Adult Acquire FlatfootDeformity refers to secondary flatfoot in symptomatic adults. There are many causes of secondary flatfoot, such as joint degeneration, trauma, diabetes, rheumatoid arthritis, neurological lesions, tumors, and posterior tibial tendon dysfunction (PTTD), etc. PTTD is considered to be the most common cause of adult acquired flatfoot, but can also be the result of various flatfoot disorders.
I. Etiology and pathology
(A) Causes of secondary foot arch collapse
1, various causes of posterior tibial tendon insufficiency.
2, joint lesions. Talofibular joint, metatarsophalangeal joint. Joint destruction of the foot in rheumatoid arthritis.
3, Medical origin, such as overcorrection of high arched foot.
4, Trauma. Abnormal healing of heel fracture, talofibular joint fracture, Lifranc injury, posterior tibial tendon contusion, injury to the spring ligament.
5, Neurological osteoarthropathy secondary to diabetes or peripheral neuropathy (Charcot joint)
6, Neuromuscular lesions. Cranial injury, cerebral palsy, poliomyelitis, nerve injury.
7, Foot tumor
8, pregnant women due to endocrine changes in the body, the relaxation of many joint ligaments throughout the body, while the increase in weight, so that the foot is subject to greater pressure, the change of the longitudinal arch.
(B) The collapse of the medial longitudinal arch causes changes in the structure of the foot.
1, Achilles tendon contracture. After the collapse of the medial longitudinal arch, the moment of the Achilles tendon acting on the ankle joint decreases, and the pulling force of the Achilles tendon cannot be effectively transmitted to the forefoot through the hard arch. In order to push the body forward and lift the heel, the Achilles tendon needs to become shorter, tighter and more powerful.
2, Laxity of the midfoot. The mid-tarsal joint cannot be locked.
3, Displacement of the forefoot. After the collapse of the medial longitudinal arch, the talus is plantarflexed, the heel is subluxed posteriorly, and the anterior tuberosity of the heel no longer supports the talar head. To accommodate this position, both the forefoot and midfoot are displaced dorsally and laterally around the talus. The forefoot is abducted and the lateral column of the foot is shortened.
4, the posterior tibial tendon stress is increased, and posterior tibial tendon strain is likely to occur. In severe cases, there may be injuries to the medial ligaments of the foot, such as the spring ligament and deltoid ligament.
5, anterior rotation of the subtalar joint and heel exostosis.
6, Instability of the midfoot puts the subtalar joint and talar navicular joint in an abnormal position for a long time, and over time, these joints degenerate and become fixed deformities. This will put the ankle joint under greater stress and eventually lead to ankle degeneration.
(C) Causes of posterior tibial tendon insufficiency
Acute and chronic tendinitis, tendon degeneration and different degrees of tendon tears and ruptures of the posterior tibial tendon caused by various reasons can make the posterior tibial tendon unable to play its normal role, and this state is also called posterior tibial tendon insufficiency. It is currently believed that posterior tibial tendon insufficiency is the most common cause of acquired flatfoot in adults, and is a common foot lesion in middle-aged and elderly people. Posterior tibial tendon insufficiency can be caused by a variety of reasons, such as trauma, overuse, inflammation, tendon degeneration, infection, hormone injections, abnormal tendon anatomy, and improper shoe wear. After a posterior tibial tendon injury, the foot is not able to complete the locking of the mid-tarsal joint well, and thus the foot cannot form a stiff lever to effectively propel the body forward. The inversion and plantarflexion of the foot are dysfunctional, and over time other ligaments (such as the spring ligament complex) that maintain the arch of the foot also tear, resulting in a variety of deformities of the foot. Such as forefoot abduction, collapse of the medial longitudinal arch, heel exostosis, Achilles tendon contracture, etc.
(d) The pathological types of posterior tibial tendon insufficiency include 1, complete avulsion of the posterior tibial tendon from the navicular bone or paravicular avulsion leading to traumatic arthritis. 2, complete rupture of the posterior tibial tendon behind the medial ankle. 3, longitudinal tear of the posterior tibial tendon without complete rupture. 4, tenosynovitis, peritendinitis, with or without tendinitis, but no rupture of the tendon.
II. Clinical manifestations and diagnosis
It usually occurs in middle-aged women, especially those who are engaged in standing workers for a long time. The onset of the disease is slow, and the arch of the foot was normal in the past, but later it is found to be gradually collapsed. Patients often cannot recall a history of acute trauma. Patients often present to the hospital with ankle pain, flattened arches, and inability to wear normal shoes. The history can last from months to years, and the onset of the disease often begins with pain under the medial ankle, when it is easily diagnosed as a sprain of the medial ankle. As the medial arch decreases, the heel bone gradually exfoliates and the impingement of the heel bone and fibula or heel bone and talus causes pain below the anterior aspect of the outer ankle. Another population with onset is young adults who prefer sports, who usually have a history of acute ankle trauma with contusion or rupture of the posterior tibial tendon.
