The pressure points and positioning of five types of heel pain: ① heel pad atrophy ② plantar fasciitis ③ Baxter’s nerve entrapment syndrome ④ heel compression fracture ⑤ ankle tube syndrome Plantar fasciitis 1, cause: the plantar fascia starts at the medial aspect of the heel base and splits into five bundles connected to the distal phalanx, these fibers are closely connected to the surrounding dermis, transverse metatarsal ligaments and flexor tendons. Especially in the first metatarsophalangeal joint, dorsiflexion increases the tension of the plantar fascia and the longitudinal arch of the foot. The inelasticity of the plantar fascia itself allows only about 4% lengthening. The disease is often caused by repeated minor trauma and excessive tension. Recently, it is considered to be a non-inflammatory reaction and is more appropriately referred to as “plantar fascia degeneration”. Reduced ankle flexion due to tension in the Achilles tendon or gastrocnemius is also associated with the development of plantar fasciitis. Obesity, excessive weight bearing, and other independent risk factors include: age, shoe discomfort, overtraining, and decreased mobility of the subtalar joint. High arches and flat feet are also important causes of plantar fasciitis. Pathological manifestations: mucinous degeneration of collagen fibers, hypertrophy and calcification of vascular fibroblasts, and infiltration of inflammatory fine packets such as polymorphonuclear leukocytes, lymphocytes and macrophages are rarely reported. 3, clinical manifestations: the patient often feels the initial pain, that is, the first step is more obvious in the morning or after a long rest, the pain is relieved after walking a few steps, but with the increase of walking time or standing time, the pain increases again. The pain is sharp and not radiating. 4. Physical examination: localized pressure pain around the heel tuberosity is obvious, and pressure pain is palpable along the fascial pathway, more obvious when the plantar fascia is tense (Figure 2), for example, when the ankle joint is dorsiflexed. Excessive dorsiflexion of the first thumb can lead to excessive stretching of the plantar fascia, causing pain. The finger shows the tense plantar fascia. 5. Diagnosis: A weight-bearing foot plain radiograph is necessary to detect bone spurs and calcifications, however, autopsy shows that the spurs are concentrated at the onset of the toe flexors rather than in the painful plantar fascia. 6. Treatment: For all cases, non-surgical treatment, rest, functional therapy, self-stretching exercises, heel pads, orthopedic devices, ice, NSAID, weight loss should be the main focus. Barefoot activities as well as unsuitable foot pads and others are not recommended. Arch restoring shoes help to reduce the dorsiflexion of the first metatarsophalangeal joint and help to reduce the maximum tension of the plantar fascia. at 8 weeks the effect of plantar fascia stretching is better compared to the effect of Achilles tendon stretching. However, the results at 2-year follow-up were average. Other treatments include: night immobilization, prescription medications, orthotic devices, and immobilization. The role of immobilization is to prevent and correct the position of the plantar fascia and gastrocnemius. As well as the application of orthopedic appliances. Only a small percentage requires the use of local injectable medications and extracorporeal ultrasound therapy. Topical steroid injections have proven to be effective in the short term but not in the long term. The side effects are also: tears of the plantar fascia, not just a separate complication. They also include: arch tension, lateral as well as dorsal midfoot tension, lateral plantar nerve dysfunction, stress fractures, and hammertoe deformity. It also includes: localized skin and fat atrophy, localized redness, damage to surrounding blood vessels and nerves. Resulting in hyperglycemia, tendon damage, infection, and facial flushing. ESWT: The use of sound waves to eliminate the inflammatory response could theoretically lead to neovascularization and repair. However there is no definitive evidence that it works significantly better than placebo for. Pulsed radiation electromagnetic field therapy, botulinum toxin type A therapy, and PRP therapy are all ineffective. Surgical treatment: limited to fasciotomy rather than removal of bone spurs. Endoscopy has gained increasing attention in the last few decades due to its short recovery time, with an efficiency of up to 76%. For patients with gastrocnemius atrophy, gastrocnemius release can be used, with pain relief in 81% of patients. Prevention and rehabilitation include: 1. release of fascia and muscles 2. stretching of fascia and muscles 3. strengthening of muscle strength training 4. neuromuscular control exercises. Heel pad atrophy 1, the cause: heel pad for the heel bone below, a piece of tissue rich in fat. The disease occurs over 50 years of age, due to the loss of water, collagen and elasticity, resulting in atrophy of the heel pad. 2, clinical manifestations: pain is mostly deep pain, non-radioactive, concentrated in the central weight-bearing part of the heel node. It is easily misdiagnosed as plantar fasciitis, which is easily induced by walking barefoot or walking on hard surfaces, and reduced by less walking. The plantar aspect of the heel node is prone to pressure pain, which correlates with the degree of swelling. The pain is usually not related to ankle and toe mobility or nodal compression. 