Complex localized pain syndrome (CRPS) refers to a clinical syndrome characterized by severe intractable and variable pain, malnutrition and dysfunction secondary to accidental injury, medically induced injury or systemic disease.
Incidence.
The incidence of complex localized pain syndrome (CRPS) in normal population is extremely small; the incidence of patients with complex localized pain syndrome (CRPS) after trauma varies from one report to another, generally at 4-8%. Burning pain (CRPS type II) is more likely to occur after nerve injury than other tissue injuries, with an incidence of 1%-15%, depending on the degree of nerve injury; it has been observed that 20% of patients with nerve injury have transient burning pain symptoms, and 2% still have persistent symptoms after 12 days; other reports show that 8.2% of patients with brachial plexus, median, ulnar, sciatic and tibial nerve injuries have persistent type II symptoms.
In adults, the distribution tends to be in the upper extremities, and 2/3 of type II lesions are located in the upper extremities; pediatric patients are less likely to have complex localized pain syndrome (CRPS); age predominates between 40 and 60 years; and the incidence in both sexes is generally thought to be higher in women, which may be related to psychological status.
Classification.
Complex localized pain syndrome (CRPS) encompasses two typical types of sympathetic pain disorders, reflex sympathetic dystrophy and burning neuralgia, namely CRPS type I and CRPS type II.
Type I is a symptom group consistent with the traditional description of RSD symptoms, i.e. abnormal neuromodulation (vasodilation and sweating disorders), sensory hypersensitivity or dullness, and tissue dystrophy.
Type II refers in particular to burning pain, and this type refers specifically to sympathetic-dependent persistent pain (SMP), which should be distinguished from sympathetic non-dependent persistent pain, or independent pain (SIP). Because the latter is the pain of the nerve injury itself, it does not belong to the category of complex localized pain syndrome (CRPS).
Clinical manifestations.
1, pain: most patients are induced by mechanical, thermal, mental, emotional stimuli, such pain includes spontaneous pain, nociceptive hypersensitivity and nociceptive hypersensitivity and other neurogenic pain. In some cases, 3-6 months or even longer after the injury, there can still be persistent pain, and spread to the surrounding area.
2, nutritional disorders: in the injury site and its surrounding tissues, often accompanied by vasomotor nerve dysfunction, swelling. Sometimes, although the swelling is not obvious, but often complains of swelling. The skin begins to sweat and mostly appears moist and flushed. The skin temperature may be variable high or low, with a tendency to decrease in the later stages, showing ischemic changes. With the progressive development of the disease, the growth rate of hair and nails changes from accelerated to slowed down, and the skin gradually becomes thin and the nails curl and lose their luster.
3.Motor function: Grip strength and fine motor function can be reduced in the early stage. As the range of motion decreases, the joints become stiff due to muscle wasting atrophy. After 6 months of the disease, the skin becomes thin and shiny due to the atrophy of the subcutaneous tissue, and the sweating of the affected skin increases or decreases. If the myofascial hypertrophy, it may also lead to joint contracture and osteoporosis.
Diagnostic criteria.
① A longer or recent history of injury or disease.
② Persistent burning-like pain with neurogenic pain manifestations.
③There is vascular and sweating dysfunction, nutritional changes such as muscle atrophy, limb edema or dehydration, and hypersensitivity to cold and other stimuli.
④Diagnostic sympathetic nerve block test is mostly positive.
Treatment.
Once complex local pain syndrome (CRPS) treatment is diagnosed, methods of pain relief should be sought as early as possible, and rehabilitation should be actively carried out at the same time.
1.Preventive treatment:The perfect treatment of trauma and adequate analgesia in the early stage of injury is very important. That is, the pain is perfectly controlled in the acute stage to prevent its development towards chronicity, and combined with psychiatric treatment, it is generally believed that better results can be achieved.
2.Nerve block treatment: sympathetic nerve block is the main treatment. Commonly used nerve blocks are: SGB, thoracic sympathetic nerve block, lumbar sympathetic nerve block, intravenous local nerve block, epidural block, subarachnoid block. The sympathetic nerve block performed clinically mainly works by blocking the pain mediated by it and dilating the blood vessels in its innervation area.
Transcutaneous electrical stimulation (TENS): TENS is an analgesic by activating endogenous opioid peptides, and it can also stimulate the thick fiber nerves at the pain site to change the sensory impulses transmitted to the central nervous system for the purpose of pain relief.
4.Drug treatment:
①Anti-depressants: commonly used are amytriptyline, promethazine, doxepin, meprotiline and other tri(tetra)cyclic anti-depressants.
② antispasmodics: representative drugs are carbamazepine, phenytoin sodium, sodium valproate, effective for nerve shock-like pain. The more widely used abroad is gabapentin, which can significantly relieve neuralgia caused by diabetes or herpes zoster.
③ Non-steroidal anti-inflammatory and analgesic drugs, neurotoxin, prostaglandin preparations, hormones, morphine drugs, etc.
5.When the pain symptoms do not improve or only temporarily improve after the anesthetic block by the authorities, the use of nerve-destroying drugs, nerve disruption or sympathectomy should be considered.
6.When the above treatments are ineffective, analgesic pacemaker or subarachnoid analgesic pump implantation can be considered.