Hammer toes, mallet toes , and claw toes are sagittal plane deformities of the lesser toes. They are common and vary from asymptomatic minor deformities to painful disabling ones. Consultation is generally sought because of shoewear difficulties or pain.

There is some overlap in aspects of these deformities, although currently agreed definitions for these deformities is discussed in this chapter. The terms hammer toe and claw toe are used somewhat interchangeably.

Mallet toe deformity is generally defined as a flexion deformity at the distal interphalangeal (DIP) joint of the toe. Mallet toes often involve the longest lesser toe.

Hammer toe deformity is defined as primarily a flexion deformity at the proximal interphalangeal (PIP) joint sometimes accompanied by a metatarsophalangeal (MTP) joint extension deformity. A hammer toe may involve several toes or just 1 toe and most commonly has a mechanical cause.

A crossover toe deformity is likely an extension of a hammer toe deformity. However, a hammer toe is a purely sagittal plane deformity, while a crossover toe has a sagittal plane deformity as well as an axial plane deformity.

A claw toe deformity is defined as a toe where the primary deformity is a hyperextension deformity at the MTP joint. There is often a PIP joint flexion deformity as in hammer toes, although claw toes commonly will have a DIP joint flexion deformity. Claw toes will more commonly be neurologic in nature (e.g., Charcot-Marie-Tooth) and more commonly involve several toes.

All the toe deformities are further classified as “rigid” or “flexible” deformities, depending on whether the deformity is passively correctable.

The primary static restraints of the toe are the thick plantar plate, plantar aponeurosis, joint capsule, and collateral ligaments. These structures allow the DIP joint and PIP joint to flex but block extension past neutral while they allow the MTP joint to flex and extend during the normal gait cycle.

The dynamic stabilizers of the toes can be divided into intrinsic (originating in the foot) and extrinsic (originating in the leg) muscles. The tibial nerve innervates all the intrinsic muscles as well as the extrinsic flexor muscles, while the peroneal nerve innervates the extrinsic extensor muscles.

The extrinsic muscles terminating at the lesser toes are the extensor digitorum longus (EDL) and flexor digitorum longus (FDL). The intrinsic muscles terminating at the lesser toes comprise the 7 interosseus muscles, 4 lumbricals, and abductor digiti minimi as well as the extensor digitorum brevis (EDB) and flexor digitorum brevis (FDB).

The EDL runs over the dorsal aspect of the MTP joint and invests the extensor hood over the proximal phalanx before inserting on both the middle and distal phalanx.

The EDL is a strong extensor at the MTP joint through its attachments at the extensor hood. However, it can extend the PIP and DIP joints only when the intrinsic muscles hold the proximal phalanx in a neutral or flexed position at the MTP joint.

The FDL runs under the metatarsal head dorsal to the FDB and inserts on the distal phalanx. As a result of having no direct connection to the proximal phalanx, the FDL serves as a strong flexor of the DIP joint but is a weak flexor of the MTP joint.

The EDB is an intrinsic muscle that sends a slip to the 2nd, 3rd, and 4th toes. The EDB tendon inserts into the lateral aspect of the EDL tendon and weakly extends the PIP joint.

The FDB runs plantar to the FDL tendon through most of its course, splitting into 2 terminal slips at the level of the proximal phalanx, and traveling over either side of the FDL before inserting on the middle phalanx. The FDB is a weak flexor of the MTP joint.

The 4 lumbricals originate from the FDL tendon, run under the intermetatarsal ligament, and insert on the tibial side of the plantar plate and the extensor hood at the level of the MTP joint. They are strong flexors of the MTP joint when the joint is in neutral but quickly lose their mechanical advantage as the joint is extended.

Prior to inserting on the extensor hood, the 7 interosseus muscles of the foot, 4 dorsal and 3 plantar, run dorsal to the intermetatarsal ligament but plantar to the axis of rotation of the metatarsal head when the toe is in a neutral position. As the MTP joint dorsiflexes, the tendons of the interossei will travel dorsally with the extensor hood closer to the axis of rotation of the joint and then eventually dorsal to the axis of rotation, converting them from flexors to extensors of the joint.

