Chronic compartment syndrome, or exercised induced compartment syndrome, is an uncommon cause of leg pain in athletes who participate in repetitive impact exercises.   The muscles, nerves, and vessels of the lower extremities are contained within four compartments; these include the anterior, lateral, superficial posterior, and deep posterior compartments. During exercise muscle weight can increase by up to 20% which forces the surrounding fascia to expand to accommodate the increased volume. When the fascia fails to expand to accommodate the increase in muscle volume compartmental pressures can increase above diastolic blood pressure.  As a result, arteriole blood is decreased and can become insufficient to meet the needs of the muscle. Inadequate tissue perfusion causes ischemia and increasing pain with activities. Athletes describe the pain as predictable, deep, and achy pain that is relieved with rest. Physical exam in the office setting is almost always normal. An MRI or bone scan is often ordered to rule out a stress fracture and medial tibial stress syndrome. The diagnosis of chronic compartment syndrome is made by measuring the resting and post-exercise compartment pressures. Normal compartment pressures are between 0 and 10 mm Hg. Chronic compartment syndrome can be diagnosed with a resting pressure > 15 mm Hg,  1-minute post exertion pressure > 30, or a 5-minute postexertional pressure > 20.  Surgical fasciotomy is the definitive treatment of choice with a return to sports rate of over 90%.

The term medial tibial stress syndrome (MTTS) describes a condition of periostitis at the muscular attachment site along the posterior medial tibia. MTTS causes exertion pain in athletes that is relieved with rest. Risk factors may include excessive foot pronation, hindfoot varus, and changes in exercise routine including intensity and duration.  On exam, pain to palpation may be noted over the posterior medial tibia. Pain may increase with resisted plantar flexion and with toe raises.  MRI or bone scan will likely show increased activity along the posteriormedial tibia. Treatment is usually successful with a period of rest, immobilization, and NSAIDs.

Stress fractures of the tibia occur when repetitive stress is placed on bone that fails to respond to mechanical loads placed upon it. This failure results in the accumulation of microfractures that can result in a stress fracture.  Women are 12 times more likely to have a stress fracture than males and 72% of stress fractures occur in runners. Athletes with stress fractures complain of increasing pain over the middle to distal posteriormedial tibia. Physical exam reveals localized boney tenderness and patients may be unable to perform a single leg hop. Radiographs are often negative, particularly early in presentation. MRI will show bone edema, and in some cases, a fracture line. Treatment is usually successful with a period of rest, immobilization, and NSAIDs. Athletes should not return to play until daily activities are pain free and no tenderness to palpation is present over the previous fracture site.

Popliteal artery entrapement syndrome (PAES) is a rare condition caused by a partial or completely obstructed popliteal artery. This may be caused by a congenitally abnormal medial head of the gastrocnemius muscle compressing on the popliteal artery. Functional popliteal artery compression has also been found to be caused by compression of the popliteus muscle during repetitive use. Symptoms include intermittent claudication that worsens with activity and is relieved with rest.  PAES occurs bilaterally in up to 25% of patients which unlike chronic compartment syndrome which occurs in up to 95% bilaterally. Decreased pulses and vascular skin changes are rarely found with PAES. Computed tomographic angiogram findings help to confirm the diagnosis. Vascular surgery consultation is the most appropriate initial step when PAES is suspected.

References
Meininger AK, Turnipseed WD, Hutchinson MR. Recognition and treatment of leg pain in athletes. Orthopedic Online Journal 2009. 7(2).

Fraipoint MJ, Adamson GJ. Chronic Exertional Compartment Syndrome. J Am Acad Orthop Surg 2003; 11; 268-276.

X-ray findings that include fused sacroiliac joints, vertebral body squaring, interspinous ligament calcification, flowing syndesmophytes (bony growth that originates inside a ligament), and posterior element fusion are consistent with the diagnosis of Ankylosing Spondylitis. Ankylosing Spondylitis (AS) is a seronegative spondyloarthropathy of unknown etiology that primarily affects the axial skeleton. HLA-B27 is positive in 90% of patients with AS. Enthesitis or enthesopathy is the main clinical feature of AS that helps differentiate it from rheumatoid arthritis. Enthesopathy is inflammation at the tendon and ligament insertion that leads to bony destruction, surrounding soft tissue ossification, and new bone formation with eventual joint ankylosis. Ankylosis and loss of spine motion leads to syndesmophyte formation with the characteristic “bamboo spine” appearance on lateral x-ray. 1,2

Systemic manifestations of AS may include uveitis, cardiac abnormalities, and a susceptibility to Klebsiella pneumoniae synovitis. Musculoskeletal manifestations may include bilateral sacroiliitis, progressive kyphosis, cervical spine fractures, and hip and shoulder arthritis. Low bone density and osteoporosis is found in up to 62% of patients with AS explaining the higher incidence of compression fractures. The modified New York Criteria is used to diagnose AS and includes 1. Lower back pain for at least 3 months which improves with exercise and is not relieved with rest 2. Limitation with lumbar spine motion 3. Chest expansion decreased relative to normal values for same age and sex 4. Radiographic criteria of bilateral sacroiliitis grade 2-4 or unilateral sacroiliitis grade 3-4. 1,2

References

1. Kubiak EN, Moskovich R, Errico TJ, Cesare D. Orthopedic Management of Ankylosing Spondylitis. JAAOS 2005; 13: 267-278.

