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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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Most flexible flat feet are asymptomatic, and do not cause pain. In these cases, there is usually no cause for concern. Flat feet were formerly a physical-health reason for service-rejection in many militaries. However, three military studies on asymptomatic adults (see section below), suggest that persons with asymptomatic flat feet are at least as tolerant of foot stress as the population with various grades of arch. Asymptomatic flat feet are no longer a service disqualification in the U.S. military.
In a study performed to analyze the activation of the tibialis posterior muscle in adults with pes planus, it was noted that the tendon of this muscle may be dysfunctional and lead to disabling weightbearing symptoms associated with acquired flat foot deformity. The results of the study indicated that while barefoot, subjects activated additional lower-leg muscles to complete an exercise that resisted foot adduction. However, when the same subjects performed the exercise while wearing arch supporting orthotics and shoes, the tibialis posterior was selectively activated. Such discoveries suggest that the use of shoes with properly fitting, arch-supporting orthics will enhance selective activation of the tibialis posterior muscle thus, acting as an adequate treatment for the undesirable symptoms of pes planus.
Rigid flatfoot, a condition where the sole of the foot is rigidly flat even when a person is not standing, often indicates a significant problem in the bones of the affected feet, and can cause pain in about a quarter of those affected. Other flatfoot-related conditions, such as various forms of tarsal coalition (two or more bones in the midfoot or hindfoot abnormally joined) or an accessory navicular (extra bone on the inner side of the foot) should be treated promptly, usually by the very early teen years, before a child's bone structure firms up permanently as a young adult. Both tarsal coalition and an accessory navicular can be confirmed by X-ray. Rheumatoid arthritis can destroy tendons in the foot (or both feet) which can cause this condition, and untreated can result in deformity and early onset of osteoarthritis of the joint. Such a condition can cause severe pain and considerably reduced ability to walk, even with orthoses. Ankle fusion is usually recommended.
Treatment of flat feet may also be appropriate if there is associated foot or lower leg pain, or if the condition affects the knees or the lower back. Treatment may include using orthoses such as an arch support, foot gymnastics or other exercises as recommended by a podiatrist/orthotist or physical therapist. In cases of severe flat feet, orthoses should be used through a gradual process to lessen discomfort. Over several weeks, slightly more material is added to the orthosis to raise the arch. These small changes allow the foot structure to adjust gradually, as well as giving the patient time to acclimatise to the sensation of wearing orthoses. Once prescribed, orthoses are generally worn for the rest of the patient's life. In some cases, surgery can provide lasting relief, and even create an arch where none existed before; it should be considered a last resort, as it is usually very time consuming and costly.
Training of the feet, utilizing foot gymnastics and going barefoot on varying terrain, can facilitate the formation of arches during childhood, with a developed arch occurring for most by the age of four to six years. Ligament laxity is also among the factors known to be associated with flat feet. One medical study in India with a large sample size of children who had grown up wearing shoes and others going barefoot found that the longitudinal arches of the bare-footers were generally strongest and highest as a group, and that flat feet were less common in children who had grown up wearing sandals or slippers than among those who had worn closed-toe shoes. Focusing on the influence of footwear on the prevalence of pes planus, the cross-sectional study performed on children noted that wearing shoes throughout early childhood can be detrimental to the development of a normal or a high medial longitudinal arch. The vulnerability for flat foot among shoe-wearing children increases if the child has an associated ligament laxity condition. The results of the study suggest that children be encouraged to play barefooted on various surfaces of terrain and that slippers and sandals are less harmful compared to closed-toe shoes. It appeared that closed-toe shoes greatly inhibited the development of the arch of the foot more so than slippers or sandals. This conclusion may be a result of the notion that intrinsic muscle activity of the arch is required to prevent slippers and sandals from falling off the child’s foot.
There are few good estimates of prevalence for pes cavus in the general community. While pes cavus has been reported in between 2 and 29% of the adult population, there are several limitations of the prevalence data reported in these studies. Population-based studies suggest the prevalence of the cavus foot is approximately 10%.
Diagnosis is made on the basis of history and a high index of suspicion. On examination there is tenderness to palpation on navicular head. Radiographs reveal typical changes of increased density and narrowing of the navicular bone
Surgical treatment is only initiated if there is severe pain, as the available operations can be difficult. Otherwise, high arches may be handled with care and proper treatment.
