X-ray. Hyper-intense T2 signal within the IFP indicates inflammation and its associated edema and hemorrhage.[25] A positive Hoffa's test and loss of extension and flexion are the usual symptoms of anterior interval scarring, scar tissue that binds the IPFP to the anterior tibia. Other symptoms include discomfort during extension and anterior knee pain. In a comparative study, Arthur et al demonstrated that individuals with clinical fat pad impingement had edema on MRI in the superolateral area of the Hoffa fat pad. However, similar edema may also be present in people without signs of fat pad impingement. Therefore, clinical assessment is very important for diagnosis rather than sole reliance on MRI findings.[29]

Nonoperative Management Physical therapy is the mainstay of treatment for Hoffa pad impingement syndrome.[30] The goal of physical therapy is to restore the biomechanics of patellar tracking via vastus medialis obliquus strengthening, taping to offload the patella tendon and fat pad, stretching, and improving pelvic control with training focused on gluteal strengthening to optimize lower extremity mechanics.[31] The goal of taping is to tilt the inferior portion of the patella anteriorly to decrease impingement and subsequent inflammation of the IFP. This is accomplished by applying tape across the proximal half of the patella with the knee fully extended. Two strips are applied in a "V" formation, with the apex at the tibial tubercle. The first part of the V tape starts at the tibial tubercle and is applied over the medial epicondyle while the patella and surrounding soft tissue are pulled inferiorly. The second strip is similarly applied at the tibial tubercle and towards the lateral epicondyle. The tape is to remain in place every day until the patient is pain-free. Patients are also instructed to avoid hyperextension and rapid extension maneuvers to decrease impingement of the IFP.[31] Muscle training focuses on closed-chain exercises targeting the quadriceps, namely the vastus medialis obliquus, to improve patellar tracking.[32] Resistance training of the gluteus medius's posterior fibers to decrease the hip's internal rotation and the resultant valgus force at the knee can be implemented to align the patella within the trochlea better. The patient may stretch the anterior hip structures to increase available external rotation if the patient has marked femoral internal rotation. House and Connell reported an improved visual analog score after injecting a mean of 4 injections of alcohol and bupivacaine under ultrasound guidance.[33] IFP pain usually responds to 1 to 3 injections of 6 ccs of 2% lidocaine combined with 40 mg of methylprednisolone acetate or 50 mg of hydrocortisone at intervals of 4 to 6 weeks. Corticosteroid injections have also been used to treat Hoffa pad impingement syndrome and have demonstrated satisfactory results.[16] Operative Management

Muscle training focuses on closed-chain exercises targeting the quadriceps, namely the vastus medialis obliquus, to improve patellar tracking.[32] Resistance training of the gluteus medius's posterior fibers to decrease the hip's internal rotation and the resultant valgus force at the knee can be implemented to align the patella within the trochlea better. The patient may stretch the anterior hip structures to increase available external rotation if the patient has marked femoral internal rotation. House and Connell reported an improved visual analog score after injecting a mean of 4 injections of alcohol and bupivacaine under ultrasound guidance.[33] IFP pain usually responds to 1 to 3 injections of 6 ccs of 2% lidocaine combined with 40 mg of methylprednisolone acetate or 50 mg of hydrocortisone at intervals of 4 to 6 weeks. Corticosteroid injections have also been used to treat Hoffa pad impingement syndrome and have demonstrated satisfactory results.[16] Operative Management Operative intervention is indicated once the patient has exhausted conservative management. Arthroscopic resection of the posterior aspect of the IFP is the primary surgical treatment of the inflamed, symptomatic fat pad.[34] It has been recommended that a high anterolateral portal and a standard anteromedial working portal be used during arthroscopic resection. A high anteromedial portal is sometimes necessary to best visualize and access the lateral ala impingement. Symptomatic infrapatellar plica has been demonstrated to respond well to arthroscopic excision. The majority (86 to 91%) of patients with solitary infrapatellar plica release experienced few to no post-operative complaints. Regardless of the approach, hemostasis is precisely maintained.[35]