Examination reveals swelling of the ankle joint, especially in the posterior lower part of the medial ankle, where the posterior tibial tendon travels. This swelling of the foot may be more pronounced when viewed from the posterior aspect of the foot. More severe patients may present with reduced arch, prominent navicular tuberosity, heel exostosis, and forefoot abduction. Depending on the length of the history, this deformity can be reversible, in which the arch is present in the non-weight-bearing state and disappears after weight-bearing, with the presence of subtalar joint movement, or it can be rigid, in which the arch disappears in the non-weight-bearing state and the foot deformity cannot be corrected passively. When the patient is allowed to stand naturally and the forefoot appears to be abducted, more lateral toes are seen than normal when viewed from the back of the foot, which is a positive “polydactyly” sign.
There may be pressure pain at the end of the navicular tuberosity of the posterior tibial tendon under the medial ankle. The posterior tibial tendon can be more easily palpated by having the patient turn the affected heel externally. In patients with posterior tibial tendon, it may be inappropriate to palpate the tendon, feel a gap between the tendons, or have thickening of the tendon. Examination of the ankle, subtalar and mid-tarsal joints for movement generally does not affect ankle movement. In patients with rigid flatfoot syndrome, the subtalar and midtarsal joints are significantly limited in motion, and the valgus heel cannot be passively corrected.
Patients may have reduced strength of the posterior tibial tendon, or if the patient is asked to lift the heel with one or both feet, if the affected foot appears weak or painful, it is called a positive heel lift test. Adult patients with acquired flatfoot syndrome often have a combination of Achilles tendon contracture. If the ankle dorsiflexion is limited when the knee is extended and increased when the knee is flexed, this indicates a gastrocnemius contracture. This is because the gastrocnemius muscle spans both the ankle and knee joints, and flexion of the knee relaxes the gastrocnemius. Conversely, if ankle dorsiflexion is limited regardless of knee extension or flexion, this indicates a contracture of the Achilles tendon.
In order to better understand the course of posterior tibial tendon insufficiency and to be able to guide treatment, Johnson and Strom divided posterior tibial tendon insufficiency into 3 stages in 1989, and later Myersom added a 4th stage. 2007 Bluman,
Title and Myerson further refined this classification in 2007.
Stage 1: inflammatory phase
Type A: synovitis
Type B: partial rupture of the tendon, without deformity
Type C: partial rupture of the tendon and mild deformity of the hindfoot
Stage 2: Hindfoot exostosis
Type A1: combined reversible forefoot entropion
Type A2: fixed forefoot pronation
Type B: forefoot abduction
Type C: medial column instability
Stage 3: Fixed hindfoot adduction
Type A: Hindfoot adduction
Type B: Forefoot adduction
Stage 4: Ankle valgus
Type A: hindfoot valgus, reversible ankle valgus, no significant arthritis
Type B: hindfoot valgus, fixed or reversible ankle valgus with significant arthritis
X-ray examination
On the anteroposterior X-ray of the affected foot in the weight-bearing position, the navicular bone is seen to have insufficient coverage of the talus, the talar heel angle is increased, and the navicular bone is semi-dislocated to the lateral side. In the lateral position, the height of the arch is reduced, the angle between the talar axis and the first metatarsal is reduced or reversed, and the angle between the talar axis and the longitudinal axis of the heel is increased. The presence or absence of talar tilt should be noted on weight-bearing ankle radiographs. The presence of stenosis and hyperplasia of the intertarsal, subtalar and ankle joints should also be noted on foot and ankle radiographs.
CT has better visualization of bone abnormalities. Such as arthritis, tarsal junction and fracture malunion.
Ultrasound has the advantages of lower price, can examine static and dynamic changes in tendons, can be confined to the patient’s painful area for examination, has short examination time, is not affected by the metal in the body, and has no radiological radiation. However, the examiner must have some experience to be able to distinguish various lesions of the posterior tibial tendon.
MIR allows evaluation of the posterior tibial tendon and its surrounding structures from multiple planes. It can show tears, degeneration and tendinitis of the posterior tibial tendon.
IV. Treatment
(i) Non-surgical treatment
1, reduce the activity, if necessary, use plaster immobilization for 4-6 weeks.