Suggested conservative management of patients with painful pes cavus typically involves strategies to reduce and redistribute plantar pressure loading with the use of foot orthoses and specialised cushioned footwear. Other non-surgical rehabilitation approaches include stretching and strengthening of tight and weak muscles, debridement of plantar callosities, osseous mobilization, massage, chiropractic manipulation of the foot and ankle, and strategies to improve balance. There are also numerous surgical approaches described in the literature that are aimed at correcting the deformity and rebalancing the foot. Surgical procedures fall into three main groups:
1. soft-tissue procedures (e.g. plantar fascia release, Achilles tendon lengthening, tendon transfer);
2. osteotomy (e.g. metatarsal, midfoot or calcaneal);
3. bone-stabilising procedures (e.g. triple arthrodesis).
The differential diagnosis for heel pain is extensive and includes pathological entities including, but not limited to the following: calcaneal stress fracture, calcaneal bursitis, osteoarthritis, spinal stenosis involving the nerve roots of lumbar spinal nerve 5 (L5) or sacral spinal nerve 1 (S1), calcaneal fat pad syndrome, hypothyroidism, seronegative spondyloparthopathies such as reactive arthritis, ankylosing spondylitis, or rheumatoid arthritis (more likely if pain is present in both heels), plantar fascia rupture, and compression neuropathies such as tarsal tunnel syndrome or impingement of the medial calcaneal nerve.
A determination about a diagnosis of plantar fasciitis can usually be made based on a person's medical history and physical examination. In cases in which the physician suspects fracture, infection, or some other serious underlying condition, an x-ray may be used to make a differential diagnosis. However, and especially for people who stand or walk a lot at work, x-rays should not be used to screen for plantar fasciitis unless imaging is otherwise indicated as using it outside of medical guidelines is unnecessary health care.
Plantar fasciitis is usually diagnosed by a health care provider after consideration of a person's presenting history, risk factors, and clinical examination. Tenderness to palpation along the inner aspect of the heel bone on the sole of the foot may be elicited during the physical examination. The foot may have limited dorsiflexion due to tightness of the calf muscles or the Achilles tendon. Dorsiflexion of the foot may elicit the pain due to stretching of the plantar fascia with this motion. Diagnostic imaging studies are not usually needed to diagnose plantar fasciitis. However, in certain cases a physician may decide imaging studies (such as X-rays, diagnostic ultrasound or MRI) are warranted to rule out serious causes of foot pain.
Other diagnoses that are typically considered include fractures, tumors, or systemic disease if plantar fasciitis pain fails to respond appropriately to conservative medical treatments. Bilateral heel pain or heel pain in the context of a systemic illness may indicate a need for a more in-depth diagnostic investigation. Under these circumstances, diagnostic tests such as a CBC or serological markers of inflammation, infection, or autoimmune disease such as C-reactive protein, erythrocyte sedimentation rate, anti-nuclear antibodies, rheumatoid factor, HLA-B27, uric acid, or Lyme disease antibodies may also be obtained. Neurological deficits may prompt an investigation with electromyography to evaluate for damage to the nerves or muscles.
An incidental finding associated with this condition is a heel spur, a small bony calcification on the calcaneus (heel bone), which can be found in up to 50% of those with plantar fasciitis. In such cases, it is the underlying plantar fasciitis that produces the heel pain, and not the spur itself. The condition is responsible for the creation of the spur though the clinical significance of heel spurs in plantar fasciitis remains unclear.
Though a neuroma is a soft tissue abnormality and will not be visualized on standard radiographs, the first step in the assessment of forefoot pain is an X-ray in order to evaluate for the presence of arthritis and exclude stress fractures/reactions and focal bone lesions, which may mimic the symptoms of a neuroma. Ultrasound (sonography) accurately demonstrates thickening of the interdigital nerve within the web space of greater than 3mm, diagnostic of a Morton’s neuroma. This typically occurs at the level of the intermetatarsal ligament. Frequently, intermetatarsal bursitis coexists with the diagnosis. Other conditions that may also be visualized with ultrasound and can be clinically confused with a neuroma include synovitis/capsulitis from the adjacent metatarsophalangeal joint, stress fractures/reaction, and plantar plate disruption. MRI can similarly demonstrate the above conditions; however, in the setting where more than one abnormality coexists, ultrasound has the added advantage of determining which may be the source of the patient’s pain by applying direct pressure with the probe. Further to this, ultrasound can be used to guide treatment such as cortisone injections into the webspace, as well as alcohol ablation of the nerve.
Shin splints can be diagnosed by a physician after taking a thorough history and performing a complete physical examination. The physical examination uses gentle pressure to determine whether there is tenderness over a 4–6 inch section on the lower, inside shin area. The pain has been described as a dull ache to an intense pain that increases during exercise, and some individuals experience swelling in the pain area. People who have previously had shin splints are more likely to have it again.
