Claw Toes

Claw toe is a triplanar deformity of a lesser toe: the MTP joint hyperextends while both the PIP and DIP joints flex. Hammer toe flexes the PIP alone and mallet toe the DIP alone; claw toe affects all three joints at once. MTP hyperextension is pathognomonic for claw toe and suggests intrinsic muscle dysfunction.

Epidemiology. Claw toes are reported in 2-20% of adults, the figure varying with age, and can occur at any age depending on the cause. There is no significant sex predominance, unlike hammer toe. Between 60 and 80% are bilateral, which suggests a systemic cause, and 80% have an underlying neurological condition or cavus foot.

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The intrinsic muscles. The lumbricals and interossei are the balancing muscles of the lesser toe. Both flex the MTP joint and extend the PIP and DIP joints, and the interossei also abduct and adduct the toes.

• Lumbricals (4) - arise from the FDL tendons and insert into the medial aspect of the extensor hood. The first is supplied by the medial plantar nerve, the second to fourth by the lateral plantar nerve
• Interossei (7: 3 plantar, 4 dorsal) - arise from the metatarsals and insert into the base of the proximal phalanx and the extensor hood. All are supplied by the lateral plantar nerve

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The balance. In the normal toe the intrinsics flex the MTP and extend the IP joints, the extrinsic flexors (FDL and FDB) flex the PIP and DIP, and the extrinsic extensors (EDL and EDB) extend the MTP. Together they hold the toe in a neutral position.

When the intrinsics fail. Weak or paralysed intrinsics leave the extrinsic muscles to dominate:

1. EDL unopposed → MTP hyperextension
2. FDL and FDB unopposed → PIP and DIP flexion
3. Loss of stabilisation → progressive deformity
4. Weight-bearing forces drive the MTP into further extension

Transfer metatarsalgia. MTP hyperextension shifts weight onto the metatarsal heads, and the result is plantar callus and pain.

Causes. Neurological causes are the most common. Neurological claw toes are bilateral and progressive, and the disease affects the intrinsic muscles first.

• Neurological - Charcot-Marie-Tooth disease (CMT), the most common neurological cause; diabetic neuropathy, through a motor component affecting the intrinsics; spinal cord pathology such as syringomyelia or tethered cord; cerebral palsy, with spasticity and muscle imbalance; peripheral nerve injury (sciatic or tibial nerve lesions)
• Biomechanical - cavus foot; gastrocnemius contracture, which increases forefoot loading; a long toe or metatarsal, a mechanical disadvantage; chronic MTP joint instability from plantar plate insufficiency
• Inflammatory - rheumatoid arthritis (synovitis → joint destruction); seronegative arthropathies (psoriatic, reactive arthritis); crystal arthropathies (gout, CPPD), less commonly
• Traumatic - compartment syndrome, with intrinsic muscle necrosis and fibrosis; crush injury
• Iatrogenic - previous forefoot surgery disrupting muscle and tendon balance; overcorrection of flatfoot by excessive plantar fascial release

The cavus foot. Hindfoot varus drives forefoot pronation, peroneus longus overpull plantarflexes the first ray, and the intrinsics are weakened by stretching.

Primary claw toe. When no cause can be identified the deformity is primary (idiopathic). It is often associated with cavus foot and progresses over time. Secondary claw toe is neurological (CMT, diabetes, spinal pathology), inflammatory (RA, seronegative arthritis), traumatic (compartment syndrome, crush injury) or iatrogenic (a post-surgical complication).

Flexibility is the classification that matters, because it determines treatment. It is graded on the flexibility test described under examination.

Symptoms. The pain maps onto the deformity:

• Dorsal toe pain - shoe pressure over the PIP and DIP joints
• Plantar forefoot pain - transfer metatarsalgia from MTP hyperextension
• Tip-of-toe pain - DIP callus and ground contact
• Interdigital pain - impingement against the adjacent toe

Function. Patients have difficulty finding comfortable footwear and cannot wear dress or athletic shoes. Walking hurts, especially barefoot; cosmetic concerns and progressive worsening over time complete the history.

Clues to the cause. Ask about weakness or numbness in the feet and legs (neurological), lateral ankle instability and chronic sprains (cavus foot), and morning stiffness with multiple joint involvement (inflammatory).