Operative intervention is indicated once the patient has exhausted conservative management. Arthroscopic resection of the posterior aspect of the IFP is the primary surgical treatment of the inflamed, symptomatic fat pad.[34] It has been recommended that a high anterolateral portal and a standard anteromedial working portal be used during arthroscopic resection. A high anteromedial portal is sometimes necessary to best visualize and access the lateral ala impingement. Symptomatic infrapatellar plica has been demonstrated to respond well to arthroscopic excision. The majority (86 to 91%) of patients with solitary infrapatellar plica release experienced few to no post-operative complaints. Regardless of the approach, hemostasis is precisely maintained.[35] Patients with discomfort and swelling around the inferior pole of the patella may find relief with arthroscopic denervation of the nociceptive nerves innervating those areas. The inferior fat pad is often surgically removed from where it inserts on the inferior patellar pole using an electrothermal cautery method.[36] After arthroscopic excision, patients with significant impingement of the fat pad and no other concurrent disease may anticipate remission or long-term improvement in their symptoms and function.[34] Kim et al reported improved clinical results with either partial or subtotal arthroscopic excision of the impinged fat pad between the patella and femoral trochlea. Given that partial resection was just as successful as subtotal resection and kept more of the fat pad, it may thus be a suitable course of therapy.[37]

Hoffa pad impingement syndrome is a diagnosis of exclusion, mainly due to the numerous conditions that cause anterior knee pain and extension block. Soft tissue pathology, such as bursitis, must be ruled out. The anterior knee has 4 bursae: the prepatellar, superficial, infrapatellar, deep infrapatellar, and pes anserine bursae, and can become inflamed with repetitive microtrauma or sports requiring repetitive knee use such as cycling.[38] Patellar tendinosis must also be considered, as it is typically seen in high-impact jumping sports. It is characterized by activity-related pain localized to the inferior pole of the patella and occurs more prominently with eccentric quadriceps contraction. Intra-articular pathologies such as plica syndrome, meniscal tears, articular cartilage injuries, and osteochondral lesions must also be ruled out. Plica syndrome occurs when the incompletely resorbed embryonic septa separating the knee joint into medial, lateral, and suprapatellar compartments become inflamed following trauma, overuse, long-standing patellar mal-tracking, diabetes, and inflammatory arthropathy.[39] Meniscus tears usually occur following a traumatic injury to the knee, resulting in pain and an intra-articular clicking/catching sensation. Mechanical blocks to full extension can also occur from hypertrophic fibrosis following ACL reconstruction. Also known as a "cyclops lesion," this nodule or hypertrophied graft tissue has been reported to occur between 1% and 10% of all ACL reconstructions. It is the second most common cause of restricted knee extension following graft impingement.[40][41] Anterior interval scarring is another common block to full knee extension, often causing pain, decreased patellar mobility, and quadriceps atrophy. The anterior interval is the space between the IFP and the anterior tibia and is also often implicated as the cause of extension block following arthroscopic ACL reconstruction.[42]

Hoffa pad impingement syndrome is most often successfully treated with conservative management such as physical therapy or steroid injections.[30] In those requiring operative intervention, the vast majority return to their pre-injury level of sporting activities following arthroscopic debridement.[34]

Missed or delayed diagnosis of Hoffa pad impingement syndrome can lead to diminished quality of life, missed playing time, and progression of inflammation into the development of fibrosis. An enlarged and fibrotic IFP can cause a knee flexion contracture, which alters gait mechanics.

Patients, especially athletes, can help avoid the development of Hoffa pad impingement syndrome by focusing on closed-chain quadriceps exercises that promote appropriate patellar tracking and avoid the initial impingement event. Those with ligamentous laxity, a history of patellar dislocation, or prior ligamentous knee injury are at increased risk of developing this pathology. Increased awareness of this disease serves as the best preventative measure.

Hoffa pad impingement syndrome is 1 of the many causes of infrapatellar knee pain. Due to the prevalence of anterior knee pain, familiarity with this disease is paramount in inappropriate diagnosis, treatment, and recovery for patients with this condition. The healthcare professional must be thoughtful and intentional during the history and physical examination to arrive at a diagnosis in a timely fashion. It has been reported that many cases of IFP syndrome have been incorrectly diagnosed and treated as meniscal pathology, which leads to inefficient use of resources and improper treatment. This pathology requires effective interprofessional communication between the clinician, athletic trainer, nurses, and physical therapist, as most cases can be treated with physical therapy alone.[30] Improving the healthcare professional's understanding of evaluating and treating this condition promptly leads to better patient outcomes.