Vascular and neurological examinations produce normal results in patients with shin splints. Radiographies and three-phase bone scans are recommended to differentiate between shin splints and other causes of chronic leg pain. Bone scintigraphy and MRI scans can be used to differentiate between stress fractures and shin splints.
It is important to differentiate between different lower leg pain injuries, including shin splints, stress fractures, compartment syndrome, nerve entrapment, and popliteal artery entrapment syndrome. These conditions often have many overlapping symptoms which makes a final diagnosis difficult, and correct diagnosis is needed to determine the most appropriate treatment.
If shin splints are not treated properly, or if exercise is resumed too early or aggressively, shin splints can become permanent.
Risk factors for developing shin splints include:
- Excessive pronation at subtalar joint
- Excessively tight calf muscles (which can cause excessive pronation)
- Engaging the medial shin muscle in excessive amounts of eccentric muscle activity
- Undertaking high-impact exercises on hard, noncompliant surfaces (ex: running on asphalt or concrete)
- Smoking and low fitness level
While medial tibial stress syndrome is the most common form of shin splints, compartment syndrome and stress fractures are also common forms of shin splints. Females are 1.5 to 3.5 times more likely to progress to stress fractures from shin splints. This is due in part to females having a higher incidence of diminished bone density and osteoporosis.
Aside from surgery, there are a few options for handling an accessory navicular bone that has become symptomatic. This includes immobilization, icing, medicating, physical therapy, and orthotic devices. Immobilizing involves placing the foot and ankle in a cast or removable walking boot. This alleviates stressors on the foot and can decrease inflammation. Icing will help reduce swelling and inflammation. Medication involves usage of nonsteroidal anti-inflammatory drugs, or steroids (taken orally or injected) to decrease inflammation. Physical therapy can be prescribed in order to strengthen the muscles and help decrease inflammation. Physical therapy can also help prevent the symptoms from returning. Orthotic devices (arch support devices that fit in a shoe) can help prevent future symptoms. Occasionally, the orthotic device will dig into the edge of the accessory navicular and cause discomfort. For this reason, the orthotic devices made for the patient should be carefully constructed.
Treatment usually involves resting the affected foot, taking pain relievers and trying to avoid putting pressure on the foot. In acute cases, the patient is often fitted with a cast that stops below the knee. The cast is usually worn for 6 to 8 weeks. After the cast is taken off, some patients are prescribed arch support for about 6 months. Also, moderate exercise is often beneficial, and physical therapy may help as well.
Prognosis for children with this disease is very good. It may persist for some time, but most cases are resolved within two years of the initial diagnosis. Although in most cases no permanent damage is done, some will have lasting damage to the foot. Also, later in life, Kohler's disease can spread to the hips.
An equinovalgus is a deformity of the human foot. It may be a flexible deformity or a fixed deformity. Equino- means plantarflexed (as in standing on one's toes), and valgus means that the base of the heel is rotated away from the midline of the foot (eversion) and abduction of foot. This means that the patient is placing his/her weight on the medial border of the foot, and the arch of the foot is absent, which distorts the foot's normal shape.
Equinovalgus mostly occurs due to tightness of plantar flexors (calf muscles) and peroneus group of muscles.
Computed tomography is the most sensitive and specific of the imaging techniques. The facial bones can be visualized as slices through the skeletal in either the axial, coronal or sagittal planes. Images can be reconstructed into a 3-dimensional view, to give a better sense of the displacement of various fragments. 3D reconstruction, however, can mask smaller fractures owing to volume averaging, scatter artifact and surrounding structures simply blocking the view of underlying areas.
Research has shown that panoramic radiography is similar to computed tomography in its diagnostic accuracy for mandible fractures and both are more accurate than plain film radiograph. The indications to use CT for mandible fracture vary by region, but it does not seem to add to diagnosis or treatment planning except for comminuted or avulsive type fractures, although, there is better clinician agreement on the location and absence of fractures with CT compared to panoramic radiography.
There are various classification systems of mandibular fractures in use.
X-rays may help visualize bone spurs, acromial anatomy and arthritis. Further, calcification in the subacromial space and rotator cuff may be revealed. Osteoarthritis of the acromioclavicular (AC) joint may co-exist and is usually demonstrated on radiographs.
MRI imagining can reveal fluid accumulation in the bursa and assess adjacent structures. In chronic cases caused by impingement tendinosis and tears in the rotator cuff may be revealed. At US, an abnormal bursa may show (1) fluid distension, (2) synovial proliferation, and/or (3) thickening of the bursal walls. In any case, the magnitude of pathological findings does not correlate with the magnitude of the symptoms.