Standing. Observe the toes weight-bearing, the hindfoot alignment (varus suggests cavus) and the height of the medial arch. Look for callus over the dorsal PIP and DIP joints and beneath the metatarsal heads.

The flexibility test. This is the critical examination, because it chooses the operation.

1. Passively flex the MTP joint to 90°, which relaxes the extrinsic tendons (FDL and EDL)
2. Attempt to passively extend the PIP and DIP joints
3. Assess the degree of correction

Complete correction with the MTP flexed means a flexible deformity: the intrinsics are present but weak, and the toe is a candidate for Girdlestone-Taylor transfer. Partial correction means semi-rigid, with an intrinsic contracture developing. No correction means rigid, a fixed contracture with joint changes that needs bone surgery.

The Kelikian push-up test. Examiners ask for it by name. The flexibility test relaxes the extrinsics by flexing the MTP; the push-up test asks a different question by pushing up on the plantar aspect of the metatarsal head to simulate weight-bearing.

• The toe corrects - the deformity is driven by MTP position, and correcting the MTP (soft-tissue release, plantar plate repair, Weil shortening) may straighten the toe without an IP procedure
• The toe stays clawed - there is a fixed IP contracture that must be addressed in its own right

Use both. Flexing the MTP tells you whether the extrinsics are the problem; pushing up the metatarsal head tells you whether the MTP is. They can disagree, and when they do the disagreement is the operative plan: a toe that corrects on push-up but not on MTP flexion needs the metatarsal addressed, not the toe.

The MTP joint. The drawer test displaces the proximal phalanx dorsally, and a positive test indicates plantar plate insufficiency. Check the MTP range of motion (extension is often limited by the capsule) and palpate for synovitis and tenderness.

Neurovascular examination.

• Sensation - light touch, two-point discrimination
• Motor - intrinsic strength (toe spread, toe grip)
• Reflexes - ankle jerk, plantar response
• Gait - high-stepping (foot drop), lateral instability
• Pulses - dorsalis pedis, posterior tibial

Associated deformities.

• Cavus foot - Coleman block test for hindfoot flexibility
• Hallux valgus - often coexists with lesser-toe pathology
• Ankle instability - chronic lateral ligament laxity
• Gastrocnemius contracture - Silfverskiöld test

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Radiographs. Weight-bearing views of the foot:

• AP - MTP joint alignment, metatarsal declination angle, joint space, erosive changes (inflammatory arthritis), metatarsal length pattern
• Lateral - MTP hyperextension angle, PIP and DIP flexion angles, calcaneal pitch (cavus assessment), metatarsal declination, forefoot-hindfoot relationship
• Oblique - MTP joint congruity, PIP and DIP joint anatomy, osteophyte formation

Measurements. A claw toe shows increased PIP and DIP flexion angles and plantar subluxation of the proximal phalanx, and the angles below separate normal from abnormal:

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Neurological work-up. Bilateral or progressive claw toes are investigated for a cause:

• EMG/NCS - identifies a peripheral neuropathy pattern
• MRI spine - if upper motor neuron signs are present
• Genetic testing - CMT panel if there is a family history
• HbA1c - screens for diabetes
• Vitamin B12 - deficiency neuropathy

Inflammatory work-up. If inflammatory arthritis is suspected: ESR and CRP, rheumatoid factor and anti-CCP, HLA-B27 for a seronegative arthropathy, and uric acid for gout.

Non-operative care. It controls symptoms but does not correct the deformity; progressive worsening is expected and surgery is often eventually required. It suits:

• Mild, asymptomatic deformity
• A flexible deformity with minimal symptoms
• A patient medically unfit for surgery
• Patient preference after counselling

Non-operative options.

• Footwear - wide, deep toe box; soft uppers to reduce pressure; cushioned insoles; custom shoes if the deformity is severe
• Orthoses - night-time toe-straightening splints; metatarsal pads to offload the metatarsal heads; custom insoles for cavus foot correction; crest pads to support the PIP joint
• Symptomatic treatment - callus debridement (podiatry); corn pads and toe sleeves; NSAIDs for inflammatory pain; physiotherapy for intrinsic strengthening

Treat the cause. Optimise diabetic control, treat rheumatoid arthritis, manage the neurological condition, and follow a gastrocnemius stretching protocol.

Absolute indications for surgery.

