anatomize
There are two lateral processes on the anterior side of calcaneal tubercle: medial process and lateral process. The smaller lateral process is the starting point of abductor digiti minimi. The medial process is large and attached to abductor pollicis, flexor digitorum brevis and plantar aponeurosis. The plantar aponeurosis consists of three parts: the central zone, the medial zone and the lateral zone. The central zone of the plantar aponeurosis (CBPF) is the thickest and strongest, which starts from the plantar surface of the medial process of calcaneal tubercle, divides into five branches forward, and merges with the flexor digitorum sheath and the lateral surface of metatarsophalangeal joint. The medial band covers abductor pollicis, but it is very weak. The lateral band is also very weak, covering abductor digiti minimi, and reinforced by strong fibrous band on its outer side, which starts from the medial or lateral process of calcaneal tubercle and ends at the fifth metatarsal tubercle. The medial plantar groove and lateral plantar groove are formed between the central plantar aponeurosis belt, medial plantar belt and lateral plantar belt, and the cutaneous branches of medial plantar and lateral plantar arteries, veins and nerves pass through these grooves. The medial sulcus is deep and the lateral sulcus is shallow, both of which are filled with adipose tissue. The tibial nerve sends out 1 ~ 2 medial calcaneal nerve at the 2 ~ 3 transverse fingers on the medial malleolus, passes through the fibrous fat pad at the bottom of the heel and distributes in the heel and medial calcaneal periosteum. The tibial nerve at the deep side of the split ligament is divided into medial and lateral plantar nerves, which enter the plantar through the deep side of abductor pollicis muscle together with the medial and lateral plantar blood vessels. A branch of lateral plantar nerve still dominates abductor digiti minimi. Schepsis [3] and others believe that plantar aponeurosis, medial calcaneal branch of tibial nerve and abductor digiti minimi branch all play a role in the formation of heel plantar pain. Berkowitz [4] and others measured the plantar aponeurosis of 8 patients with PF/HSS with MRI, and found that the thickest part was 7.40mm in sagittal plane and 7.56mm in coronal plane. However, the average sagittal plane was 3.22mm and the average coronal plane was 3.44 mm in 5 age-matched control groups, and the average sagittal plane was 3.00mm and the average coronal plane was 3.00 mm in 5 young male control groups, which showed that PF/HSS plantar aponeurosis was obviously thickened. But at present, there are no measurement reports of a large number of cases (including normal values).
etiology
According to Bogman [1], Zachary may be the first person to describe the symptoms of heel pain. 1860, when discussing a heel disease, he wrote that the patient's pain was obvious in the morning and relieved after standing and walking for an hour or two. This is a typical symptom of PF/HSS, but it was not recognized at that time. 1900, Plettner accidentally found calcaneal spur on the patient's X-ray. Since then, more and more theories about the causes of calcaneal spur and the symptoms of calcaneal pain have been seen in the literature. The real reason of PF/HSS has been debated for many years. Baer proposed in 1906 that bone spur was caused by gonorrhea, which lasted for about a quarter of a century, and was later denied by Von Lachum and Palomeque. 19 15 Scholl suggested that calcaneal spur was caused by gonorrhea, but it was often accompanied by flatfoot. In the late 1930s, it was generally believed that local mechanical abnormality was the cause of calcaneal tingling. 1934 often resects bone spurs and the starting point of plantar aponeurosis with Milter. 1937 Spitz advocates only plantar tendinous neurotomy to treat heel pain. Hauser believes that the repeated pulling of aponeurosis and muscle attachment points causes bone spurs. When bone spurs protrude from soft tissues, inflammation will cause pain. 1942, Gould believes that there is a male sex-linked genetic tendency [1]. Since then, the causes are fat pad degeneration, foot strain, tuberculosis, obesity, direct compression of bone spurs, nerve entrapment and so on [6].