In patients with bursitis who have rheumatoid arthritis, short term improvements are not taken as a sign of resolution and may require long term treatment to ensure recurrence is minimized. Joint contracture of the shoulder has also been found to be at a higher incidence in type two diabetics, which may lead to frozen shoulder (Donatelli, 2004).
Orthotics and corticosteroid injections are widely used conservative treatments for Morton’s neuroma. In addition to traditional orthotic arch supports, a small foam or fabric pad may be positioned under the space between the two affected metatarsals, immediately behind the bone ends. This pad helps to splay the metatarsal bones and create more space for the nerve so as to relieve pressure and irritation. It may however also elicit mild uncomfortable sensations of its own, such as the feeling of having an awkward object under one's foot. Corticosteroid injections can relieve inflammation in some patients and help to end the symptoms. For some patients, however, the inflammation and pain recur after some weeks or months, and corticosteroids can only be used a limited number of times because they cause progressive degeneration of ligamentous and tendinous tissues.
Sclerosing alcohol injections are an increasingly available treatment alternative if the above management approaches fail. Dilute alcohol (4%) is injected directly into the area of the neuroma, causing toxicity to the fibrous nerve tissue. Frequently, treatment must be performed 2–4 times, with 1–3 weeks between interventions. A 60–80% success rate has been achieved in clinical studies, equal to or exceeding the success rate for surgical neurectomy with fewer risks and less significant recovery. If done with more concentrated alcohol under ultrasound guidance, the success rate is considerably higher and fewer repeat procedures are needed.
Radio Frequency Ablation is also used in the treatment of Morton's Neuroma The outcomes appear to be equally or more reliable than alcohol injections especially if the procedure is done under ultrasound guidance.
If such interventions fail, patients are commonly offered surgery known as neurectomy, which involves removing the affected piece of nerve tissue. Postoperative scar tissue formation (known as stump neuroma) can occur in approximately 20%-30% of cases, causing a return of neuroma symptoms. Neurectomy can be performed using one of two general methods. Making the incision from the dorsal side (the top of the foot) is the more common method but requires cutting the deep transverse metatarsal ligament that connects the 3rd and 4th metatarsals in order to access the nerve beneath it. This results in exaggerated postoperative splaying of the 3rd and 4th digits (toes) due to the loss of the supporting ligamentous structure. This has aesthetic concerns for some patients and possible though unquantified long-term implications for foot structure and health. Alternatively, making the incision from the ventral side (the sole of the foot) allows more direct access to the affected nerve without cutting other structures. However, this approach requires a greater post-operative recovery time where the patient must avoid weight bearing on the affected foot because the ventral aspect of the foot is more highly enervated and impacted by pressure when standing. It also has an increased risk that scar tissue will form in a location that causes ongoing pain.
Cryogenic neuroablation is a lesser known alternative to neurectomy surgery. Cryogenic neuroablation (also known as cryo injection therapy, cryoneurolysis, cryosurgery or cryoablation) is a term that is used to describe the destruction of axons to prevent them from carrying painful impulses. This is accomplished by making a small incision (~3 mm) and inserting a cryoneedle that applies extremely low temperatures of between −50 °C to −70 °C to the nerve/neuroma. This results in degeneration of the intracellular elements, axons, and myelin sheath (which houses the neuroma) with wallerian degeneration. The epineurium and perineurium remain intact, thus preventing the formation of stump neuroma. The preservation of these structures differentiates cryogenic neuroablation from surgical excision and neurolytic agents such as alcohol. An initial study showed that cryo neuroablation is initially equal in effectiveness to surgery but does not have the risk of stump neuroma formation.
Recently, an increasing number of procedures are being performed at specialist centers which offer a range of procedures to treat Morton's neuroma under ultrasound guidance. Recent studies have shown excellent results for the treatment of Morton's neuroma with ultrasound guided sclerosing alcohol injections, ultrasound guided radiofrequency ablation, and ultrasound guided cryo-ablation.
An accessory navicular bone is an accessory bone of the foot that occasionally develops abnormally in front of the ankle towards the inside of the foot. This bone may be present in approximately 2-21% of the general population and is usually asymptomatic. When it is symptomatic, surgery may be necessary.
Surgery can be performed at any age because it does not alter any other bones.
Symptoms of an accessory navicular bone may include plantar fasciitis, bunions and heel spurs.
