RSD REFLEX SYMPATHETIC DYSTROPHY 2
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Possibly the worst pain syndrome is Reflex Sympathetic Dystrophy, referred to as RSD. People suffering from RSD experience continual pain that feels like their skin is on fire. To an RSD patient, touching a piece of tissue paper or a bed sheet with the affected limb feels like touching fire.
In 1986, the International Association for the Study of Pain Subcommittee on Taxonomy defined Reflex Sympathetic Dystrophy as continuous pain in an extremity with sympathetic hyperactivity. This generally occurs from a trauma such as a bone fracture.
The name of the condition was later changed to Sympathetically-Mediated Regional Pain Syndrome. It is a pain syndrome that occurs due to an increase in the activity of the sympathetic nervous system. RSD is very similar to fibromyalgia, in that many people are labeled with both of these conditions when, in fact, they have ligament or tendon laxity. Ligament laxity can cause severe, burning extremity pain. Just as with fibromyalgia, traditional treatments usually provide only temporary benefits.
Stages of RSD
RSD is a deteriorating disease, progressing in three stages. In stage I, the acute phase, the pain is described as burning or aching which is exacerbated by touch, emotional upset, or active/passive movement. The pain is often tremendous, much more than is expected with the original injury. For example, two months after a stubbed toe, severe pain may develop far beyond what would normally be expected for such a mild injury. The involved limb becomes edematous (filled with fluid) and may be hot or cold. A bone scan may reveal an increased uptake of the radioactive phosphate compound in the affected area, indicating increased uptake of red blood cells to the area.
In stage II, the dystrophic phase of RSD, the pain is constant and is exacerbated by any sensory input. Excruciating pain is elicited by touching, vibrating, moving, or even blowing on the affected limb. The limb becomes more edematous, cool, and hyperhidrotic (sweaty). The bone scan typically shows a decreased uptake of red blood cells and x-ray films reveal the initial stages of osteoporosis.
Finally, in stage III, the atrophic phase, irreversible damage occurs to the extremity. Because of limited movement of the extremity, the affected limb contracts and the skin becomes cool, thin, and shiny. Because of scar tissue, it is nearly impossible to move the joint, and arthritis and osteoporosis are prevalent, resulting in a permanently frozen or contracted limb. At this time, the pain begins to subside; however, the limb is now essentially useless. The progression from stage I to stage III occurs over several months or years. Unfortunately, this process may repeat itself in other parts of the body.
Causes of RSD
Factors that predispose people to RSD are arthritis, brain injury, spinal cord injury, fracture, herpes, immobilization with a cast or splint, infection, heart attack, soft tissue injury, surgery, nerve injury, sprain, tendonitis or bursitis, vasculitis, and others. RSD experts conclude that trauma is the usual initiating event in the development of RSD.
People experiencing chronic pain attempt to decrease inflammation, most often by taking anti-inflammatory medicines, thereby unknowingly diminishing the chance of healing. The majority of people with RSD have also taken anti-inflammatory medicines after their injury, thereby diminishing their chances of healing. In every case of RSD we have treated, the patient was previously advised to immobilize the limb, generally the foot or hand, for a prolonged period of time. Immobilizing an injured joint for a prolonged period of time will guarantee inadequate healing of the soft tissue injury.
The traditional treatment for soft tissue or bony injuries is Rest, Ice, Compression, and Elevation (RICE). Rest has the following detrimental effects on the bones and soft tissues of the joints after two weeks of immobilization: fibrosis of periarticular tissue (contracture and weakening of joint capsules and ligaments); cartilage deterioration, producing an overgrowth of bone; atrophy in weight-bearing areas; and regional bony eburnation, sclerosis and resorption (fancy terms for arthritis and osteoporosis). Many of these effects are irreversible.
It is not uncommon for RSD patients to relay a treatment course of resting the limb for a few days, a doctor wrapping it for a week or two, and another doctor casting it for a month. The patient eventually immobilizes the limb because of the severity of the pain. The immobility triggers the arthritic process and potentially the RSD process as well. Immobility is especially detrimental to the articular cartilage that lines the bones in the joints. The articular cartilage has no blood vessel supply. It depends on the compressive force of the bones to provide joint fluid into the articular cartilage for nourishment. An immobilized joint starves the articular cartilage. Immobility causes a reduction in the cartilage-water content, a decrease in the glycosaminoglycan content, and a loss of hexamines from the periarticular tissue. In other words, the articular cartilage degenerates, beginning a slow death of the cartilage.
It is common medical knowledge that immobility causes osteoporosis, or weakening of the bones, due to the urinary excretion of calcium from the resorption of bone. This osteoporosis process begins as soon as the limb becomes immobile. The strength of the bones is dependent upon muscle contraction through production of an electrical current with each contraction. The greater the immobility, the greater the osteoporosis. When a tissue is injured, anti-inflammatories and immobility should be avoided. Movement, Exercise, Analgesics, and Treatment (MEAT) as opposed to RICE after an injury, in many cases, will prevent the onslaught of RSD.
It is not uncommon after a cast is removed for pain in the limb to remain. The orthopedist interprets this as a normal occurrence caused by stiffness and recommends physical therapy to resolve the problem. Unfortunately for many, therapy does not resolve the problem; consequently, the patient sees another physician. Many do not find relief and, although they may not develop RSD, they have a chronic pain problem. The solution to their problem may be found with a physician familiar with Prolotherapy.
Imagine the magnitude of force required to break a bone. What happens to the ligaments that support the joint around the broken bone? The ligaments are injured. The blood supply to bone is excellent, whereas blood supply to ligament tissue is poor. Small feeder blood vessels, which are sheared during the initial injury, are designed to supply the ligaments with essential nutrients. This worsens the nutritional support that the ligaments receive. Combine this with NSAIDs and immobility, and the ligaments have essentially no hope of healing. This is why patients have chronic pain after their cast is removed despite good physical therapy. Post-casting, post-broken bone pain that does not respond to physical therapy is most likely a ligament injury. Weakened ligaments will not heal with physical therapy. Chronic ligament laxity has only one curative treatment, Prolotherapy.
RSD is often triggered by a traumatic event. This initial injury causes soft tissue damage involving the ligaments. The sympathetic nervous system shuts down to allow increased blood flow to the area in order to heal the injury. This is why initial bone scans clearly reveal RSD. Because the ligaments do not heal, joint deterioration continues. As the joint continues to deteriorate, the sympathetic nervous system’s output increases because the ligament injury has not healed.
Physiological Changes Occurring in RSD
What is the source of RSD pain? As the name implies, the sympathetic nervous system becomes hyperactive. Adrenaline activates the sympathetic nervous system when you are nervous. What causes and maintains the hyperactivity of the sympathetic nervous system? The sympathetic nervous system is part of the autonomic nervous system, meaning that it is not under our conscious control. We do not consciously direct our blood vessels to dilate from 1.2 mm in diameter to 1.3 mm because it is a hot day. This happens automatically.
The result of sympathetic stimulation on the blood vessels causes them to constrict, therefore, decreasing the blood supply to the tendons, ligaments, bones, and skin of the limb. Decreased blood supply will also decrease the immune system’s ability to heal and will lead to osteoporosis, as the tendons and ligaments become fibrosed or shortened. The skin becomes shiny and pale. Because of impaired joint movement, the articular joint degenerates. The end result of the increased sympathetic activity is a contracted useless limb. It is imperative to properly treat RSD at the onset of its symptomatology.
In 1949, I. Korr, M.D., published the first of a series of papers on sympathetic hyperactivity related to alterations in the sensory input from the musculoskeletal system. He described how muscle, joint, or soft tissue injury caused an increase in the activity of the sympathetic nervous system at the injured limb. Bio-mechanical stress, such as tilting the pelvis or wearing a heel lift, could cause the hyperactivity. Other studies have shown that any type of noxious mechanical deformation or chemical irritation of the soft tissues or joints alters the sensory input to the sympathetic nervous system. This causes the sympathetic nervous system to fire the nerves and the blood vessels to constrict in the limb, triggering the progression of RSD.
Treatment of RSD
The traditional treatment for RSD involves various forms of sympathetic nerve blocks, consisting of injections of anesthetics into the sympathetic ganglion in the neck and back. These sympathetic ganglion blocks cause an immediate increase in temperature to the limb due to the increased blood flow. Often the patient experiences immediate pain relief.
Unfortunately, this treatment is only temporarily effective. RSD patients may receive multiple sympathetic blocks, to the point of having anesthetic pumps placed in their backs, or even have the sympathetic nerves severed in an attempt to find relief from their pain.
Treating the ligament injuries to stabilize the joint during stage I and stage II will eliminate the symptoms of RSD. An evaluation by a physician familiar with Prolotherapy is crucial for proper diagnosis and treatment for anyone who has had a simple injury that has not healed after several months. Prolotherapy injections to repair injured ligaments will keep a simple injury, simple. The further the progression of RSD, the harder it is to treat. If Prolotherapy is performed prior to the stage III changes, the condition is reversible. Prolotherapy can halt the progression of RSD because the initial etiological basis for the disease, ligament injury, is corrected. For example, RSD of the feet is often due to an injury to the anterior talofibular and its accompanying ligaments.
Prolotherapy stimulates the body to improve blood flow because it causes inflammation at the fibro-osseous junction. Prolotherapy cannot reverse the destructive changes that have occurred, but can be very helpful in eliminating the pain from RSD.
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