2, physical therapy.
3, non-steroidal anti-inflammatory and pain-relieving drugs.
4, arch support pad, medial heel pad and ankle support (Ankle Foot
Orthoses (AFO). Such as the University of California Biomechanics Laboratory orthosis (University of California Biomechanics Laboratory orthosis) designed by the United States.
Laboratory orthosis
(UCBL), designed to correct lax forefoot and hindfoot deformities, has the ability to support the medial arch while pushing against the lateral wall of the heel bone and supporting the lateral edge of the 5th metatarsal stem to keep the foot in the foot pad. Other commonly used ankle supports include Arizona
AFO, various walking boots, etc., all have the function of limiting the movement of the ankle joint, reducing the weight-bearing of the foot and correcting the deformity. For pregnant women with flat feet caused by physiological changes, the use of arch support pads can protect the tendons and ligamentous structures of the foot and prevent permanent flat feet from being caused later.
5, wear shoes with hard soles to achieve effective support for the sole of the foot, and shoes with rocker soles can reduce the stress on the ankle when walking. For those with lesions in the ankle joint, walking boots can be worn to reduce symptoms.
(ii) Surgical treatment
If the non-surgical treatment fails, the corresponding surgical treatment can be chosen according to the type of lesion.
1.
For stage 1 patients, surgical removal of the inflamed tendon sheath and peritendinous tissue can reduce symptoms. However, this surgery does not change the other abnormalities of the foot and the long-term results are not good. It is rarely used alone anymore. After removal of the diseased tendon due to tendinitis resulting in tendon degeneration, the posterior tibial tendon can be strengthened by direct suturing or by flexing the long toe tendon.
2.
The main goals of treatment for stage 2 lesions are to strengthen the posterior tibial tendon, correct the abduction of the heel exostosis, stabilize the medial column of the foot, and preserve the motion of the subtalar joint. Since the deformity of the foot is reversible, the deformity can be corrected by soft tissue and osteotomy surgery to preserve joint motion.
If the tendon is avulsed at the navicular tuberosity or paracarpal arthritis, the posterior tibial tendon is reconstructed at the navicular bone after removal of the paracarpal bone. Torn or ruptured tendons can be directly sutured after resection of the diseased tendon, and those who cannot be sutured can be reconstructed with other tendons.
For medial column instability, fusion of the talonavicular, navicular wedge or metatarsal wedge joints is required.
In cases of posterior tibial tendon insufficiency, the posterior tibial tendon can be reconstructed using flexor digitorum longus tendon or flexor digitorum longus tendon transfer, but the result of posterior tibial tendon reconstruction alone is not satisfactory, and it is often necessary to perform internal heel osteotomy at the same time to achieve the effect of double tendon transfer.
Abduction of the foot can be corrected by fusion of the heel cuneiform joint implant or by lengthening the lateral column of the foot with an osteotomy implant at the neck of the heel.
The repair and reconstruction of the spring ligament complex is also important when it is degenerated or torn. In the case of Achilles tendon contracture, it is necessary to distinguish between Achilles tendon contracture and gastrocnemius contracture, and in the former case, Achilles tendon lengthening is performed; in the latter case, only gastrocnemius lengthening is usually done, and if Achilles tendon lengthening is also done at this time, it may cause weakness of plantarflexion of the ankle joint during walking.
In recent years, the use of subtalar joint block has been reported for the treatment of stage 2 adult acquired flatfoot syndrome, which uses an endograft implanted in the tarsal sinus to allow for partial motion of the subtalar joint. The implant can later be removed as needed to fully restore joint motion.
In stage 3 lesions, the deformity of the foot is fixed and requires fusion of the subtalar joint or a combination of subtalar fusion or even triple fusion to correct the deformity and stabilize the joint.
4. Stage 4 lesions may require triple fusion, quadruple fusion, or artificial joint replacement with subtalar joint fusion.
For tendon surgery, the ankle joint should be fixed in a mild plantarflexion and inversion position after surgery, and the cast should be removed after 4 weeks to start ankle mobility exercises, and after 6 weeks to start muscle strength exercises and partial weight bearing in a walkable boot, and after 8 weeks to walk with full weight bearing and continue functional exercises of the ankle joint. Full functional recovery usually takes 6-8 months.
For joint fusion, plaster fixation takes 6 weeks. If the bone heals satisfactorily, the patient can walk with partial weight bearing in the walking boot and start to gently move the joint without fixation, and then gradually increase the mobility and muscle strength exercises. 12 weeks later, the X-ray will be reviewed and the bone will be completely healed before starting to walk with weight bearing.