Knee Loss of Motion

Gregory C. Fanelli

Justin D. Harris

Daniel J. Tomaszewski

John A. Scanelli III

DEFINITION

Loss of motion is a generic term that can refer to a loss of flexion, extension, or both. It does not specifically imply a particular etiology.
Flexion contracture implies a loss of extension secondary to contracture or relative shortening of the posterior soft tissues (capsular or muscular).
Arthrofibrosis describes knee loss of motion (ie, flexion, extension, or both) caused by diffuse adhesions or fibrosis within a joint.
Ankylosis describes immobility of a joint, usually secondary to fibrous, cartilaginous, or bony overgrowth.
Knee loss of motion is a common and serious complication of knee ligament injury or reconstruction. Surgeon understanding of the pathogenesis, preventive measures, and surgical management of this condition is vital for optimum patient care.

ANATOMY

The knee has been described as a ginglymus (simple hingetype) articulation.
- In actuality, knee motion is complex and requires at least 6 degrees of freedom (ie, translation in the anteroposterior, mediolateral, and tibial axial planes with rotational moments corresponding to abduction-adduction, flexionextension, and internal-external rotation).
The knee joint consists of three independent articulations: the patellofemoral, medial tibiofemoral, and lateral tibiofemoral articulations.
Constraint of the knee joint is complex and dynamic. It depends on the position of the knee, the direction and nature of a given load, and the integrity of its bony and soft tissue restraints.
The knee joint is the largest in the body. Its capsular attachments extend from the suprapatellar pouch proximally to posteromedially and from the posterolateral recesses distally.
- Fibrosis can occur anywhere within these confines and ultimately may lead to loss of motion.
Normal knee motion varies from person to person.
- Most people achieve some degree of recurvatum in full extension, with men averaging 5 degrees and women averaging 6 degrees of hyperextension.
- Normal knee flexion ranges from 140 degrees in men to 143 degrees in women.
Slight losses of flexion are much better tolerated than slight losses of extension.²,²⁴ Full extension is required to allow quadriceps relaxation during the stance phase of gait. Small deficits in terminal flexion may go unnoticed by all but the elite athlete.

PATHOGENESIS

Loss of motion after a knee injury can vary depending on patient predisposition, the extent and nature of the injury, the timing and technique of surgery, and postoperative management (Table 1).
Motion loss in an injured or reconstructed knee can be associated with any of a wide variety of conditions.
A complete understanding of the terminology associated with knee loss of motion is essential to diagnose and communicate the patient’s condition appropriately (Table 2).¹⁵
Each area has its own pathoanatomy and relevant physical findings.

NATURAL HISTORY

Loss of knee motion, particularly extension, can have a tremendous effect on clinical outcomes and overall patient satisfaction.
Pressures across the patellofemoral joint during stance increase from 0% to 30% of body weight when comparing full extension to a 15-degree flexed position.²⁴
These altered mechanics can lead to pain, apprehension regarding motion, and, ultimately, worsening stiffness. Aggressive intercession via a carefully directed physical therapy protocol or appropriate surgical intervention is essential.

Table 1 Pathogenesis of Knee Loss of Motion

Patient factors	Underlying arthritis or neuromuscular imbalance can affect final motion.
Injury pattern	Knee dislocations and multiple-ligament injured knees typically do worse in regard to incidence and extent of motion loss. This may result from the greater extent of injury, surgery, or both.
Timing of surgery	Acute ligament repair has been identified by some as a risk factor for restricted motion postoperatively.⁹,¹⁷,²⁸ Surgery in patients with a robust postinjury inflammatory response and subsequent loss of motion should be delayed, if possible, until normal motion can be achieved.
Technical factors	Improper graft positioning and tensioning will prevent normal knee kinematics and has resulted in motion loss.⁸ Performing concomitant extra-articular procedures has resulted in poorer postoperative motion.⁹
Postoperative factors	Prolonged immobilization, poor rehabilitation, infection, and reflex sympathetic dystrophy all can contribute to motion loss after surgery.

Table 2 Terms Associated with Knee Loss of Motion

Term	Definition
Arthrofibrosis	Diffuse fibrosis or adhesions
ACL nodule	Described as a “cyclops lesion,” this is a dense fibrous scar that can form after bone-patellar tendon-bone autograft for ACL reconstruction. It typically is located anterolateral to the tibial tunnel and can lead to impingement on the intercondylar notch, preventing full extension.
Infrapatellar contracture syndrome	Pathologic fibrous hyperplasia of the anterior fat pad leads to adherence of the patellar tendon to the tibia. This leads, in turn, to limited patellar excursion and can be a cause of patella infera.
Soft tissue calcifications	Calcification and contracture of the capsuloligamentous structures about the knee are a less common, but well-described, cause of motion limitation.
Muscle contracture	Prolonged immobilization, in either flexion or extension, may lead to deficits in motion due to muscle contracture.