• Intractable pain despite conservative measures
• Skin breakdown or ulceration
• Functional limitation affecting quality of life
• Progressive deformity with a risk of skin compromise

Relative indications.

• Cosmetic concerns (patient-driven)
• Difficulty with footwear
• Recurrent callus formation
• Mild pain with activity

Patient selection. The patient should be medically fit for surgery, with realistic expectations, able to comply with postoperative restrictions, and with an adequate vascular supply and no active infection. The flexibility grade then chooses the operation.

Intraoperative

Neurovascular injury. Digital nerves or arteries can be injured during dissection, more commonly in scarred or inflamed tissue. Prevention is careful dissection with identification of the structures; repair primarily if the injury is identified, and observe if it is minor.

Inadequate correction. Residual deformity after the procedure; undercorrection is more common than overcorrection. Prevention is intraoperative assessment and adequate release. Accept mild residual deformity and revise significant deformity.

K-wire problems. Pin migration and breakage, as well as pin-tract infection (below). Prevention is proper technique and pin care.

Early (less than 6 weeks)

Wound complications. Superficial infection in 2-5%, delayed healing in 5-10% and wound breakdown in less than 5%, managed with local wound care, antibiotics and debridement.

Pin-tract infection. Occurs in 5-10% with percutaneous K-wires and presents as erythema and drainage around the pin. Pin care and oral antibiotics treat it, with early removal of the wire if it is severe.

Swelling. Expected, and it can be significant, typically lasting 2-3 months. Elevation, compression and ice manage it.

Late (more than 6 weeks)

Floating toe. The most common complication, in 10-20% after PIP arthroplasty: the toe sits elevated off the ground and lacks purchase. Excessive bone resection or a tight transfer causes it. It is usually asymptomatic but cosmetically concerning; most are observed, and a symptomatic toe is revised to an arthrodesis.

Recurrence. 5-15%, depending on the procedure. It is more common if the underlying cause has not been addressed and more likely after flexible procedures than after arthrodesis. Treat it conservatively first and revise if needed.

Stiffness. Expected, and intended, after arthrodesis. It can affect the adjacent joints and may limit footwear options; shoe modifications and stretching help.

Nonunion and malunion. Nonunion occurs in 5-10% at the PIP and in less than 5% at the DIP; malunion (rotational or angular deformity) in 5%. Smoking, diabetes and poor fixation are the risk factors, and revision arthrodesis is for the symptomatic toe.

Transfer metatarsalgia. Pain under the adjacent metatarsal heads from the altered biomechanics after surgery. Prevention is addressing metatarsal length discrepancies; metatarsal pads, and possibly a Weil osteotomy, treat it.

Vascular compromise. Rare but serious, and more common in smokers, diabetics and patients with peripheral vascular disease; it can lead to toe ischaemia and necrosis. Prevention is careful patient selection and preserving the vascular supply. A viable toe is observed; a necrotic one is amputated.

• Why it happens. The toe floats when its plantar-flexing / ground-purchase force at the MTP is lost or overpowered by a dorsal force:
  • PIP resection arthroplasty shortens the toe and disrupts the flexor and plantar-plate purchase, so the toe loses the plantarflexion that holds the pulp down.
  • An over-tight FDL-to-EDL transfer pulls the toe into too much MTP flexion-correction and dorsiflexion, lifting the tip.
  • A Weil osteotomy translates the metatarsal head plantarward and proximally, which shifts the intrinsic (interosseous/lumbrical) tendons dorsal to the MTP axis of rotation - the intrinsics then act as MTP extensors instead of flexors, producing a dorsal contracture and a floating toe (the classic Weil pitfall).
• How to prevent it. Resect minimal bone, tension the transfer so the toe rests plantigrade with the ankle neutral (not over-corrected), preserve or repair the plantar plate, limit Weil shortening and avoid excessive plantar translation, and stabilise the MTP (temporary K-wire) while it heals.
• How to treat a symptomatic floating toe. Most are asymptomatic and observed. A symptomatic one is addressed by flexor tenodesis / FDL transfer to restore plantar pull, plantar plate reefing, MTP capsular release of the dorsal contracture, or, if a Weil has malpositioned the head, a corrective (e.g. more proximal / less plantar) revision.