2. Ankylosing Spondylitis. http://www.orthobullets.com. Accessed on 1/14/17.

The two most common post-operative complications following hip arthroplasty include leg length discrepancy and hip dislocation. Leg discrepancy after hip arthroplasty is relatively common with an incidence as high as 20 to 50%. Maintaining equal leg lengths intra-operatively is a challenge orthopedic surgeons face to ensure normal gait and hip function post-operatively. In order to achieve increased hip stability the surgeon may choose to use a larger prosthesis which may result in an increased leg length compared to the contralateral side. However, leaving an extremity shortened may result in post-operative hip instability which is far more devastating. 1, 2

The pre-operative assessment should carefully screen for leg length discrepancies which include a hip contracture, pelvic obliquity, and congenital discrepancies. Pre-operative hip x-rays are used by orthopedic surgeons to template the hip and determine the appropriate size of implants that should be used during surgery. Achieving hip stability generally takes priority during surgery and a small length discrepancy is thought to be acceptable in most cases. Few patients with an increased leg length will ever notice or have symptoms. However large discrepancies may cause post-operative nerve injury to the leg, gait disorders, and lower back and hip pain. A large leg length discrepancy after total hip arthroplasty is a significant source of dissatisfaction after hip arthroplasty and one of the most common reasons for lawsuits against orthopedic surgeons. Up to 10 mm or approximately 3/8 inch leg length discrepancy is well tolerated in most patients. A > 1 cm, or approximately 7/16 inch, discrepancy is noticeable in up to 50% of patients; of those patients 15-20% require shoe correction to resolve symptoms caused by the discrepancy. Small leg length discrepancies can be treated with heel lift shoe inserts but a lift greater than 3/8 of an inch generally doesn’t fit well in a shoe. A 7/16 of an inch or greater discrepancy generally requires a shoe lift at the shoe bottom. A discrepancy greater than 2 cm generally requires surgical correction. Muscle tightness, pelvic tilt, and altered gait after hip arthroplasty causing leg length discrepancies usually corrects within 6 months following surgery so generally shoe lifts aren’t used until after this time period. 1,2

References

1. Maloney WJ, Keeney JA. Leg Length Discrepancy after Total Hip Arthroplasty. The Journal of Arthroplasty 2004. Volume 19, number 4. 108-110.

2. Desai AS, Board TN. Leg length discrepancy after total hip arthroplasty: a review of literature. Curr Rev Musculoskelet Med. 2013 Dec; 6(4): 336–341.

The most common conditions seen by foot and ankle specialists include the lesser-toe deformities (e.g., mallet toes, hammer toes, and claw toes). These toe deformities are often attributed to the wearing of fashionable shoes because they are more prevalent in women and with increasing age. An understanding of toe anatomy is necessary to identify and appropriately treat these conditions. Each lesser toe is composed of 3 bones, the proximal, middle, and distal phalanges, which are connected by the metatarsophalangeal (MTP), proximal interphalangeal (PIP), and distal interphalangeal (DIP) joints, respectively. The joints are held together by the collateral ligaments, the plantar plate, the joint capsule, and the surrounding tendons. The flexor digitorum longus (FDL) tendon attaches to the distal phalanx and flexes the DIP joint. The flexor digitorum brevis (FDB) tendon divides around the FDL, inserts on the middle phalanx, and flexes the PIP joint. The extensor digitorum longus (EDL) tendon and the extensor digitorum brevis (EDB) tendon are attached to the middle and distal phalanges. These extensor tendons attach to the plantar capsule of the MTP joint with a sling of tissue. This sling mechanism helps the tendons to exert a strong extension force at the MTP joint.

Of the lesser-toe deformities, hammer toe is the most common. Hammer toe is characterized by plantar flexion of the middle phalanx on the proximal phalanx (PIP joint flexion). The MTP joint is often hyperextended, and the DIP joint may be flexed, extended, or in a neutral position. The hyperextended MTP joint is caused by an over-pull of the EDL tendon and an imbalance of the intrinsic muscles. The etiology of a hammer-toe deformity is multifactorial and may include hallux valgus, trauma, arthritis, a contracted FDL, neuromuscular abnormalities, and postural abnormalities. The longer lesser toe is most commonly affected, but the deformity also may occur in the other lesser toes. Pain from a hammer-toe deformity occurs with contact pressure on the PIP joint. This pressure often makes it difficult for patients to wear shoes, and a hypertrophic callus can develop on the dorsal aspect of the digit from repetitive contact.

