IS IT PAIN OF SYMPATHETIC ORIGIN? UPDATE ON RSD AND SMP
BY
Bernard M. Abrams, M.D.

    The detection of reflex sympathetic dystrophy is extremely important in the care and well being of patients who manifest these pain syndromes, because of the possibility of early intervention and prevention of difficult and debilitating complications. There is a school of thought that reflex sympathetic dystrophy is a dubious entity- (1) This holds that, "RSD is not a syndrome; RSD is a phenomenology. RSD phenomenology: a) Can be seen in multiple medical disorders (vascular, inflammatory, neurological, etc.), in other words RSD imitators. b) Can occur as a product of mere immobilization in the context of significant pain, avoidance behavior, and at times psychiatric disorders, c) Can be man made as part of a factitious disorder with either "internal" (psychological) secondary gains (Munchausen's g ' s (malinger), or syndrome, etc-), or "external" (financial, drug related, etc.,) secondary gain d) Can he seen as part of a complex set of neuropathogenic phenomena occurring in the context of nerve injury or even it's absence. (2)

    Reflex sympathetic dystrophy is now characterized as a complex regional pain syndromes. CRPS Type 1, replaces the term RSD and CRPS Type 11, replaces the term causalgia.

    CRPS Type I (RSD) is usually related to trauma resulting in local tissue damage in an extremity, e.g-, visceral (myocardial infarction), as well as central (stroke) pathology as reported in the literature to cause CRPS Type 1. Causalgia or CRPS Type II differs from CRP'3 Type I (RSD) in that the injury does involve a major nerve trunk,

    The pathogenesis of CR?S Type I has been the subject of much investigation. Evidence is mounting to staggering that there is an abdominal interaction between the sympathetic efferents and the nociceptive afferents. These two systems perpeptuate each other creating a vicious cycle of pain along with sympathetic discharge. This is the basis for sympathetic blockade. Symptoms can occur insidiously over weeks or months or can occur abruptly. Symptoms spread proximally and are usually non-dermatomal. The severity of symptoms does not correlate with the severity of the injury. (3)

    In any event the diagnosis of reflex sympathetic dystrophy or complex regional pain syndrome should be considered if the majority of the following questions can be answered in the affirmative.

1. Is the pain disproportionate to the extent of the injury?
2. Is there associated hyperpathia?
3. Is there a burning quality to the pain?
4. Are there associated cyanosis, redness, or skin temperature changes?
5. Are the nails cracked and grooved?
6. Is the skin smooth and shiny?
7. Is there increased hair growth in the painful extremities?
8. Is there joint swelling or stiffness?
9. Is there edema of the extremities)
10.Is there osteoporosis or abnormal uptake on the bone scan?


      In RSD a scoring scale has been suggested. (3) Diagnostic criteria are a history of spontaneous evoked pain, sensory changes in the affected extremity, at least two signs of sympathetic dysfunction, and absence of other anatomic, physiological or psychological pathology. Vasomotor- changes, sudomotor chances, and trophic changes should be considered.

        An RSD scoring table is as follows:

        Allodynia/hypopathia
        Burning pain
        Edema
        Color/hair growth changes
        Sweating
        Temperature changes
        X-ray changes
        Vasomotor/sudomotor changes
        Bone scan
        Response to sympathetic blockade

             

Less than three factors indicates it is not RSD. Three to 4-1/2 factors, possible RSD, more than five factors probable RSD.

    There are generally considered to be three stages of RSD although they are certainly not mutually exclusive. The first stage (acute or hyperemic) commends at the time of injury but may be delayed for weeks. It is associated with spontaneous pain of a burning quality and usually aggravated by movement of the extremity. There is localized tissue edema, muscle spasm, and tenderness The patient will experience allodynia (a painful vasodilatation, warm, red, and dry skin. this is also the stage where sympathetic blockade and physical therapy has its greatest benefit.

    The second stage (dystrophic or ischemic) is associated with increasing, pain that may radiate proximally or distally from the injured site, There is joint stiffness and edema. The extremity is moist, cyanotic, and the skin cold and shiny. This is the vasoconstrictive stage. Sympathetic blockade and aggressive physical therapy can still remain therapeutic at this stage.

Third stage (atrophic) is still characterized by pain but there is a decrease in blood flow to the skin resulting in marked trophic changes. There is also muscle atrophy, contractures, hair loss, and osteoporosis noted in these. At this stage sympathetic blockade and physical therapy usually have lost their therapeutic benefit.

 

DIAGNOSIS: At this time there remains no specific laboratory or radiological tests for CRPS Type 1. The diagnosis is usually made by exclusion and clinical presentation. A three phase bone scan may demonstrate a reduction of blood flow during the early stages but does show increased peri-articular uptake during the third stage. The sensitivity of the bone scan is approximately 60% and a specificity 86%. Negative bone scans may occur in up to 40% of cases. A recent article on the value of autonomic testing in reflex sympathetic dystrophy by Chelimsky (8) suggested that sweating abnormalities correlate strongly with the clinical syndrome of RSD ,and alterations in the resting skin temperature might be superior to clinical findings in predicting the response to sympathetic block. There was a comparison of three autonomic tests; resting sweating-output, resting skin temperature, and quantitative sudomotor axon reflex test (QSart). The increased RSO predicted a diagnosis of RSD wit 94% specificity, and a specificity was 9801/1, when RSO was considered in conjunction with an abnormal Q-Sart result. However Ochoa, (1) also called that study into question. Thermography at one time was felt to be the diagnostic procedure of choice but has fallen into disuse.

TREATMENT:

TREATMENT: The treatment for CRPS Type I and Type II is sympathetic blockade with pain relief adequate to allow the patient to participate in Injury-specific physical therapy. Weight bearing, range of motion, and strengthen- exercises are necessary to bring these patient back to recovery. Sympathetic blocks can be performed with several techniques. The lower extremity is treated with lumbar sympathetic nerve blocks. Continuous sympathetic blocks can be performed with an epidural or paravertebral catheter. Upper extremity sympathetic blocks are performed using stellate ganglion blocks or cervicothoracic epidural catheter for continuous sympathetic blocks if indicated. It should also be noted that a brachial plexus differential block often gets fibers which may escape the stellate ganglion block. Intravenous regional techniques include the use of bretylium and labetalol. Medication management is essential. CRPS Type I and Type 11 represent a type of neuropathic pain which is more opioid resistant than the nociceptive; therefore adjuvant drugs are used to help manage their pain. Tricyclics play an important role in pain reduction as well as normalizing sleep patterns. Procardia (,Nlfedepine) is also useful doses of 10 mg po t.i.d., and increasing doses to 20 mg t.i.d. Netirontin is showing utility in counteracting the pain. The starting dose is 300 mg t.i.d., and may be increased to 3600 daily. Anticonvulsants including Tegratol, nonsteroidals, and a variety medications have been used. Catapres TTS patches are sometimes useful on the affected limb. A TENS unit and acupuncture with an end result to decrease the patient's pain, to block the sympathetic cycle, and to allow the patients to perform aggressive physical therapy are indicated.