At the DIP joint, the FDL provides a strong flexion force, while the EDL provides a relatively weak extension force, and then only if the intrinsic muscles are able to hold the proximal phalanx in a neutral alignment.

At the PIP joint, the FDL provides weak flexion, while the FDB provides strong flexion through its direct insertion on the middle phalanx. As at the DIP joint, the EDL provides a relatively weak extension force if the intrinsic muscles are able to hold the proximal phalanx in a neutral alignment.

At the MTP joint, the EDL is a strong extensor. The FDL and FDB, with no direct insertions on the proximal phalanx, provide weak flexion power, while the lumbricals and the interossei provide the majority of the flexion power to oppose the EDL.

The strong pull of the intrinsic muscles is dependent on the position of the proximal phalanx. With MTP joint extension, the flexion power is greatly diminished, as the interossei muscles become extensors of the joint, as their mobile tendons travel dorsally, and the lumbrical muscles lose their mechanical advantage.

A mallet toe is a flexion deformity at the DIP joint. Through trauma or impingement of tight shoes, the EDL tendon at the DIP joint attenuates or ruptures, creating a strong unopposed flexion by the FDL tendon at the DIP joint.

A hammer toe (a flexion deformity at the PIP joint) is thought to occur as the result of impingement of the end of the toe against the shoe or MTP joint synovitis causing the MTP joint to dorsiflex. This results in the FDB and FDL strongly flexing the PIP joint without the EDL being able to oppose the flexion, as it can extend the joint only when the proximal phalanx is neutrally aligned.

A claw toe is notable for dorsiflexion deformity at the MTP joint and flexion deformity at the PIP joint and DIP joint. It often involves more than 1 toe and has a neurologic origin. It develops as the extrinsic muscles overpower the intrinsic muscles of the foot; the EDL overpowers the lumbrical and interossei muscles, creating dorsiflexion at the MTP joint. As the dorsiflexion deformity increases, the lumbricals lose their ability to flex the MTP joint. The interossei tendons pass dorsal to the axis of rotation of the MTP joint and function as extensors, leaving the FDL and FDB overwhelmed by the EDL extension force at the MTP joint, resulting in MTP joint extension deformity. With the resultant MTP dorsiflexion deformity, the FDL and FDB flex the PIP joint, and the FDL flexes the DIP joint without the counterbalancing extension by the EDL, which cannot extend these joints with the MTP joint dorsiflexed.

A history should elicit as precisely as possible the patients’ problem, as they see it. If they are complaining primarily of pain, the exact location as well as the degree and frequency of discomfort should be recorded.

The shoewear requirements for the patient’s occupation as well as the patient’s shoewear desires are important to understand, as successful nonoperative treatment will usually require shoewear modification.

Lesser toe deformities usually present with toe complaints in 1 of 3 areas: The tip of the toe, the dorsal aspect of the PIP joint, or under the foot at the MTP joint. These areas should be evaluated for evidence of callus or corn formation.

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  The pain at the tip of the toe results from the shoe rubbing on the toe or the relatively unpadded toe tip resting on the ground or grabbing the ground as the patients walk.

  
  
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  The PIP joint pain occurs from the shoes rubbing on the toe box.

  
  
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  Pain at the metatarsal head occurs as the proximal phalanx dorsiflexes on the metatarsal head, increasing the plantar pressures on the metatarsal head. In addition, as the proximal phalanx dorsiflexes, it takes the plantar fat pad with it, relatively uncovering the metatarsal head.

Checking the ankle range of motion and strength is an important part of the examination. Equinus deformity or weakness of the anterior tibial muscle will result in the recruitment and compensatory overpull of the EDL tendon, potentially leading to a claw toe deformity.

The push-up test involves passively pushing up under the metatarsal heads on the non-weight-bearing foot until the ankle is brought to neutral. In the case of a flexible toe deformity, the toes should correct to a neutral alignment, whereas in a rigid deformity, they will not.

Most lesser toe deformity problems will improve with the general recommendation of shoewear modification, specifically switching to a shoe with a wider &/or higher toe box.

Other nonoperative treatments target the specific area of discomfort. Pain under the metatarsal heads can be improved with a metatarsal pad.