PIP joint flexion can be either fixed, semiflexible, or flexible. The degree of rigidity is important to identify because this helps to determine the course of treatment. A deformity that can be corrected passively is considered flexible. A deformity than cannot be corrected passively or with ankle plantar flexion is considered rigid. Nonsurgical management focuses on relieving dorsal pressure over the PIP joint, relieving pressure off of the corresponding metatarsal head, and reducing pressure off of the distal tip of the toe. Nonoperative treatment includes shoes with a high toe box, low-heeled shoes, and a silicone toe sleeve. Patients with a fixed deformity may be treated with a toe crest that elevates the toe, or a foam toe cap that reduces pressure on the tip of the toe. There are a number of surgical procedures available to correct a hammer-toe deformity if nonoperative treatment is unsuccessful. These procedures include soft-tissue releases, tendon transfers and releases, joint resection, arthroplasty, and arthrodesis, or a combination of these procedures. A fixed deformity will not be corrected with a soft-tissue procedure alone, and will require an osseous corrective procedure such as a PIP joint arthroplasty or arthrodesis.

Suggested Reading
Coughlin MJ. Lesser-toe abnormalities. J Bone Joint Surg Am. 2002;84(8):1445-69.

Coughlin MJ, Dorris J, Polk E. Operative repair of the fixed hammertoe deformity. Foot Ankle Int. 2000 Feb;21(2):94-104.

Shirzad K, Kiesau CD, DeOrio JK, Parekh SG. Lesser toe deformities. J Am Acad Orthop Surg. 2011 Aug;19(8):505-14.

The ulnar collateral ligament (UCL) is the primary stabilizer against valgus stress and volar subluxation at the MCP joint. Injury can cause the ligament to be stretched, partially torn, or completely torn. Injury to the ligament can weaken grip and pinch strength and cause disability. The ability to perform tasks such as turning a door knob or a key, writing, and grasping objects can be severely impaired with an incompetent UCL. Acute injury typically occurs with a sudden abduction and valgus force to the MCP joint. The forceful valgus stress typically causes an avulsion of the UCL from the proximal phalanx. The injury is classically described as a “skier’s thumb” because the injury commonly occurs in skiers who fall with their pole in hand. However, any type of fall or thumb collision can result in a UCL tear.

The UCL consists of 2 distinct bundles, the proper and accessory collateral ligaments. The proper collateral ligament is located dorsally and is taut in flexion and lax in extension. The accessory collateral ligament, located on the volar aspect of the MCP joint, is taut in extension and lax in flexion. Valgus laxity in both flexion and extension indicates disruption of both the proper and accessory collateral ligaments of the UCL. A Stener lesion can occur when an avulsion of the UCL occurs proximally and the UCL is blocked from healing at its site of insertion by the adductor aponeurosis. A Stener lesion may be felt as a tender mass on the ulnar side of the MCP joint.

To determine the degree of UCL laxity, the thumb metacarpal is stabilized with one hand while a valgus stress is placed on the MCP joint with the other hand. Stability should be tested in full extension and in 30° of flexion to determine the stability of both the proper and accessory collateral ligaments. Examination of the contralateral hand should be performed to compare stability and to better determine if a Stener lesion may be present.

Radiographs may show an osseous avulsion of the metacarpal or the proximal phalanx. An avulsion may represent a true avulsion fracture of the UCL, but many are actually isolated fractures that are associated with a complete UCL rupture. MRI is the most accurate study in detecting UCL ruptures. MRI is recommended if the diagnosis is uncertain clinically or if a Stener lesion is suspected. In this case, the painful bump on the ulnar side of the proximal phalanx is suspicious for a Stener lesion and, therefore, MRI should be ordered.

Treatment: Nonoperative treatment of stable partial UCL ruptures typically includes immobilization with a thumb spica cast for 4 to 6 weeks. Grip and pinching activities can be initiated at 6 weeks. Generally, partial tears go on to heal without residual disability. Surgical treatment is indicated in patients with complete or unstable UCL tears. Additionally, indications include >35° of valgus laxity (normal averages 6° in extension and 12° to 15° in flexion), a displaced or rotated fracture, and a suspected Stener lesion. Valgus laxity of >15° compared with that of the contralateral side and a “soft” end point with valgus stress may also indicate a complete UCL rupture and the need for surgical repair.

Suggested Reading
1. Tang P. Collateral ligament injuries of the thumb metacarpophalangeal joint. J Am Acad Orthop Surg. 2011 May;19(5):287-96.
2. Rhee PC, Jones DB, Kakar S. Management of thumb metacarpophalangeal ulnar collateral ligament injuries. J Bone Joint Surg Am. 2012 Nov 7;94(21):2005-12.