The interphalangeal joint of the hallux

Dorsal impingement with spur formation similar to that seen in the first metatarsophalangeal (MP) joint can occur in this joint. It can be a sign of degenerative joint disease (DJD) but usually is secondary to stiffness and lack of motion in the adjacent MP joint. When hallux rigidus forms in the first MP joint, the interphalangeal (IP) joint will be forced into excessive dorsiflexion in an attempt to compensate for the lack of motion in the proximal joint. At times this can be dramatic. I once saw a female dancer who was born with congenital ankylosis of both first MP joints. They were totally rigid. She had Grecian (Morton’s) feet with short first rays and had developed 90 degrees of dorsiflexion in her IP joints so that she had a full demi-pointe relevé. Rigidity in this joint can be treated similarly to the condition found in the first MP joint. One should remember, however, that this joint is forgiving, and surgery is rarely necessary.

The lesser metatarsophalangeal joints

Dorsal impingement in these joints usually is associated with Freiberg’s disease.¹ This condition is no more common in athletes and dancers than it is in the general population. One should remember, however, that it can be symptomatic for as long as 6 months before it appears on x-ray and should be considered in unexplained metatarsalgia in young patients. A bone scan or magnetic resonance imaging (MRI) usually will confirm the diagnosis before plain radiographic changes are evident. Freiberg’s infarction comes in the following four variations.¹

Type I

The head of the metatarsal (MT) dies and then heals by “creeping substitution” (Phemister²). In this form it may heal completely, with little or no collapse, leaving the articular surface intact and almost as good as it was before the event occurred. Surgery often is not necessary.

Type II

The head collapses during revascularization and the articular surface settles and remains intact, but peripheral osteophytes form along the dorsal margin of the joint, limiting dorsiflexion. This type is amenable to a dorsal clean-out (cheilectomy), which should leave the joint intact and restore dorsiflexion. (The surgeon should remember to remove more bone than he or she thinks is necessary when performing this operation.)

Type III

The head collapses and the articular surface loosens and falls into the joint, leaving the joint totally destroyed. Obviously simply removing the osteophytes will not suffice in this case—an arthroplasty is required. All the necrotic bone must be excised from the MT head and all the dorsal osteophytes must be removed. Usually the plantar portion of the head is left when this has been done. The surgeon should be generous in the excision to permit full dorsiflexion later, but the entire MT head should not be removed. Either a dorsiflexion osteotomy of the MT head or a capsular arthroplasty, similar to the one described for use in the first MP joint, can be useful in this situation.

Type IV

Multiple heads are involved in the process (Fig. 2-1). This type is rare and actually may be a form of epiphyseal dysplasia. Each MT head must be evaluated and treated individually.

Figure 2-1 A rare case of multiple Freiberg’s disease.

A Freiberg-like syndrome can occur in the fifth MT head following a nondisplaced or minimally displaced fracture of the distal MT shaft, similar to the “boxer’s fracture” of the fifth metacarpal (Fig. 2-2).

Figure 2-2 “Boxer’s fracture” of the distal fifth metatarsal (arrow).

Lesser MP joint instability

Metatarsalgia is not common in the young, healthy athletic population. When it is encountered, one should suspect either early Freiberg’s disease or MP instability.¹ This subtle problem often goes unrecognized because the x-rays are normal. The patient presents with isolated metatarsalgia. There is plantar tenderness under the MT head and dorsal tenderness where the phalanx subluxes on top of the head when the patient relevés or goes up on the ball of the foot. The subluxated phalanx pushes the head of the metatarsal downward, producing the metatarsalgia, the so-called dropped metatarsal. It is recognized easily on physical examination if one remembers to observe for it. The Lachman test of the MP joint will be positive.¹ The base of the proximal phalanx is grasped in the fingers, and a dorsal-plantar force is applied. The instability is recognized easily when the phalanx subluxes on the top of the MT head (Fig. 2-3).

Figure 2-3 Lachman test of the metatarsophalangeal (MP) joint.