At present, it is generally believed that the fundamental reason of PH/HSS is the abnormal biomechanical mechanism of foot. When the foot touches the ground, it bears a great force, which is about 2 ~ 3 times its weight. The key to disperse this force is the internal rotation mechanism of the foot [7]. In normal walking gait, plantar aponeurosis has undergone an alternating transition from relaxation to tension, from pronation force when the foot touches the ground to supination force when the middle of the foot touches the ground, and then to toe off the ground. The tension of plantar aponeurosis increases in the middle of the whole foot landing and reaches the peak when the toes leave the ground. The tense plantar aponeurosis is like a bowstring, maintaining the arch-shaped foot bones [10]. Therefore, plantar aponeurosis is an important static structure to maintain longitudinal arch. Most of the forces acting on the longitudinal arch are borne by the plantar aponeurosis, especially the protruding points in the calcaneal tubercle. Pronation and supination movements are very important to the function of the foot, because the foot bears loads through special anatomical structures in very fine continuous movements [9]. Abnormal joint mechanics may prolong the pronation force in gait cycle, and as a result, the normal load is not borne by the main structures such as bones and ligaments, but by the secondary structures such as joint capsules and collateral ligaments [9]. When the force borne by plantar aponeurosis exceeds its physiological limit, this repeated long-term overload will induce inflammatory process, form degeneration and fibrosis, and lead to plantar aponeurosis [3,9]. Most researchers believe that pain is caused by micro-tearing of plantar aponeurosis caused by repeated minor injuries, or by inflammatory reaction secondary to micro-tearing of plantar aponeurosis [1, 3,8 ~1].
Plantar aponeurosis can occur in both flat foot and high arch foot deformity. The former increases the tension of the inner heel due to excessive pronation of subtalar joint, and the latter can not disperse the force from the heel to the whole foot landing due to internal structural defects, both of which increase the plantar aponeurosis load [9].
It is generally believed that calcaneal spur is not the cause of pain [1, 3, 6, 8, 10, 12 ~ 14], and it can only cause pain when the calcaneal fat pad shrinks due to old age or repeated hormone injection [10]. Foremann and Green [15] found that calcaneal spur was located at the attachment point of flexor digitorum brevis and abductor pollicis, but not in plantar aponeurosis. The plantar aponeurosis hangs under the calcaneus and is located on the plantar side of calcaneal spur. They believe that bone spur is the result of the compensatory reaction of the foot to stabilize itself during abnormal internal rotation. In the pronated foot, abductor pollicis and flexor digitorum brevis began to contract at the 0 th and 26 th percentiles in the standing stage respectively until the toes left the ground, while in the normal foot, these two muscles began to contract at the 38 th and 40 th percentiles respectively until the toes left the ground. Therefore, the muscle contraction of pronation foot is earlier and longer than that of normal foot. At the same time, the forefoot is unstable because the pronated foot is still pronated from the middle stage of gait standing to the propulsion stage, and the tarsal joint is not locked. In order to compensate for the instability, it is necessary to increase the activity of the internal muscle compared with the normal foot, so that the internal muscle is overstretched at the starting point. Repeated micro-trauma causes periostitis, calcification occurs over time, and finally calcaneal spur is formed.
diagnose
At present, the diagnosis of PF/HSS mainly depends on the medical history and clinical manifestations [8]. The onset of this disease is hidden, and the patient has no history of trauma, but he may have a history of excessive exercise or sudden change of exercise [8, 16]. Some people think that middle-aged and obese women are prone to this disease [17]. The patient felt pain and burning sensation on the plantar side of the heel. The pain is the most serious in the first step or two or after a period of rest every morning. After a few steps, the pain is relieved [8, 18], but it is gradually aggravated with the increase of daytime activities [8, 9, 17]. Typical pain appears in the advancing period of gait cycle [9], which can be aggravated when going upstairs [4]. With the development of the disease course, any weight-bearing activity feels pain, and patients can't run or jump [3]. The pain of the patient standing for a long time can radiate to the arch of the foot [8].
Physical examination showed that there was no inflammation in the heel [9, 17], and there were often signs of biomechanical abnormality in the foot [17]. The stopping point of CBPF is equivalent to the local tenderness at the medial process of calcaneal tubercle [8,9, 18], which can be induced by passive toe extension [8], but some people think that passive toe extension does not aggravate the symptoms [16].
X-ray film can show calcaneal spur, but it is not helpful to diagnose this disease, and can be used to exclude calcaneal cyst or fatigue fracture [9]. On MRI, the normal plantar aponeurosis shows a uniform low-signal image, with the same or slightly thinner thickness from near to far. The thickness of plantar aponeurosis is obviously thicker than that of the control group, and the thickened area has different signal enhancement areas [4]. Intinzo [14] thinks that Tc-99m three-phase bone scanning has certain significance for the diagnosis of plantar aponeurosis. In plantar aponeurosis, the dynamic phase showed hyperemia of the affected heel, the blood pool phase showed increased blood vessels on the plantar aponeurosis surface, and the delayed static phase showed local concentration of calcaneus plantar side.