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• The indication. A flexible claw or hammer toe with a tip-of-toe (apex) ulcer or impending ulcer, classically in a diabetic neuropathic (or neuroischaemic) foot - the setting where a formal open reconstruction or arthrodesis carries unacceptable wound and vascular risk.
• The procedure. A percutaneous stab on the plantar surface just proximal to the flexion crease divides the FDL and FDB tendons; the flexible toe then straightens and the tip lifts off the ground, offloading the apex. It is done under local anaesthetic, needs no fixation, and the incision heals by itself.
• Why it works and its evidence. Releasing the deforming flexor pull lets the neuropathic toe sit plantigrade so the ulcer offloads and heals (Rasmussen: 93% healed, median 21 days, no infections or amputations), and prophylactic tenotomy of an at-risk toe prevents ulceration. It is explicitly a limb-sparing alternative to amputation in the poorly-vascularised foot.
• The limits. It only works while the toe is flexible - a rigid contracture will not correct with tenotomy alone and needs PIP arthrodesis (or resection) as elsewhere in this topic; and dividing the flexors can leave a small floating-toe tendency, usually well tolerated in this population.

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Weeks 0-2. Keep the compression dressing clean and dry, elevate the foot above heart level to reduce swelling, and weight-bear as tolerated in a stiff-soled shoe or boot. Ice for 20 minutes every 2-3 hours, give oral analgesics as needed, and clean any K-wire daily with an alcohol wipe.

First review at 10-14 days. Remove the sutures, assess wound healing and check the alignment for rotation. Change to a lighter dressing or toe sleeve and continue weight-bearing in the protective shoe.

Weeks 2-6. Protected weight-bearing continues with any K-wire left in place. Buddy-tape the toe to its neighbour, start gentle passive motion of the unfused joints, control swelling with compression and elevation, and watch for pin-tract infection.

Review at 6 weeks. The K-wire comes out in the office under local anaesthetic and radiographs assess alignment and early fusion. The patient moves into a regular supportive shoe and begins active motion, with a physiotherapy referral if the toe is stiff.

Weeks 6-12. Progress weight-bearing to normal, with active and passive motion, intrinsic strengthening exercises and scar massage. Return to regular activities gradually, and assess shoe fitting.

Review at 12 weeks. Final radiographs confirm fusion, the functional outcome is assessed, residual swelling or stiffness is addressed, and the patient is cleared for full activities if healed.

3-12 months. Swelling may persist for 3-6 months, and numbness around the surgical site gradually improves. Modify shoes as needed, monitor for recurrence or adjacent toe deformity, and review annually if there is a neurological condition.

Primary prevention in at-risk groups.

• Neurological conditions (CMT, diabetes) - regular foot examinations, early intrinsic strengthening, custom orthotics for cavus foot, proper diabetic foot care and optimised glucose control
• Cavus foot - early identification and treatment, lateral column lengthening if progressive, a gastrocnemius stretching programme and appropriate footwear
• Inflammatory arthritis - DMARD therapy to control disease, early soft-tissue procedures if deformity is developing, and regular rheumatology and podiatry follow-up

Preventing recurrence after surgery. Address the underlying neurological or biomechanical cause, keep to proper footwear long term, continue intrinsic strengthening, and monitor the adjacent toes, with revision surgery if the deformity recurs.

Prognosis. Young age, a single toe, a flexible deformity and no systemic disease are favourable. A progressive neurological condition, multiple toes, rigid deformity, diabetes and smoking are unfavourable.

The long view. Patients with a progressive neurological condition are likely to develop deformities of the adjacent toes, and a cavus foot carries a high recurrence risk if it is not addressed. The isolated idiopathic claw toe has good long-term outcomes with appropriate surgery.

Global Epidemiology

• Diabetes burden: ~537 million adults live with diabetes worldwide (IDF, 2021); distal symmetrical polyneuropathy develops in roughly 30-50% over time and is a leading driver of acquired claw toe and plantar pressure redistribution.
• Charcot-Marie-Tooth disease: prevalence ~1 in 2,500 globally - the commonest inherited neuropathy and the classic cause of bilateral, progressive claw toes with cavovarus feet.
• Lesser-toe deformity: prevalence rises steeply with age; population foot studies report clawing/hammering in a substantial minority of older adults, more in women (footwear and hallux valgus association) but with no sex bias in neurological claw toe.
• Resource-setting variation: in high-resource settings deformity is often elective/cosmetic-driven; in limited-resource settings the same deformity more often presents late with ulceration, infection or osteomyelitis because of delayed access and barefoot/ill-fitting footwear.

