Surgical correction of checkrein deformity following

Surgical correction of checkrein deformity following
malaligned distal tibia fracture
Eric Barp D.P.M., FACFAS, Eric Temple D.P.M., Timothy Holcomb D.P.M.
Iowa Methodist Medical Center, The Iowa Clinic
INTRODUCTION
Checkrein deformities are rare and involve entrapment or fixed tethering of
the flexor hallucis longus (FHL) tendon in the posterior foot, just proximal to the
flexor retinaculum of the ankle (1-3). The deformity occurs secondarily to nonsurgical or surgical correction of fractures of the distal tibia and has been observed
after fibular, calcaneal, and talar fractures or the removal of fibular grafts (1-4).
Radiographic imaging has suggested that the deformity can result from entrapment
of the FHL in callus formation at a fracture site or within scar tissue (5). In general,
deformities present with flexion contracture at the interphalangeal (IP) joint of the
hallux with extension contracture of the metatarsophalangeal joint and occasionally
affect the second and third toes. Complications of compartment syndrome can also
cause contracture of the deep posterior muscle compartment and produce a fixed
length phenomenon of the long toe flexors inducing the checkrein deformity (6).
Pain related to the deformity is normally elicited in the posteromedial ankle upon
dorsiflexion of the ankle or hallux, inducing tension on the FHL (1). Passive
dorsiflexion about the ankle enhances the deformity at the hallux, while
plantarflexion at the ankle partially corrects the deformity.
Case reports have described different surgical interventions for the checkrein
deformity such as release of adhesions at the fracture site, Z-plasty lengthening of
the FHL tendon at the fracture site with release of adhesions, and Z-plasty of the
FHL at the midfoot without release of adhesions (5). A paucity of information exists
on this rare deformity and available surgical techniques used for correction. The
aim of this study was to report the etiology of a checkrein deformity case, describe
the method of treatment, and provide and compare operative results of the case
with other treatment modalities in the literature.
The tendon was transected and retracted giving rise to the joint. All cartilaginous
surfaces were removed from joint and it was reduced (Fig. 5). A 4.0, 46 mm cannulated
screw was placed and retrograded back down through toe providing compression. Light
fluoroscopy demonstrated appropriate screw placement and position of toe. Extensor
tendon was re-approximated with fiber wire and skin was closed in layers. Post closure
the forefoot was loaded (Fig. 6) demonstrating correction of the checkrein deformity. An
ankle block was administered using 30cc of 0.5% bupivacaine hydrochloride and foot
and ankle was wrapped in a Robert Jones compression dressing. Patient was
transferred to a Post Anesthesia Care Unit with stable vital signs and vascular status
intact.
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CASE STUDY
A 19-year old male presented at a foot and ankle clinic with a flexion
deformity at the IP joint of his left hallux and proximal IP joints of the left second and
third toes. The deformity had progressed over the past five years since treatment of
a distal tibia fracture, which had healed in a malaligned position. Patient denied
sudden 'lock up', snapping sensation, clicking sensation, 'catching' during
movements, feeling of instability, joint looseness, or feelings of displaced joints in
affected toes. The patient was unable to actively straighten the deformed joints, and
admitted pain upon palpation and ambulation. Stiffness was noted in the left great
toe joint and left second toe joint. The IP joint of the hallux as well as the proximal
IP joint of second and third toes were only partially reducible with passive reduction.
The flexion deformity was enhanced with dorsiflexion of left ankle and was partially
corrected with plantarflexion. All remaining joints of left foot and ankle maintained
normal range of motion. No neurological deficits were noted upon examination and
no visible swelling of left forefoot.
Bilateral foot and ankle radiographs were obtained, with left foot lateral
radiograph (Fig.1) demonstrating hallux IP dislocation and hammering at second
digit. Clinical examination of non-weight bearing left foot (Fig.2) illustrated a
checkrein deformity while loaded foot when dorsiflexed (Fig. 3) revealed increased
deformity. Surgical correction of deformity was explained to patient and parent as
well as risks and benefits of surgical procedures. Both parties agreed and elected to
proceed with surgical intervention.