Histological examination showed that the plantar aponeurosis was obviously thickened near the starting point, with obvious fibrosis and chronic inflammatory reaction [3, 4].
differential diagnosis
The diagnosis of PH/HSS is based on typical clinical manifestations and effective conservative treatment. Other rare causes should be considered for cases with ineffective conservative treatment or atypical symptoms [17]. Therefore, it is of great significance for clinical diagnosis and treatment to fully understand other diseases.
1 plasma negative spondyloarthropathy
Plasma negative spondyloarthropathy is a group of closely related diseases in clinic. Include ankylosing spondylitis, psoriatic arthritis, Wright syndrome, colitis arthropathy, Still's disease and reactive arthritis. They have some similar clinical features: joint inflammation changes, easy to invade the spine and sacroiliac joints and other central axes. When the peripheral joints are invaded, they are often distal joints such as interphalangeal joints, which are asymmetrical; Often encroach on tendons and ligaments, causing inflammatory pain; HLA B27 is often positive; Skin mucosal injury; Eye involvement; Rheumatoid factor in plasma was negative [17].
Heel stagnation is a common manifestation of ankylosing spondylitis, Reiter's syndrome and psoriatic arthritis, but it is not common in other diseases [17].
The positive rate of HLA B27 was 8% in normal whites and 2% in blacks. Among patients with ankylosing spondylitis, the positive rate of whites is 92%, and that of blacks is 50%. The positive rate of Wright syndrome was 72% for whites and 40% for blacks. The positive rate of other plasma negative arthropathy is between 20% and 80% [17].
Feet have two manifestations: joints and skin. It involves the formation of "sausage toes" between interphalangeal joints. The lesion is purulent keratosis. Patients with toenails showed atrophy and deformation of multi-toenails, similar to progressive fungal infection [17].
In the course of the disease, patients may have many complications, such as uveitis, spinal fracture, atlantoaxial subluxation, cauda equina syndrome, cardiopulmonary diseases and so on [17].
The clinical and X-ray features are helpful to distinguish spondyloarthropathy from rheumatoid arthritis, including: (1) having the same family history of arthritis or psoriasis; (2) Enteritis or uveitis; (3) History of uveitis; (4) Have a history of psoriasis; (5) systemic arthritis; (6) Wandering intermittent rheumatalgia; (7) Acute arthritis occurs immediately after diarrhea and urethritis; (8) Asymmetric aseptic arthritis of lower limbs, or single first metatarsophalangeal arthritis without uric acid crystals. Negative rheumatoid factor is the basic condition for the diagnosis of spondyloarthropathy, and positive HLA B27 supports the diagnosis. Laboratory examination is helpful to exclude other diseases, but not to distinguish them from each other [15].
Ankylosing spondylitis (1) [5, 17] is common in young men aged 20-30. Mainly involving axial joints, manifested as back pain, aggravated at rest and improved after exercise. The peripheral joints of 20% patients are the first to get sick. In the foot, the hind foot (ankle and heel) is more easily involved than the front foot (metatarsophalangeal joint and interphalangeal joint), and skin and toenail lesions are less common.
(2)2) The clinical manifestations of Wright syndrome [5, 17] are triad and/or tetralogy, including conjunctivitis, nongonococcal urethritis, polyarthritis, skin and buccal mucosa damage (oral ulcer, balanitis). Achilles tendon, knee pain and purulent keratinization of skin may also occur. Laboratory tests are consistent with spondyloarthropathy. In addition, 80% patients have very high HLA B27 and ESR. Joint involvement is mainly in the lower limbs, especially at the anchorage of achilles tendon, which is characterized by mild to moderate swelling and no redness. On the X-ray film, the triangle between the posterior superior calcaneus and achilles tendon decreases.
(3) Psoriatic arthritis [5, 17] is characterized by skin erythema with silver flakes on the extended side of the body, and Auspitz's sign (+) (punctate bleeding except silver flakes). In some cases, it may be pustular psoriasis, which is similar to tinea pedis when it occurs on the plantar side. There may also be psoriasis toenail changes, similar to fungal infections, but usually there are concave changes on the toenails. Tenosynovitis of flexor tendon and interphalangeal arthritis form a typical "sausage toe" 10 ~ 30% patients have heel pain, which is secondary to psoriatic arthropathy. On the X-ray film, there are pencil-shaped and cup-shaped changes between metatarsals and phalanges.
