Complex regional pain syndrome (CRPS) type I is a regional pain syndrome that usually develops after tissue trauma. Allodynia (the perception of a nonpainful stimulus as painful), hyperpathia (an exaggerated pain response to a painful stimulus), and spontaneous pain occur. Symptoms are unrelated to the severity of the initial trauma and are not confined to the distribution of a single peripheral nerve. CRPS type II is a regional pain syndrome that develops after injury to a peripheral nerve, usually a major nerve trunk. Spontaneous pain initially develops within the territory of the affected nerve but eventually may spread outside the nerve distribution.
- Early mobilization with physical therapy or a brief course of glucocorticoids may be helpful for CRPS type I.
- Other treatments include the use of adrenergic blockers, NSAIDs, calcium channel blockers, phenytoin, opioids, and calcitonin.
- Stellate ganglion blockade is a commonly used invasive therapeutic technique that often provides temporary pain relief, but the efficacy of repetitive blocks is uncertain.
Treatment: Autonomic Nervous System Disorders - Of particular importance is the removal of drugs or amelioration of underlying conditions that cause or aggravate symptoms. For example, OH can be related to angiotensin-converting enzyme inhibitors, calcium channel blocking agents, tricyclic antidepressants, levodopa, alcohol, or insulin.
- Nonpharmacologic approaches are summarized in Table 186-3. Adequate intake of salt and fluids to produce a voiding volume between 1.5 and 2.5 L of urine (containing >170 meq of Na+) each 24 h is essential. Sleeping with the head of the bed elevated will minimize the effects of supine nocturnal hypertension.
- Prolonged recumbency should be avoided. Pts are advised to sit with legs dangling over the edge of the bed for several minutes before attempting to stand in the morning. Compressive garments such as compression stockings and abdominal binders may be helpful if they can be tolerated. Anemia should be corrected, if necessary, with erythropoietin; the increased intravascular volume that accompanies the rise in hematocrit can exacerbate supine hypertension. Postprandial OH may respond to frequent, small, low-carbohydrate meals.
- If these measures are not sufficient, drug treatment might be necessary.
- Midodrine is a directly acting α1-agonist that does not cross the blood-brain barrier. The dose is 5-10 mg orally three times a day, but some pts respond best to a decremental dose (e.g., 15 mg on awakening, 10 mg at noon, and 5 mg in the afternoon). Midodrine should not be taken after 6 P.M. Side effects include pruritus, uncomfortable piloerection, and supine hypertension.
- Droxidopa was recently approved for treatment of neurogenic OH associated with autonomic failure, Parkinson's disease, or MSA; the oral form is converted to norepinephrine and has been shown to be effective in short-term clinical trials.
- Pyridostigmine appears to improve OH without aggravating supine hypertension by enhancing ganglionic transmission (maximal when orthostatic, minimal supine).
- Fludrocortisone (0.1-0.3 mg PO twice daily) will reduce OH, but it aggravates supine hypertension. Susceptible pts may develop fluid overload, congestive heart failure, supine hypertension, or hypokalemia.
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For a more detailed discussion, see Low PA, Engstrom JW: Disorders of the Autonomic Nervous System, Chap. 454, p. 2637, in HPIM-19. |