Patient was placed in supine position in operating room and put under
general anesthesia. The left lower extremity was prepped and draped in normal
sterile fashion. Attention was directed to plantar aspect of toes one, two, and three
where stab incisions were made with a 15-blade to tenotomize flexor tendons (Fig.
4). Correction was achieved and incisions flushed and closed. Next, a curvilinear
incision was made over IP joint of the hallux and was carried down to level of
extensor tendon.
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LITERATURE REVIEW
The FHL muscle belly arises from the inferior two-thirds of the posterior surface of the fibula
and the interosseous membrane (7). Since Clawson (1974) first described claw toes following
fractures of the tibia, checkrein deformity has been observed in other circumstances (8).
Typical causes for tendon entrapment include, but not limited to, talar fractures, calcaneal
fractures, and ankle fractures. These fixed flexion deformities of the hallux cause significant
pain for patients, particularly when the ankle is passively dorsiflexed, causing the deformity to
become prominent and rigid (6). Due to the rarity of this deformity, few reports have been
cited in the literature. The reported case described a malaligned tibia fracture resulting in a
progressing deformity requiring surgical correction. Currently there is little available
information in the literature on etiologies and standard treatments of deformity.
Compartment syndrome has been reported as an etiology for developing clawing of the
toes from delayed or inadequate treatment with decompression. Feeney et al. (6) reported
contracture of multiple digits in nine patients, of which only one had an acute compartment
syndrome present. The absence of any contracture of tibialis posterior in the case suggested
the etiology may not have been related to compartment syndrome. The surgical treatment
involved lengthening the FHL alone in four of the patients, and the FHL and flexor digitorum
longus (FDL) in the remaining five patients through a retromalleolar incision. All patients had
full correction of the deformities with no recurrence. Follow-up at 12 months or longer
revealed all patients reported relief from pain, ease of shoe-fitting and subjective
improvement of gait. Inter-tendinous connection between the FDL and the FHL ultimately
determines whether lengthening the FHL alone is sufficient. Feeney et al. suggested
lengthening the FHL first if clawing of the hallux is present, and if there is persistent clawing of
the lesser toes on maximum passive ankle dorsiflexion, then lengthen FDL additionally (6).
Lee et al. (5) reported on surgical repair of 11 patients with checkrein deformities of
hallux, providing the largest available patient sample in the literature. Five patients underwent
release of adhesions with Z-plasty lengthening at the musculotendinous junction above the
ankle at fracture site, and the remaining six had lengthening of the FHL in midfoot. Of these
five patients with lengthening sites above the ankle, three patients had a recurrence and one
required a secondary operation. No patients in the midfoot group had recurrence. At final
follow-up of 20 months, 9 out of 11 patients had lost some flexion of the IP joint, but without
loss of function. Though the patient groups in the study were small, authors suggested
lengthening the FHL tendon by Z-plasty in midfoot, due to a relatively simple incision with less
chance of adhesions recurrence.
These authors assert that release of adhesions can improve movement but tendon
lengthening or release needs to be performed to correct deformity. Tenotomy of flexor tendon
at the level of the IP joint may be an option to treat checkrein deformity, particularly in
recurrent cases (9). Some authors suggest soft tissue correction distal to the retromalleolar
level or arthrodesis on individual digits does not correct the deformity (5,6), however there is
no evidence-based studies to substantiate these claims. Due to the rarity of the deformity, no
single surgical technique has been defined as standard. In the presented case, the checkrein
deformity developed after a distal tibia ankle fracture that healed malaligned, which resulted
in adhesions of the FHL and FDL to the callus of the tibial fracture. The case received flexor
tenotomy to digits 1-3 and IP arthrodesis to hallux. Immediate correction of deformity was
achieved intraoperatively. As of two months post-surgery the patient had no reoccurrence of
deformity or complaints.
CONCLUSIONS
•Checkrein is a rare deformity caused by traumatic injury to the posterior aspect of the
foot and ankle leading to impingement of FHL and occasionally FDL tendons.
•Previous surgical corrective intervention have been described in the literature as a
release of adhesions with or without Z-plasty lengthening of tendons in midfoot and
supramalleolar region.
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Feeney et al. Selective lengthening of the proximal flexor tendon in the management of acquired claw toes. JBJS 2001; 83-B: 335-338.
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