Conservative treatment consists of padding to unload the painful MT head and taping or wearing a toe retainer to try to control the instability (Fig. 2-4). It often is a frustrating situation for the dancer or athlete because he or she does not want to undergo surgery, but once the ligaments and plantar plate are stretched, they can be tightened again only by surgery. The surgical options for this problem in a dancer are tricky. The usual operations for this condition (stabilizing procedures such as the Girdlestone-Taylor operation³) are inappropriate for athletes because they stabilize the joint but also limit dorsiflexion—an unacceptable solution for dancers, gymnasts, and so forth. We have had success in a limited number of dancers and athletes with a resection arthroplasty and partial syndactyly, especially in the fourth MP joint, which seems especially prone to this problem. As previously noted, one should not remove too much of the proximal phalanx (one-fourth to one-third at most), and one should remove the plantar condyles of the MT head, use a toe wire, and remove it early (2 weeks).

Figure 2-4 Taping to control metatarsophalangeal (MP) instability.

Idiopathic synovitis

Idiopathic synovitis⁴ is characterized by MP swelling, the so-called sausage toe. Its cause is controversial. (It usually is not caused by systemic inflammatory diseases, but of course these must be ruled out.) It usually is associated with laxity of the joint and MP instability. Whether the looseness irritates the joint and leads to chronic synovitis or the synovitis loosens the joint is not known. Conservative therapy involves stabilizing the joint by using tape or toe retainers (see Fig. 2-4); having the patient reduce activities and take anti-inflammatory medication; and, if necessary, giving the patient one or two (at most) intra-articular injections of steroids. If this fails, exploration and appropriate surgery are indicated. Surgical options include (1) extensor tendon lengthening with resection of the plantar condyles of the MT head, (2) Girdlestone-Taylor³ procedure, (3) DuVries-type arthroplasty,³ and (4) resection arthroplasty with partial syndactyly to the adjacent digit.

Medial midfoot impingements

True impingements in the midfoot are rare. Occasionally, accessory ossicles can be seen between the bases of the metatarsals or the cuneiforms; symptoms may warrant their removal. These bones, more often than not, will be asymptomatic.

An isolated osteophyte on the dorsum of the midfoot occasionally can cause entrapment of the deep peroneal nerve or irritation of the extensor hallucis longus (EHL) tendon as they pass over it. Initially, extra padding on the undersurface of the tongue of the shoe may resolve pain. If this fails, removal of the osteophyte may be necessary. The painful accessory navicular is not due to an impingement and is discussed in Chapters 8, 14, and 27.

Lateral midfoot impingements

In the lateral midfoot, three related conditions are a combination of impingement and subluxation: (1) derangement of the cuboid—base of the fourth and fifth metatarsal joints, (2) cuboid subluxation, and (3) sinus tarsi syndrome.

Subluxation of the cuboid⁵ and derangement of the cuboid—base of the fourth and fifth metatarsal joints—often are seen together. The subluxing cuboid is a common but poorly recognized condition. It presents as lateral midfoot pain and an inability to “work through” the foot. Pressing on the plantar surface of the cuboid in a dorsal direction is painful. The normal dorsal-plantar joint play is reduced or absent when compared with the uninjured side. (Because of this immobility, the condition sometimes has been referred to as a “locked cuboid.”) Often there is a shallow depression on the dorsal surface, a palpable fullness on the plantar aspect of the cuboid, and subtle forefoot valgus. Documentation by x-ray, computed tomography (CT) scan or MRI is difficult because of the normal variations found in the relationship between the cuboid and its surrounding structures. The diagnosis must be made on the basis of the history and physical findings. Treatment involves recognition of the pathology and manual reduction by a therapist or physician familiar with the condition and follow-up to be certain that it remains in place. Therapists and orthopaedists involved in the care of athletes and dancers should be aware of the subluxed cuboid and be able to recognize it when it occurs. When the cuboid subluxes plantarward, the bases of the fourth and/or fifth metatarsals often are elevated, causing the head of the fourth metatarsal to be depressed (Fig. 2-5, Table 2-1).

Figure 2-5 A “dropped” fourth metatarsal head resulting from elevation of its base.

From Marshall PM, Hamilton WG: Am J Sports Med 20:170, 1992.