PIP joint discomfort can be treated with various toe pads or a Budin splint to try to hold the dorsally prominent PIP joint down.

Discomfort at the tip of the toe can often be improved with a soft toe cap or a toe crest that fits under the toes and helps relieve the pressure on the tip of the toe.

As a rule, most flexible toe deformities tend to respond much better to conservative care than do rigid deformities.

The number 1 predictor of patient satisfaction after toe surgery is realistic preoperative expectations. Toe surgery will generally lead to a toe that is shorter and more swollen with less motion and less volitional control. This is the surgical trade-off for a toe that is less painful, straighter, and “shoeable.” The toe is not “normal.”

Toe surgery also carries significant neurovascular risk, especially if the patient has peripheral vascular disease, has had previous toe surgery, or is in need of an extensive toe procedure. A common complication of surgery is some recurrence of deformity.

Mallet toe

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  A flexible mallet toe is generally treated with a simple flexor tenotomy from a plantar approach with pinning of the DIP joint for 3 weeks.

  
  
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  A fixed mallet toe deformity is generally treated with a DIP joint resection followed by pinning of the DIP joint for 6 weeks ± a flexor tenotomy, depending on the degree of correction obtained with the bony resection.

Hammer toe

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  A flexible hammer toe deformity can be treated with a flexor to extensor tendon transfer. The FDL tendon is released from its insertion at the distal phalanx through a plantar approach. The tendon is then split in 2 and passed dorsally at the level of the proximal phalanx. The 2 limbs are reunited on the dorsal aspect of the toe and secured to the EDL. This FDL transfer removes the deforming flexion force of the FDL tendon at the DIP joint and PIP joint and establishes a secure attachment of the FDL to the proximal phalanx, making the FDL a strong flexor at the MTP joint.

  
  
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  A fixed hammer toe deformity is treated with a dorsal approach to the PIP joint with resection of the PIP joint and pinning of the toe for 6 weeks.

Claw toe

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  A flexible claw toe deformity is generally treated similarly to a flexible hammer toe deformity with a flexor to extensor tendon transfer.

  
  
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  A fixed claw toe deformity is generally treated in a stepwise fashion from proximal to distal, attempting to correct the deformity. The MTP deformity is addressed with an EDL Z-lengthening and EDB tenotomy. If the deformity remains, sequentially the MTP joint capsule is released, followed by the dorsal 1/3 of the medial and lateral collateral ligaments. Further correction may necessitate a metatarsal shortening osteotomy. The fixed claw toe deformity at the PIP joint is treated with a PIP joint resection similar to a fixed hammer toe deformity.

Second MTP joint instability is a painful condition typically arising from a progressive failure of the restraints to dorsal translation of the phalanx on the metatarsal at the MTP joint.

Although acute rupture of the plantar plate can cause spontaneous 2nd MTP joint instability, the more common situation is gradual attenuation of the plantar plate as the result of mechanical overload. This subluxation during the toe-off portion of gait causes synovitis, which can lead to significant pain and functional limitation.

Predisposing factors include a relatively long 2nd metatarsal, hypermobile 1st ray, equinus deformity, hallux rigidus, and hammer and claw toe deformities, which can all lead to increases in 2nd MTP joint pressure and begin the cycle of synovitis, static restraint compromise, and joint subluxation.

The 2nd proximal phalanx is firmly attached to the metatarsal through a thick plantar plate as well as medial and lateral collateral ligaments. The plantar plate, along with the collateral ligaments, acts to block dorsal translation of the MTP joint as it is loaded.

As the 2nd MTP joint is mechanically stressed, the synovium of the joint becomes inflamed. The synovitis erodes the collateral ligaments and plantar plate. As the static restraints of the toe are weakened, the toe will begin to sublux to a greater degree with less force exerted on it. At the MTP joint, the increased subluxation will mechanically make it difficult for the dynamic restraints (FDL, FDB, intrinsic muscles, and lumbricals) to resist subluxation of the toe.