2 Rheumatoid arthritis [5, 19]
The etiology of rheumatoid arthritis is unknown, which may be related to heredity and immunity. The population incidence rate is 1 ~ 3%. Women get sick easily. The incidence rate increases with age, reaching a peak at 40-60 years old. The basis of differentiation from spondyloarthropathy is that rheumatoid factor is positive and HLA B27 is negative.
The foot is the second most easily affected part after the knee joint. Forefoot involvement such as metatarsal erosion is common, but calcaneus is also often involved. There is a synovial sac in the triangle between the posterior superior calcaneus and achilles tendon. When synovial sac is involved and inflamed, the posterior upper part of calcaneus is eroded and becomes rough.
The affected parts of calcaneus are: ① the posterior surface of calcaneus; ② Near the posterior surface of calcaneus above the achilles tendon anchorage; ③ The posterior surface of calcaneus is equivalent to the stopping point of achilles tendon; ④ The plantar surface of calcaneus at the stop of plantar aponeurosis; ⑤ The plantar surface of calcaneus in front of plantar aponeurosis.
In rheumatoid arthritis, the above areas ① and ② show erosive changes. ③ The posterior distance and plantar distance are formed in area ④. The pathological changes of ankylosing spondylitis and psoriatic arthritis are in ② ⑤ area. The lesions of Reiter syndrome are often located in ① ② ④ area.
On the X-ray film, the foot of rheumatoid arthritis mainly shows osteoporosis near the joint, toe deviation to fibula side and subluxation.
3 Mi chronic idiopathic skeletal hypertrophy (DISH) [19]
DISH patients have ossification, which is common in middle-aged or elderly men. It is characterized by bone hypertrophy at the attachment points of tendons, ligaments and fascia. The population incidence rate is 12%. It mainly involves the spine, and extraspinal manifestations are also common. The most commonly involved parts outside the spine include pelvis (iliac crest, sacroiliac joint, pubic symphysis), shoulder, elbow (olecranon of ulna), knee (femur, tibial condyle, tibial tubercle) and foot.
The cause of DISH is unknown, which may be related to hyperglycemia, obesity, excessive vitamin A, abnormal growth hormone or fluoride poisoning.
About 70% patients have foot deformities, mainly hypertrophic changes, such as dorsal talus, dorsal and medial scaphoid, lateral and metatarsal cuboid and the basal part of the fifth metatarsal. The performance of the foot can coexist with the performance of the spine, or it can appear alone. About 23% patients have heel pain. The calcaneal spur is often large and irregular, but the boundary is clear, and there is no reactive osteosclerosis, periosteal reaction, erosive changes and non-inflammatory manifestations. Osteogenesis of plantar aponeurosis or plantar ligament may also occur.
4 gout [2 19]
Gout includes four stages: asymptomatic hyperuricemia, acute gouty arthritis, intermittent gout and chronic gritty gout. When gout affects the foot, metatarsophalangeal joint 1 is most often involved, and ankle joint and tarsal joint can also be involved, but less. Under the cartilage accumulated by urate crystals, a bone defect near the articular surface is formed, and the bone around the lesion is hardened with clear boundaries. Its joint space is generally normal, which is different from rheumatoid arthritis. When calcaneus is involved, it also forms an erosive bone defect with clear boundary and sclerosis around the focus. Heel pain often occurs in the fourth stage, and the basis of pain is that sodium urate crystals are deposited at the achilles tendon stop, forming chronic foreign body granuloma.
5 nerve compression [2, 3, 20]
Tarsal tunnel syndrome (tibial nerve compression) has a burning sensation, which radiates to the plantar side of toes, often accompanied by hypoesthesia and dyskinesia. Neurological examination is necessary. A positive Tinel sign indicates nerve entrapment. Electromyography is helpful for diagnosis. Others such as medial calcaneal nerve compression, medial calcaneal neuritis and neuroma can cause heel pain.
6 others
Stress fracture of calcaneus [3], atrophy of heel fat pad [16,20], calcaneus tumor such as bone cyst, aneurysmal bone cyst, osteoid osteoma [5], foot reactive arthritis [2] caused by various infections (bacteria, viruses, fungi, parasites), osteoarthritis [5], arteriosclerosis [Green
Therefore, detailed medical history, comprehensive physical examination, necessary laboratory and X-ray examination are the basis of correct diagnosis.
deal with
The treatment of PH/HSS includes conservative treatment and surgical treatment.
1 conservative treatment
Lamelle [1 1] thinks that more than 90% patients with PF/HSS can be completely relieved after conservative treatment. Barret and Day [2 1] point out that the above estimate is too optimistic, and the remission rate is about 70 ~ 80%. It can be seen that conservative treatment plays an extremely important role in PF/HSS treatment.
