1998 Clinical and Scientific Meeting

Peter C. Rowe, MD

Dept of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

New Clinical Insights in The Treatment of CFS

Although neurally mediated hypotension (NMH) is now recognized as the most common cause of orthostatic intolerance in those with CFS, and postural orthostatic tachycardia syndrome (POTS) is also relatively common, we do not yet have definitive data from randomized controlled trials to confirm that therapy of either disorder does more good than harm. Until such data become available, we have developed the following recommendations for those who elect to begin empiric treatment of NMH and POTS in their patients with CFS, recognizing that some of these recommendations change rapidly. Treatment of NMH and POTS is not optimal unless careful attention is directed to general medical problems including inflammatory disorders (such as food allergy, allergic rhinitis, asthma), painful conditions (such as endometriosis), as well as panic disorder and depression, as each of these conditions can exacerbate orthostatic symptoms.

Reduced blood volume, excessive orthostatic pooling of blood, and excessive levels of catecholamines are thought to be the main contributors to symptoms in NMH and other orthostatic intolerance syndromes. Treatment begins with avoidance of the conditions that (1) lead to excessive venous pooling (such as prolonged quiet sitting or standing, excessive histamine release, vasodilating medications), (2) lead to lowered blood volume (such as inadequate sodium and fluid intake, excessive environmental heat, diuretics), or (3) lead to excessive catecholamine levels (adrenergic agonist medications). To reduce venous pooling, non-pharmacologic maneuvers include compression stockings, as well as abdominal binders to reduce pooling in the splanchnic circulation, and postural maneuvers that increase muscular activity in the legs or raise blood pressure (such as standing in a legs-crossed position, squatting, sitting in the knee-chest position or with the knees higher than the hips, bending forward, or putting a foot on a chair while standing). To increase blood volume, a simple method is to increase intake of dietary sodium chloride, accompanied by at least a 2 liter per day intake of fluids. In those whose orthostatic symptoms can be supported sufficiently to allow it, a progressive exercise program may help by increasing plasma and red blood cell volume. In those with asthma and CFS, inhaled glucocorticoids reduce reliance on the adrenergic agonists that can activate the vaso-vagal reflex.

There is no consensus about which medications are most effective for neurally mediated hypotension, and the efficacy of each remains to be established. Fludrocortisone in doses from 0.05 to 0.2 mg per day, always with supplemental potassium intake, is the most frequently used method of expanding blood volume. Vasoconstrictors such as midodrine, methylphenidate, dextroamphetamine, and psuedoephedrine may be particularly effective for those with excessive venous pooling. Drugs that reduce activation of C-fiber mechanoreceptors in the left ventricle can reduce the frequency with which the vaso-vagal reflex is activated, and among these are atenolol and pindolol (usually avoided in those with asthma), or disopyramide. In open trials, selective serotonin reuptake inhibitors (SSRI) improve both the tolerance of upright tilt and the frequency of clinical symptoms in non-depressed patients with NMH refractory to other measures. Other drugs used in the setting of orthostatic hypotension may have a role for those with NMH, including erythropoietin, but have not been studied in those with NMH and CFS. The use of several medications (a vasoconstrictor, a mineralocorticoid, a beta-blocker) concurrently may be necessary for the improvement of severe NMH.


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