Table 2-1 Cuboid subluxation

There usually are two types of cuboid subluxations: acute and chronic/recurrent. Treatment consists of recognition and manual reduction by a therapist familiar with the condition. The cuboid then must be held in place by taping and padding for several weeks to prevent recurrence. If the subluxation has gone unrecognized and the joint has been subluxed for any length of time, reduction can be difficult. The forefoot valgus must be corrected and the lateral column lengthened manually before the reduction can be performed. In the chronic condition, it may not be possible to keep the cuboid reduced if it goes in and out at random. In these cases, athletes often can be taught to reduce the subluxation themselves (Fig. 2-6).

Figure 2-6 Reduction of a subluxed cuboid by the patient.

Sinus tarsi syndrome⁴ is a controversial condition that produces pain deep in the sinus tarsi that increases with activity and is exacerbated by impact (jumping and running) and pronation. It is often, but not always, a sequel to a sprained ankle. On physical examination, there is discrete tenderness, or a “trigger point” deep in the sinus tarsi, and forceful abduction-pronation of the heel and midfoot may be painful. The condition usually can be confirmed with an injection of 0.5 ml of lidocaine into the trigger point. If the pain is relieved by the local anesthetic, a second injection of 0.15 ml of corticosteroids often can be highly effective. The condition is thought to have several etiologies: (1) soft tissue entrapment or partial tear of the interosseous talocalcaneal ligament, (2) osteophyte impingement (Fig. 2-7), (3) neural entrapment (motor nerve to the extensor digitorum brevis [EDB]), (4) degenerative arthrosis, and (5) arthrofibrosis. It can be difficult to differentiate this syndrome from subtalar dysfunction, and osteophytes can be found in the sinus tarsi that are not causing symptoms. The two areas are anatomically close together. One of the best ways to differentiate one from the other is to pay close attention to subtalar motion. Mann and Coughlin³ have shown how important subtalar motion is to normal foot mechanics. Subtle loss of this motion, such as arthrofibrosis of the subtalar joint from bleeding into the joint in conjunction with an ankle sprain, can cause residual symptoms after the sprain has healed.

Figure 2-7 Sinus tarsi syndrome; note osteophytes (arrow).

Conservative treatment consists of anti-inflammatory medication, physical therapy, a medial heel wedge or arch support to open up the sinus tarsi, and, if necessary, the previously mentioned cortisone injection. If symptoms persist and the diagnosis has been confirmed with lidocaine injection, surgical exploration and clean-out is indicated. This is one area in which an injection—if placed in the right spot—often is dramatically effective and will avoid surgery. Finally, the sinus tarsi syndrome often is found in conjunction with lateral ankle ligament laxity, and, in these cases, sinus tarsi exploration and debridement should be considered if ankle ligament reconstruction is planned. More about the subtalar joint can be found in Chapter 15.

The ankle

When considering ankle impingement, one should remember the basic anatomy of the ankle. The talus sits sidesaddle on the os calcis so that the axis of the talus is roughly in line with the first web space of the foot and the axis of the os calcis is in line with the fourth web space (Fig. 2-8). In dorsiflexion, bony impingement occurs anteromedially between the neck of the talus and the anterior lip of the tibia. In plantarflexion, bony impingement occurs posterolaterally between the os calcis and the posterior lip of the tibia. Therefore anteromedial and posterolateral problems usually are associated with bony impingement, whereas anterolateral and posteromedial problems usually are soft tissue in origin (there is no bony impingement in these areas). The anterior ankle is an extremely common location for impingement, but impingements can be found in all quadrants around the ankle: anterior, lateral, posterior, and medial.

Figure 2-8 Axis of talus versus axis of os calcis.

Anterior (medial, central, lateral)

Anteromedial ankle pain often comes from impingement of the anterior portion of the medial malleolus against an impingement spur on the medial shoulder of the talus. This spur is hard to see on x-ray because it cannot be visualized on standard lateral radiographs. However, nonweight-bearing, oblique x-rays of the foot may detect these spurs. The spur often can be palpated on physical examination and should be looked for in any anterior ankle clean-out. It is easy to miss, the “hidden spur.” To visualize and resect this spur arthroscopically, the surgeon must hold the ankle in dorsiflexion.

Anterocentral is the location of the classic anterior ankle impingement. It comes in the following four types: