1, reflex sympathetic dystrophy syndrome overview (reflex sympathetic dystrophy syndrome is what disease?) .
Reflex sympathetic dystrophy syndrome (RSDS) is a clinical syndrome characterized by severe pain in the distal extremities with autonomic dysfunction.
The symptoms often appear rapidly within a few hours after the injury, but can also appear gradually in the days or weeks after the injury, and last for weeks to years. The pain is characterized by the following features: burning pain, which can be intense with light touch or repeated mild stimulation, pain that is not proportional to the severity of the injury, and pain that lasts longer than the expected healing time. Pain in the affected limb is often accompanied by diffuse pressure and swelling, and manifestations of autonomic dysfunction, such as cold and hot, red and white, dryness or sweating. The lesions progress slowly, and atrophy and contracture of the skin and subcutaneous tissues appear in the late stage.
2.Reflex sympathetic dystrophy syndrome symptoms and signs (What are the symptoms of reflex sympathetic dystrophy syndrome?) .
RSDS is usually recognized by its characteristic clinical manifestations. Symptoms often appear rapidly within a few hours of injury, but may also appear gradually over days or weeks after injury and persist for weeks to years. The pain is characterized by a burning pain, which can be intense with light touch or repeated mild irritation, pain that is not proportional to the severity of the injury, and pain that lasts longer than the expected healing time. The pain in the affected limb is often accompanied by diffuse pressure and swelling, and manifestations of autonomic dysfunction, such as hot and cold, red and white, dryness or sweating of the limb. The lesions are slow RSDS and are usually recognized by their characteristic clinical presentation. Symptoms often appear rapidly within a few hours after the injury, but may also appear gradually over days or weeks after the injury and persist for weeks to years. The pain is characterized by a burning pain, which can be intense with light touch or repeated mild irritation, pain that is not proportional to the severity of the injury, and pain that lasts longer than the expected healing time. Pain in the affected limb is often accompanied by diffuse pressure and swelling, and manifestations of autonomic dysfunction, such as cold and hot, red and white, dryness or sweating. The lesions progress slowly, with atrophy and contracture of the skin and subcutaneous tissues appearing in advanced stages. The hands and feet are the most common sites of pain, while others such as the knee, patella, shoulder, face, and individual fingers or toes may also occasionally be painful. When the distal part of the upper extremity is involved, the shoulder joint on the diseased side may become painful and limited in movement, resulting in shoulder-hand syndrome.
There are generally 3 clinical phases.
1. Acute phase is the post-traumatic pain phase. It is characterized by burning pain and vasodilation of the affected limb, congestion and edema of the affected limb, and increased skin temperature in the injury area.
2. Dystrophic phase characterized by vasoconstriction, cool skin with reticular pigmentation and cyanosis, hair loss, hardened and brittle nails in the affected area.
3. Atrophic phase The limb pain develops proximally, the skin becomes thin and shiny, the fingers become thin, the fascia becomes thin and flexion contracture
3. Diagnostic tests for reflex sympathetic dystrophy syndrome (what tests are needed to confirm the diagnosis of reflex sympathetic dystrophy syndrome?) ：
Diagnosis: Diagnosis strictly depends on clinical manifestations, and the diagnostic criteria proposed by Genant et al. include the following six items: ① pain and tenderness in the limbs; ② soft tissue swelling; ③ reduced motor function; ④ nutritional skin changes; ⑤ vasomotor instability; ⑥ patchy osteoporosis. Experimental diagnosis can be made by nerve closure if diagnosis is difficult. Laboratory tests: no abnormalities in laboratory tests. Radiological examinations usually show segmental bone deficiency, and typical cases can be… [Display] Diagnosis: The diagnosis is strictly dependent on clinical manifestations, and the diagnostic criteria proposed by Genant et al. include the following six items: ① pain and tenderness in the limbs; ② soft tissue swelling; ③ reduced motor function; ④ nutritional skin changes; ⑤ vasomotor instability; ⑥ patchy osteoporosis. patchy osteoporosis. If the diagnosis is difficult, nerve closure can be used for experimental diagnosis.
Laboratory tests: no abnormalities in laboratory tests.
Other auxiliary examinations.
Radiological examination X-ray films usually show segmental bone deficiency, typically with patchy decalcification and soft tissue edema in long bones of the limbs and short bones of the hands and feet. High-resolution radiographs may also show subperiosteal resorption, striae formation, subperiosteal holes and tunnel formation. CT and MRI of the affected extremities appear to be of little or no diagnostic value.
2. triple phase bone scanning (TPBS) After intravenous injection of nuclide (usually 99mTc) for 5s, 1~5min and 3~4h, the changes of blood flow imaging, blood pool imaging and delayed imaging were observed respectively, and it can be seen that the uptake of nuclide at the affected area is significantly higher than that of normal tissue. It is suitable for those with early limited RSDS or negative X-ray examination.
4.Reflex sympathetic dystrophy syndrome treatment plan (how to treat reflex sympathetic dystrophy syndrome?) : The earlier the diagnosis, the better the outcome.
The earlier the diagnosis, the better the outcome. Shoulder-hand syndrome is treated with high intensity physical therapy to restore shoulder function, including heat therapy, acupuncture, and transcutaneous electrical nerve stimulation. Pharmacological treatment includes sympathetic nerve block, high dose short course corticosteroids, amitriptyline, etc. Sympathetic nerve block or severance is effective for this disease. Traditionally, local anesthetic drugs or epidural anesthesia are used for ganglion block, but now chemical drugs such as systemic intravenous phentolamine or subcutaneous injection or intranasal calcitonin are used to block the nerve, which is more effective than traditional… [Show] The earlier the diagnosis, the better the outcome. Shoulder-hand syndrome is mainly treated with high-intensity physical therapy to restore shoulder function, including heat therapy, acupuncture, and transcutaneous electrical nerve stimulation. Pharmacological treatment includes sympathetic nerve block, high dose short course corticosteroids, amitriptyline, etc. Sympathetic nerve block or dissection is effective for this disease. Traditionally, local anesthetic drugs or epidural anesthesia are used for ganglion block, but now chemical drugs such as systemic intravenous phentolamine or subcutaneous injection or nasal inhalation of calcitonin are used to block the nerve, which is more effective than traditional ganglion block, so in addition to treatment, it is also often used as a diagnostic treatment test.
Physiotherapy: cold and wet compression, heat therapy, wax therapy, stellate nerve ultrasound therapy, acupuncture and electroacupuncture are simple and easy to use, and can directly improve the function of limb movement. Transcutaneous implanted electrode stimulation can selectively stimulate the larger myelinated nerve sensory fibers to stimulate the inhibitory system and relieve pain. Massachusetts General Hospital treated 44 cases of RSDS with electrode implantation method, 1/3 of them had long-term relief and 1/3 of them had pain recurrence due to local scar formation.
2. Drug treatment.
(1) Sympathetic nerve block or dissection.
(1) Local anesthetic or epidural block: the ganglion below the stellate ganglion can be closed for upper limb involvement. If the pain is still not relieved, use 1% procaine 20-30 ml for intrathecal injection of brachial plexus nerve. For lower extremity involvement, saline, 0.2% procaine (sympathetic nerve block concentration), 0.5% procaine (sensory nerve block concentration), and 1% procaine (motor nerve block concentration) 5ml each can be injected epidurally every 10 min.
Schultzer et al. replaced guanethidine with lisdexamfetamine for sympathetic blockade and obtained similar results. Dellemijn used intravenous phentolamine for sympathetic blockade and achieved good results. Mays treated 10 patients with RSDS with 2 mg morphine diluted in 7 ml physiological saline as a method of planetary ganglion closure, resulting in complete remission in 8 cases and no recurrence in 7 cases within 2-8 months.
Shumacker reported 34 RSDS patients with 35 limbs underwent sympathectomy, and the results were cured except for 4 cases with mild sequelae. week synthesized the efficacy of sympathectomy in 231 RSDS cases by 6 authors, and the efficiency was 82%.
(2) glucocorticoids: corticosteroids have a significant effect on RSDS, especially for those who refuse or cannot tolerate sympathetic nerve block therapy. Generally, high-dose short-course therapy, prednisone 60-80mg/d, divided into 4 oral doses, 2 weeks after the gradual reduction, 3-4 weeks after discontinuation. In some patients, a small dose of prednisone 5-10 mg/d is needed for long-term application to control symptoms. 13 patients with RSDS were treated with Christensen, and 75% had improvement in symptoms. 17 patients with RSDS were treated with Kozin, and 82% had significant results. In some patients, intramuscular calcitonin or local intravenous ketanserin can provide long-term pain relief.