PHYSICAL FINDINGS

Knee motion after ligament reconstruction must be monitored vigilantly.
Motion should be compared with the contralateral extremity.
- Any loss of motion in the flexion or extension plane should be considered abnormal.
- A complete examination of the knee is essential and can help determine the etiology.
Inspection
- Swelling or erythema may indicate infection, reflex sympathetic dystrophy, or reinjury.
Palpation
- Effusion may indicate infection or reinjury.
- Allodynia may indicate reflex sympathetic dystrophy.
- Crepitus may indicate fibrosis, soft tissue calcification, or an anterior cruciate ligament (ACL) nodule.
- A “clunk” may indicate an ACL nodule.
Range of motion (ROM)
- Extension loss may indicate posterior capsular contracture, infrapatellar contracture syndrome, medial collateral ligament (MCL) calcification, hamstring contracture, notch impingement, ACL nodule, or graft malposition or tension.
- Loss of flexion may indicate quadriceps contracture, infrapatellar contracture syndrome, graft malposition or tension, patellar entrapment, or suprapatellar adhesions.
- Loss of flexion and extension may indicate arthrofibrosis, infection, soft tissue calcification, infrapatellar contracture syndrome, or graft malposition or tension.

IMAGING AND DIAGNOSTIC STUDIES

Plain radiographs—including anteroposterior, lateral, sunrise, and tunnel views—are the essential first step in imaging.
- Hardware failure, osteochondral defects, MCL calcifications, patellar height, patellofemoral alignment, and tunnel placement can be assessed with these images.
Magnetic resonance imaging (MRI) can be obtained to more clearly evaluate the soft tissues.
- The extent and nature of adhesions, graft position, graft failure, and the presence of an ACL nodule can be clarified by MRI.

DIFFERENTIAL DIAGNOSIS

Arthrofibrosis
ACL nodule
Graft malposition
Infection
Infrapatellar contracture syndrome
Muscle contracture
Reflex sympathetic dystrophy

NONOPERATIVE MANAGEMENT

Rest, ice, and anti-inflammatory medications should be the first-line intervention for any knee with an acute process as found on physical examination, that is, an inflamed, warm, swollen knee with motion loss.
Controlled, guided physical therapy is an excellent tool to help regain motion.
- Quadriceps strengthening, active ROM exercises, use of continuous passive motion (CPM) machines, hanging weights, and extension bracing or casting may all have a role. Each intervention depends on the clinical picture and pathogenesis.
Our rehabilitation protocol for a multiple ligament knee reconstruction typically involves four phases (Table 3).
Manipulation under anesthesia has been used by some to improve postoperative motion.⁶
- Manipulation should be done with caution because the procedure itself can cause an inflammatory reaction and lead to further fibrosis.

SURGICAL MANAGEMENT

Failure to progress with nonoperative treatment is a general indication for operative management.
Identification of the primary cause of the knee stiffness is essential to maximize outcomes.
Indications for surgical intervention include the following:
- Loss of flexion of 10 degrees or more
- Extension deficits of 10 degrees or more
- Failure to improve despite 2 months of intense therapy
The primary goal of operative treatment is restoration of normal knee motion without causing iatrogenic damage to the joint.
In both acute and chronic knee stiffness, resolution of the inflammatory phase of the condition is mandatory before proceeding with surgical intervention.
Epidural or regional anesthesia can be used to assist with postoperative pain control to allow more intensive physical therapy in the immediate postoperative period.
Millett et al¹²,¹⁶ have outlined a systematic nine-step evaluation of potential causes for knee loss of motion, all of which must be addressed whether surgical intervention is performed in an open fashion or arthroscopically.

Open Surgical Treatment

In severe cases of loss of motion of the knee, open releases may be indicated.

Table 3 Rehabilitation of Knee Loss of Motion

Goals	Program
Phase I: 0-6 wk
Maximum protection of grafts during early healing phase	Full-leg hinged knee brace locked in extension for 3 wk; may begin passive ROM exercises in neutral wk 4-6 and beyond
Maintain patellar mobility	Patellar mobilization exercises
Maintain quadriceps tone	Straight-leg raises in brace
Control pain and swelling	Cryotherapy
Maintain full passive extension	Non-weight bearing with crutches
Phase II: 6-12 wk
Increase flexion ROM	Begin full flexion in brace
Initiate weight bearing	Partial weight bearing; slowly progress to full weight bearing by postoperative wk 10
Quadriceps strengthening	Stationary bike, patella mobilization, prone hangs
Proprioceptive training	Closed chain strengthening after full weight bearing
Phase III: 3-6 mo
Increase knee flexion to within 10 degrees of uninvolved side by end of 6th mo	Aggressive ROM exercises
Improve strength and proprioception
Incorporate functional drills	Advance proprioceptive training
Phase IV: 6-12 mo
Return to sport if minimal pain and swelling, functional strength within 10% of uninvolved side, successful participation in practice drills	Agility drills/sport-specific practice sessions without contact at 6th mo
Multidirectional functional brace recommended for sports up to 18 mo

Indications for open débridement and soft tissue release typically include patients with severe arthrofibrosis or patients who have failed previously attempted arthroscopic releases.
Our general approach is to restore flexion by releasing capsular contractures, by lysing intra-articular fibrosis, and by mobilizing the extensor mechanism.
Extension is restored by addressing notch pathology, posterior capsular contractures, and anterior fibrosis.

Positioning

The patient is placed supine on the operating table.
A pneumatic tourniquet is placed high on the thigh over a cotton wrap. It is not routinely inflated.

Preoperative Planning

Examination under anesthesia is performed.
Flexion, extension, and patellar mobility should all be assessed preoperatively.
With the patient fully anesthetized, the hip should be flexed to 90 degrees.
Gravity should then be allowed to flex the knee. This reveals the true flexion limit.
With the hip extended, the heel should be supported; the extension limit is then measured.
Patellar mobility should then be documented with regard to superior—inferior glide, mediolateral glide, and patellar tilt.
Comparison to the normal, uninvolved knee is extremely useful.