Conservative treatment methods include rest, ice compress, stretching, adhesive tape fixation, orthopedic pad, physical therapy, non-steroidal drugs, local closure and so on. [ 1, 3, 5, 6, 12, 16].
Proper rest is the basis of conservative treatment.
Local ice compress is especially suitable for after strenuous exercise, and the time is generally 20 ~ 30 minutes.
There are two methods of traction therapy: one is to lean forward against the wall while keeping the heel in contact with the ground; Second, fix it with a small splint at night. Both can stretch plantar aponeurosis and achilles tendon. According to the statistics of the American Society of Foot and Ankle Osteology, in the first 8 weeks of treatment, only stretching Achilles tendon and plantar aponeurosis can improve the heel pain symptoms of about 70% patients [16]. It can be seen that this method is simple and effective.
Winding and binding can temporarily support the arch, control the heel valgus, keep the subtalar joint in a neutral position, and change the heel ground position. The general fixation time is 1 ~ 2 weeks, and the effective cases need further control by orthopedic pad. Scherer reported that the symptoms of 89% patients can be relieved by more than 80% or completely only by using adhesive tape and orthopedic pad.
Orthopedic pad (orthosis). According to the different biomechanical abnormalities of the affected foot, the corresponding orthopedic pad is specially made. The therapeutic mechanisms of various orthopedic insoles are as follows: ① The abnormal pronation of the foot is controlled by raising different parts of the forefoot or hind foot in a wedge shape, so as to avoid excessive traction at the plantar aponeurosis and muscle stops. (2) Grooving the orthopedic insole corresponding to the medial process of calcaneal tubercle can reduce the pressure on the inflamed part. ③ The use of sponge material at the heel can increase the shock absorption capacity.
Bogman adopts two-step therapy. The first step is to use orthopedic insoles made of semi-hard viscoelastic materials for patients. After local pain is relieved, the second step is to use functional orthopedic insoles made of hard materials for patients to achieve the purpose of long-term control, and the curative effect is remarkable.
Bogman pointed out in particular that when PF/HSS is unilateral, it should be noted that orthopedic pads with the same height should also be used when using orthopedic insoles in the contralateral normal foot, so as to prevent the unequal length of lower limbs caused by human beings and further aggravate the stretching of plantar aponeurosis of the affected foot. Because when the lower limbs are unequal in length, the foot of the shorter limb will be forced to rotate backward to increase the limb length, while the foot of the longer limb will be forced to rotate forward to shorten the limb length. In this way, the plantar aponeurosis of the longer limb (that is, the affected foot) will be overstretched because it is forced to further pronate.
Physical therapy, such as pulsed ultrasound, acoustic electroosmosis and iontophoresis, has limited curative effect.
Non-steroidal antibiotics are effective for acute cases, and the medication time is generally 2 ~ 3 weeks. It is not effective for chronic intractable pain cases.
Local injection of corticosteroids is sometimes effective for intractable cases, but multiple injections are not suitable because it may cause atrophy of calcaneal fat pad and tear of plantar aponeurosis. The number of injections is generally no more than 2 ~ 3 times.
In addition, for runners and patients, it is necessary to find and correct training mistakes in time. Someone investigated the patients of 40 athletes and found that 16 had training errors. The most common mistakes are suddenly increasing the training distance and training on steep slopes. Another 8 athletes wore ill-fitting or worn-out running shoes, resulting in excessive stretching of plantar aponeurosis. In addition to conventional conservative treatment, it is suggested to shorten the training distance, slow down the training speed, reduce or cancel the speed training, and change the training items such as cycling and swimming.
It should be noted that the improvement of symptoms is a slow and gradual process, and some need one year. So both patients and doctors need patience. After the symptoms are relieved, exercise should be gradually resumed to prevent the recurrence of symptoms. Early diagnosis and early treatment are easy to achieve good results. The longer the course of the disease, the less likely conservative treatment will be successful.
2 surgical treatment
Almost all authors believe that all conservative treatment measures should be taken before surgical treatment. Schepsis [3] suggests conservative treatment for at least 6 months before operation, and if the symptoms improve, continue conservative treatment for at least 6 months. Therefore, clinicians should bear in mind that surgery is only applicable to a few cases of chronic intractable pain that have failed to be treated conservatively for a long time. There are many surgical approaches and methods, and their evolution process is shown in table 1.