In most people, ligaments (which are the tissues that connect bones to each other) are naturally tight in such a way that the joints are restricted to 'normal' ranges of motion. This creates normal joint stability. If muscular control does not compensate for ligamentous laxity, joint instability may result. The trait is almost certainly hereditary, and is usually something the affected person would just be aware of, rather than a serious medical condition. However, if there is widespread laxity of other connective tissue, then this may be a sign of Ehlers-Danlos syndrome.
Ligamentous laxity may also result from injury, such as from a vehicle accident. It can result from whiplash and be overlooked for years by doctors who are not looking for it, despite the chronic pain that accompanies the resultant spinal instability. Ligamentous laxity will show up on an upright magnetic resonance imaging (MRI), the only kind of MRI that will show soft tissue damage. It can be seen in standing stress radiographs in flexion, extension, and neutral views as well, and also digital motion X-ray, or DMX.
An advantage to having lax ligaments and joints is the ability to withstand pain from hyperextension; however, this is also a disadvantage as a lack of perceived pain can prevent a person from removing the ligament from insult, leading to ligament damage. This can also lead to death if you tear the wrong ligament. People with hypermobile joints (or "double-jointed" people), almost by definition, have lax ligaments.
Although the precise mechanism of injury is unclear, the injury occurs in children who have fallen heavily with their arm trapped under the body. In his original description of the injury, Hume suggested that the injury occurred as a result of hyperextension of the elbow leading to fracture of the olecranon, with pronation of the forearm leading to the radial head dislocation.
Those who have loose ligaments in the legs and feet often mistakenly assume that they have flat feet. While their feet have an arch when not supporting weight, when stood upon, the arch will flatten. This is because the loose ligaments cannot support the arch in the way that they should. This can make walking and standing painful and tiring.
Pain will usually occur in the feet and lower legs, but can also spread to the back due to abnormal standing and walking habits. Wearing shoes that have good arch support can help minimize the discomfort. The underlying problem, however, is not solved by wearing shoes with arch supports or worsened by wearing shoes without arch support. There is currently no cure for the condition.
In addition, people with ligamentous laxity often have clumsy or deliberate gaits, owing to the body having to overcompensate for the greater amount of energy required to offset the weakened ligaments. The feet may be spread apart at a wide angle, and the knees may flex backwards slightly after each stride.
Those who have this disease may experience sprained ankles more frequently than other people.
Non-displaced or minimally displaced fractures may be treated conservatively. Open reduction and internal fixation is reserved for cases that are severely angulated or comminuted. The purpose of fixation is to restore the normal appearance of the face. Specific attention is given to the position of the malar eminence and reduction of orbital volume by realigning the zygoma and sphenoid. Failure to correct can result in rotational deformity and increase the volume of the orbit, causing the eye to sink inwards.
Fractures with displacement require surgery consisting of fracture reduction with miniplates, microplates and screws. Gillie's approach is used for depressed zygomatic fractures. The prognosis of tripod fractures is generally good. In some cases there may be persistent post-surgical facial asymmetry, which can require further treatment.
In the original description by Hume, where the olecranon fractures were not displaced, treatment consisted of closed reduction of the radial head dislocation under general anaesthesia by supination of the forearm. This was followed by immobilisation of the arm in a plaster cast with the elbow flexed at 90° and the forearm in supination for 6 weeks.
Where the olecranon fracture is displaced, open reduction internal fixation is recommended. Once the olecranon has been repaired, closed reduction of the radial head dislocation is usually possible. This is followed by immobilisation with the elbow flexed to 90° and the forearm in the neutral position. The duration of immobilisation depends on clinical assessment of the joint, and mobilisation may be possible after as little as 4 weeks.
The use of surgery to treat a Jefferson fracture is somewhat controversial. Non-surgical treatment varies depending on if the fracture is stable or unstable, defined by an intact or broken transverse ligament and degree of fracture of the anterior arch. An intact ligament requires the use of a soft or hard collar, while a ruptured ligament may require traction, a halo or surgery. The use of rigid halos can lead to intracranial infections and are often uncomfortable for individuals wearing them, and may be replaced with a more flexible alternative depending on the stability of the injured bones, but treatment of a stable injury with a halo collar can result in a full recovery. Surgical treatment of a Jefferson fracture involves fusion or fixation of the first three cervical vertebrae; fusion may occur immediately, or later during treatment in cases where non-surgical interventions are unsuccessful. A primary factor in deciding between surgical and non-surgical intervention is the degree of stability as well as the presence of damage to other cervical vertebrae.
Though a serious injury, the long-term consequences of a Jefferson's fracture are uncertain and may not impact longevity or abilities, even if untreated. Conservative treatment with an immobilization device can produce excellent long-term recovery.