3. Diagnosis: Lateral radiographs of the heel bone can be used to measure the thickness of the heel pad, and MRI is not required, but its can indicate swelling and atrophy of the heel pad. Lateral image of the heel: AB represents the level of the skin, CD represents the level of the heel node, EF is the line between the two, and its length represents the thickness of the heel pad 4, Treatment: NSAIDs, proper shoes, special orthopedic braces, silicone cups. As the disease is mostly caused by mechanical reasons, reducing compression and weight bearing is an effective method. Local injections of corticosteroids should be avoided because of their tendency to cause further atrophy in the long term. Surgical methods are also not recommended, and there is no effective way to dispose of or replace it with a new heel pad. Instead, it is prone to other complications such as skin necrosis. Baxter’s nerve entrapment syndrome 1. Cause: The first branch of the lateral plantar nerve, the only nerve located under the bunion muscle and the toe dorsiflexor, while on the square muscle. It governs the square muscle, the toe dorsiflexor, the little finger abductor, and the sensation of the lateral plantar skin, the periosteum of the heel, and the ligament along the plantar. Areas prone to entrapment 2. The nerve passes through the medial heel tuberosity. Two points where the Baxter’s nerve is susceptible to entrapment: 1, between the bunion adductor, the toe dorsiflexor and the plantar square. 2, when the nerve bypasses the medial heel tuberosity in front of the clinical manifestations: the pain is mostly located 4-5 cm in front of the heel bone, or distal to the heel tuberosity, and the pain is mostly incandescent and radiates along the lateral plantar aspect of the foot. The pain is often coexisting with plantar fasciitis. Physical examination includes atrophy of the gastrocnemius flaccida muscle and force lines in the posterior part of the foot. The symptoms can be exacerbated by valgus in the posterior part of the foot due to insufficient strength of the posterior tibial tendon and valgus in the horseshoe foot. The lateral plantar pressure is highest when the foot is plantarflexed and rotated forward. Pain can be induced by percussion. Lateral plantar sensation is reduced in chronic disease. Neurophysiogram can be used to diagnose the presence of nerve entrapment at the site of stenosis. Treatment: Early stages include: rest, ice-o, NSAIDs, orthopedic correction of abnormal force lines at the back of the foot, and local physical therapy. If conservative treatment fails and symptoms persist for 3 months, surgical decompression may be considered. This includes: release of the deep and superficial fascia of the bunion muscle covering the surface of the nerve. There are conflicting opinions on whether to eliminate the anterior heel bone. However, for open surgery, the satisfaction rate is high in 89% of patients. Stress fractures of the heel 1. Causes: Compression fractures of the heel, the largest tarsal bone in the body, are uncommon and occur only after the metatarsals. It occurs in athletes, military personnel, and elderly people with osteoporosis. It is caused by repeated overload and inconsistent bone resorption and osteogenesis. Compression fracture of the heel bone: the arrow in the lateral view of the heel bone 2. It is aggravated by activity and weight-bearing, and does not decrease at rest. There is pressure pain along the lateral aspect of the heel bone, and the heel bone crush test is positive. Diagnosis: Lateral radiographs of the heel bone can show destruction of the heel trabeculae 2-8 weeks after the onset of symptoms, although these images are mostly considered normal in the early stages of the disease. A sclerotic bone line perpendicular to the normal trabeculae predicts healing of the compression fracture. When pain persists and there is no evidence on plain radiographs, MRI or bone scan may be useful for diagnosis. 4. Treatment: Includes aggressive management with immobilization of the short leg in a cast for 4-8 weeks. It also includes VD supplementation and a bone density test. After immobilization, normal activities can be resumed. The prognosis is good and surgery is rarely required. Severe misalignment with abnormal force lines is uncommon and the likelihood of non-union is low. Ankle canal syndrome 1. Cause: A symptom of compression of the vascular nerve bundle of the posterior tibial nerve in the ankle canal. This syndrome is relatively uncommon and easily overdiagnosed. Flat feet are most likely to cause ankle canal syndrome due to the tendency of hindfoot valgus and forefoot abduction to cause nerve compression. Other causes include: fractures, narrowing of the ankle canal space, and tenosynovitis. Systemic systemic inflammatory arthropathy, diabetes, rheumatoid, etc. 2. Clinical manifestations and physical examination: The patient’s subjective sensation is vague and difficult to locate, however, the pain and numbness mostly occur in the ankle joint and the inner posterior part of the heel, and mostly radiates to the sole of the foot. The pain and numbness occur mostly in the ankle and heel, and radiates to the bottom of the foot. Sensory dullness affects sleep. In particular, the pain and numbness are particularly pronounced when there is significant entrapment, resulting in decreased muscle strength, first in the toe abductors and then in the little toe abductors. TINEL syndrome along the ankle canal and irreparable hyperalgesia along the tibial nerve distribution are the most important symptoms. Other stimulation methods, such as dorsiflexion and stretching of the tibial nerve, also tend to induce lesions. 3. Diagnosis: MRI is important for diagnosing anatomical abnormalities of the ankle canal and tibial nerve compression due to occupancy. Nerve conduction velocity and electromyography help to confirm the diagnosis. However, it has false negatives. 4. Treatment: Non-surgical methods include NSAIDs, and immobilization. Special orthopedic shoes should be worn for patients with flat feet. Caution is needed with local injections of corticosteroids, as there is a risk of tendon rupture and intravascular injection. Surgery is indicated for those patients for whom non-surgical treatment has not been effective and who have significant preoccupation, including careful removal of the flexor support band and, in some cases, the recommendation to completely release the medial plantar nerve by removing the diaphragm under the adductor muscle.