As the toe continues to sublux with gait, the synovitis within the joint will increase, and the static supports will be further compromised, causing the toe to drift up with the subsequent development of a flexible and then fixed hammer toe deformity. As the collateral ligaments attenuate, medial deviation may develop as well (crossover toe deformity).

Pain is typically activity related and can be significant. A history of shooting pain into the toes or burning in the forefoot may indicate a traction neuritis but may also indicate the existence of a neuroma, which can accompany this condition.

Acute 2nd MTP joint instability will present with a patient giving the history of a “pop” in their foot. The pop will be accompanied by swelling and pain in the area of the 2nd MTP joint.

Inspection should focus on the presence of any deformity, swelling, and bruising. Occasionally, a separation of the 2nd and 3rd toes can be seen, indicating 2nd MTP joint synovitis and chronic forefoot overload.

The areas of maximal tenderness should be sought; metatarsalgia pain will often be directly underneath the metatarsal head, whereas neuroma pain will typically be a little more distal and in the webspace. It can sometimes be difficult to clinically differentiate these 2 pathologies on clinical exam. Range of motion of the MTP joints, ankle joint, and 1st MTP joint is important. Restricted range of motion of the ankle joint will lead to increased forefoot pressures, most commonly in the 2nd MTP joint. The presence of an equinus contracture should be sought.

The drawer test is specific for metatarsalgia; the foot is held stable with one hand, while the other exerts a dorsal pressure on the phalanx. A positive test will typically have increased superior translation as well as causing the patient significant pain.

Radiographs should be reviewed for predisposing causes of 2nd MTP joint overload: Hallux valgus, hallux rigidus, or a relatively long 2nd metatarsal.

An MR can sometimes, but not always, differentiate metatarsalgia from an interdigital neuroma. Occasionally, a selective anesthetic injection into the MTP joint can help to differentiate the 2, although most surgeons will simply start with empiric nonoperative treatment.

Nonoperative treatment involves 2 parts: Alleviating the patient’s pain and then addressing the predisposing factors that may lead to recurrence. The nonoperative treatment course is based on the severity of the symptoms. The patient should be counseled that the treatment goal is to decrease pain and that any toe deformity that has occurred to this point most likely will remain without operative care.

Mild discomfort can be treated with splinting or taping of the toe with unloading of the metatarsal head with a metatarsal pad. Addressing the patient’s equinus deformity with a daily stretching program can be initiated after the initial acute phase has resolved.

A variety of procedures have been described, including plantar condylectomy and pinning, metatarsal osteotomy, plantar plate repair, or some combination of all these options.

Plantar condylectomy involves removing 25-33% of the plantar metatarsal head and is often performed with extensor lengthening and possible release of the dorsal capsule and portion of the collateral ligaments. The toe is pinned for 3 weeks followed by a course of taping for another 3 weeks.

A shortening metatarsal osteotomy is meant to take pressure off the plantar metatarsal head. A Weil-type osteotomy is made parallel to the plantar surface of the foot through the dorsal aspect of the metatarsal head or just superior to the cartilage of the metatarsal head. The toe is shortened until it falls into the normal cascade between the 1st and 3rd metatarsal heads. Pinning of the MTP joint is optional.

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  Because the plane of the osteotomy is not parallel to the plantar surface of the foot, shortening with a horizontal (Weil) osteotomy displaces the metatarsal head plantarly, and surgeons will often make a 2nd cut, taking out a wafer of bone so as to counteract this declination of the metatarsal head.

  
  
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  A metatarsal osteotomy can lead to a floating toe deformity, whereby the toe sits in a relatively elevated position. Care should be taken not to shorten the metatarsal too much.

While most of these surgical treatments are performed in an effort to address the baseline mechanical defect, the often insufficient plantar plate can also be directly repaired so as to provide an immediate restraint to dorsal subluxation at the MTP joint. Much work has been done recently to better characterize the nature of injuries to the plantar plate and the role of plantar plate repair in the treatment of metatarsalgia.

It is important to recognize that metatarsalgia does not exist in a vacuum and often exists as a syndrome, whereby a lax 1st tarsometatarsal joint, arthritic 1st MTP joint, or gastrocnemius equinus may play a significant role in the pathology and merit surgical correction to fully address the pathology.