(3) Nifedipine (cardiac pain): a calcium antagonist, can relax smooth muscle, increase peripheral blood circulation, can counter the effect of norepinephrine, not only to relieve pain and stabilize vasomotion. prough reported the application of nifedipine oral treatment of 13 patients diagnosed with RSDS, 10mg each time, 3 times / d, can be increased if not effective, and then stop taking the drug after 3 weeks. The results were complete remission in 7 cases, partial remission in 2 cases, ineffective in 1 case, and discontinuation in 3 cases due to intolerance of drug reactions. Other drugs such as amitriptyline, phenibut, propranolol, and bisphosphonates have also been reported for the treatment of RSDS.
5, reflex sympathetic dystrophy syndrome prevention and prognosis (how to prevent reflex sympathetic dystrophy syndrome?) : The
Prognosis.
The lesion progresses slowly, with atrophy and contracture of the skin and subcutaneous tissue in the late stages. It can last from several weeks to several years. The symptoms, such as burning pain, can be severe with light touch or repeated mild stimulation, and the pain is not proportional to the severity of the injury. However, the prognosis is good.
Prevention.
1, eliminate and reduce or avoid the onset of factors, improve the living environment space, develop good habits, prevent infection, pay attention to dietary hygiene, reasonable dietary allocation. Avoid trauma.
2, pay attention to exercise, increase the body’s ability to resist disease, do not overwork, overexertion, quit smoking and alcohol. Maintain a balanced psychology and overcome anxiety and tension.
3, early detection and early diagnosis and treatment, establish confidence in overcoming the disease and adhere to treatment.
Clinical diagnostic criteria (Table 1).
Table 1Gibbons et al. RSD score diagnostic items.
1, allodynia, nociceptive hypersensitivity; 2, burning pain; 3, edema; 4, changes in skin rather color and cilia; 5, changes in sweating; 6, bone decalcification images on X-ray; 7, temperature changes; 8, vasomotor disorders, quantitative determination of sweating disorders; 9, bone scintigraphy seen; 10, sympathetic nerve block effect.
Evaluation of the scoring totals for each diagnostic item.
Positive II 1 score over 3.0: not RSD.
False positive one 0.5 points 3.5 to 4.5: possible RSD.
Negative evaluation two O points) 5.0:RSD is the most likely.
The disease can be clinically divided into three stages.
Stage 1 patients present with pain in the affected limb (including burning sensation, throbbing pain and diffuse painful discomfort, etc.) and local edema and varying degrees of vasoconstriction disorder, resulting in changes in limb color and temperature. x-rays may be normal or may show patchy bone hypodensity if left untreated, and may progress to stage 2 in 3-6 months.
Stage 2 is progressive and is highlighted by progressively increasing soft tissue swelling, skin and joint thickening, muscle wasting and skin stiffness. This stage can also last for 3-6 months.
Stage 3 is the most severe and is characterized by restricted movement, shoulder-hand syndrome, finger flexion, waxy dystrophy-like skin changes and friable nail crests, with severe osteoporosis visible on x-ray of bone.
I. Classification of CRPS.
Type I CRPS (RSD); Type I CRPS or RSD is a syndrome that is usually secondary to an initial noxious stimulus and is not limited to a single peripheral nerve distribution area, often incompatible with the stimulus condition. It is accompanied by marked edema, altered skin blood flow, abnormal sweating behavior, sensory abnormalities and/or nociceptive hypersensitivity. Common complaints of patients are hyperalgesia to cold pain and abnormal sensation to mechanical stimuli, and on examination, significant thermal hyperalgesia and abnormal vibratory sensation may be found.
Type II CRPS (burning neuralgia).
Type II CRPS or burning neuralgia is a burning pain, abnormal sensation, and nociceptive hypersensitivity that often occurs after injury to a major peripheral nerve portion of the hand or foot. The most common injuries that accompany type II CRPS are injuries to the median and sciatic nerves.