Side-by-Side Guidance

There is no implant registry specific to lesser-toe surgery; outcome data derive from case series (see Evidence Base) rather than national arthroplasty registries such as NJR/AJRR/AOANJRR. Intramedullary IP fusion implants are tracked only through device-surveillance schemes, not joint registries.

Practice Variation

• High-resource: day-case surgery, intramedullary headless implants, MRI-confirmed plantar plate repair, formal gait/neuromuscular work-up.
• Limited-resource: emphasis on footwear, callus care and simple K-wire arthrodesis or percutaneous flexor tenotomy; earlier resort to amputation when ulceration is neglected or vascular supply is poor.

• Arthroplasty vs arthrodesis for rigid PIP deformity: arthrodesis gives more reliable alignment and lower recurrence but at the cost of a stiff toe and a small nonunion rate; resection arthroplasty is quicker and easier to revise but has a higher floating-toe and recurrence rate. Robust comparative (Level I) data are lacking.
• K-wire vs intramedullary implant for IP fusion: newer buried intramedullary devices avoid pin-tract infection and external wires, but high-quality evidence of superior fusion or function over the cheap, familiar K-wire remains limited, and implants add cost.
• Does the plantar plate always need formal repair? For MTPJ instability driving a claw/crossover toe, some advocate anatomic dorsal plantar plate repair with Weil osteotomy, while others argue a Weil osteotomy plus flexor transfer alone restores enough stability - the marginal benefit of suturing an often-attenuated plate is debated.
• Prophylactic surgery in the neuropathic foot: percutaneous flexor tenotomy can heal and prevent tip-of-toe ulcers, but how widely to apply prophylactic tenotomy in asymptomatic at-risk diabetic claw toes is unsettled.
• Extent of cavus correction: how aggressively to correct the hindfoot at the index operation (osteotomy/tendon transfer) versus staging it remains a judgement call, balanced against recurrence risk if the cavus driver is left untreated.

1. Coughlin MJ, Mann RA. Lesser toe deformities. J Am Acad Orthop Surg. 2007;15(9):567-576.

2. Myerson MS, Jung HG. The role of toe flexor-to-extensor transfer in correcting metatarsophalangeal joint instability of the second toe. Foot Ankle Int. 2005;26(9):675-679.

3. Nix SE, Vicenzino BT, Collins NJ, Smith MD. Characteristics of foot structure and footwear associated with hallux valgus: a systematic review. Osteoarthritis Cartilage. 2012;20(10):1059-1074.

4. Burns J, Crosbie J, Hunt A, Ouvrier R. The effect of pes cavus on foot pain and plantar pressure. Clin Biomech. 2005;20(9):877-882.

5. Highlander P, VonHerbulis E, Gonzalez A. Complications of the Weil osteotomy. Foot Ankle Spec. 2011;4(3):165-170.

6. Hicks JH. The mechanics of the foot: II. The plantar aponeurosis and the arch. J Anat. 1954;88(1):25-30.

7. Coughlin MJ, Schutt SA, Hirose CB. Metatarsophalangeal joint pathology in crossover second toe deformity. Foot Ankle Int. 2012;33(6):463-470.

8. Barbari SG, Brevig K. Correction of clawtoes by the Girdlestone-Taylor flexor-extensor transfer procedure. Foot Ankle. 1984;5(2):67-73.

9. Caterini R, Farsetti P, Ippolito E. Long-term follow-up of toe flexor-extensor transfer in adolescent and adult patients with pes cavus. Foot Ankle Int. 1994;15(6):295-298.

10. Gallentine JW, DeOrio JK. Removal of the second toe for severe hammertoe deformity in elderly patients. Foot Ankle Int. 2005;26(5):353-358.

11. Hamer AJ, Stanley D, Smith TW. Surgery for curly toe deformity: a double-blind, randomised, prospective trial. J Bone Joint Surg Br. 1993;75(4):662-663.

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

13. Wetmore RS, Drennan JC. Long-term results of triple arthrodesis in Charcot-Marie-Tooth disease. J Bone Joint Surg Am. 1989;71(3):417-422.