II. Causes of initiation of CRPS.
The typical causes of CRPS are traumatic injuries to the limb such as sprains, dislocations, fractures, crush injuries and lacerations or surgery, or peripheral nerve injuries. It has also been reported to occur from minor injury processes such as routine venipuncture or epidural injections of steroids. There is no association between the severity of the injury and the intensity of the final patient’s symptoms. It is also associated with other conditions such as diabetic neuropathy, multiple sclerosis, cerebrovascular accident, myocardial infarction and cancerous infiltration of the nerve plexus. Sometimes no cause can be identified.
The true incidence of CRPS is unknown because of its variable clinical presentation and frequent misdiagnosis. There are few published data to assess the epidemiology of CRPS. In the United States, many clinical studies have confirmed a high prevalence of the disease in middle-aged adults, but it is present in all age groups, including children. The high prevalence in people of working age reflects the association of this disease with injury at work. The disease affects all ethnic groups, although it shows a high prevalence in women, Caucasians, and Northern Europeans.
III. Etiology and pathogenesis of CRPS.
Despite the numerous theories on the subject, the definitive etiology and pathogenesis of CRPS remain elusive.
1, increased sympathetic activity; 2, sensitization of peripheral mechanical and nociceptive receptors; 3, alteration of central afferents; 4, neurogenic inflammation; 5, alteration of central processing; 6, initiation and maintenance of WDR neuronal sensitization.
IV. Clinical manifestations of CRPS.
The main clinical symptoms, the triad of sensory, autonomic and motor dysfunctions, vary greatly in their manifestations and course.
1, abnormal sensory neuron function pain.
Pain associated with CRPS is the most prominent and disabling symptom. Pain is usually constant and spontaneous, but often worsens paroxysmally under physical or psychological stress. Its severity can range from mild discomfort to severe and unbearable pain, with the pain being worst at night. The nature of the pain can be described as burning, aching, tearing, squeezing, stabbing, or cutting pain. In most patients, the pain is of multiple natures. Initially, pain may be confined to the site of injury, but later manifests as a non-anatomic distribution that does not follow a single peripheral nerve distribution. The pain is often described as a glove or sock-like distribution. Over time, the pain may extend to encompass the entire limb. The following phenomenon has also been described: the pain extends beyond the end of the affected limb to the contralateral limb, sometimes to the ipsilateral limb or to the side of the entire torso.
Sensory changes Sensory hypersensitivity (increased sensitivity to stimuli) is an almost constant component of CRPS. The patient is characteristically protective of the affected limb. If the attending physician attempts to touch the affected limb, the patient will intentionally withdraw the limb and refuse any contact. Patients with CRPS may also complain of unpleasant or uncomfortable, but not painful, sensations when cold (ice, halothane), vibration (tuning fork), or light touch is applied to the affected limb. In addition, there is a delayed nociceptive hypersensitivity, which is a delayed overreaction to stimuli and sensory legacy.
2. Autonomic symptoms.
Autonomic dysfunction is commonly present in patients with CRPS. It may manifest as either vasoconstriction, producing pale, cyanotic and chilled skin, or vasodilation, resulting in warmth and erythema of the extremities, and commonly marked edema and abnormal sweating (hyperhidrosis or hypohidrosis). As the disease progresses, progressive nutritional changes occur, including changes in skin thickness and luster; atrophy of muscles; bone decalcification; thickened and brittle nails; dull hair; and slowed growth of hair and nails.
3. Motor malfunction.
Muscle stiffness is the most frustrating physical examination finding for patients with CRPS, and it is more severe than in patients with trauma, surgery, and other common conditions.CRPS patients are often unable to initiate movement. Without treatment, muscle stiffness can worsen as the disease progresses. Other signs and symptoms of kinetic abnormalities include muscle spasms, intentional or postural tremor, decreased muscle strength, and hyperreflexia.
4. Other.
Another group of clinical findings includes reactive psychological disorders. These include anxiety, depression, and despair.
Although most cases of CRPS have been reported to occur in the extremities, facial pain syndromes have also been reported following maxillofacial tumor surgery, bullet penetrating wounds, head injuries, and treatment of difficult dental disease. The clinical manifestations of facial CRPS may be similar to those of extremity CRPS.