Autonomic dysfunction: A guide for FPs

Gastrointestinal dysfunction

In patients with diabetes, GI autonomic neuropathy can result in altered esophageal motility leading to gastroesophageal reflux disease (GERD) or dysphagia, gastroparesis, or diabetic enteropathy.¹⁴ Gastroparesis often presents as nausea, vomiting, and bloating.¹ It may be diagnosed via gastric emptying studies (scintigraphy), and often requires a multidimensional approach to treatment.

Management. Food may be chopped or pureed to aid in digestion. Metoclopramide is the most commonly used prokinetic agent, but avoid its use in patients with parkinsonism. In more severe cases, consider adding domperidone and erythromycin as prokinetic agents. Recommend antiemetics, such as diphenhydramine, ondansetron, and prochlorperazine for management of nausea and vomiting. Severe cases of gastroparesis may merit a venting gastrostomy tube for decompression and/or feeding via a jejunostomy tube.¹⁵ Impaired intestinal mobility may lead to stasis syndrome, causing diarrhea.

Hypermobility caused by decreased sympathetic inhibition can also contribute to diarrhea. Altered anal sphincter function tone may contribute to fecal incontinence. Management should focus on balancing electrolytes, maintaining adequate fluid intake, and relieving symptoms. Consider antidiarrheals such as loperamide, but use them with caution to avoid toxic megacolon.¹⁶

Constipation. Another common manifestation of autonomic dysfunction in the GI tract is severe constipation.¹ This may be managed conservatively with hydration, increased activity, and increased fiber intake. If such measures prove inadequate, consider stool softeners and laxatives.

Patients with constipation due to spinal cord lesions may benefit from a routine bowel regimen. To provide predictable defecation, advise patients to begin by inserting a stimulant rectal suppository. Follow with gentle digital stimulation of the distal rectum for one minute or less. They’ll need to repeat the process every 5 to 10 minutes until stool evacuation is complete. A forward-leaning position may assist with evacuation. It is helpful to perform this routine at the same time each day.¹⁷

Orthostatic (postural) hypotension

The autonomic nervous system plays an important role in maintaining BP during positional changes. The sympathetic nervous system adjusts the tone in arteries, veins, and the heart. Baroreceptors located primarily in the carotid arteries and aorta, are highly sensitive to changes in BP. When the baroreceptors sense the slightest drop in pressure, a coordinated increase in sympathetic outflow occurs. Arteries constrict to increase peripheral resistance and BP, and heart rate and contractility increase, all in an attempt to maintain BP and perfusion.¹⁸

The most common causes of orthostatic hypotension are not neurologic in origin,⁹ but rather involve medications, hypovolemia, and impaired autonomic reflexes. The condition is common in the elderly, with one study demonstrating a prevalence of 18.2% in those ≥65 years.¹⁹

Orthostatic hypotension may present with dimming or loss of vision, lightheadedness, diaphoresis, diminished hearing, pallor, and weakness. As a result, it is a risk factor for falls. Syncope results when the drop in BP impairs cerebral perfusion. Signs of impaired baroreflexes are supine hypertension, a heart rate that is fixed regardless of posture (the heart rate should increase upon standing), postprandial hypotension, and an excessively high nocturnal BP.¹

Orthostatic hypotension is diagnosed when, within 3 minutes of quiet standing after a 5-minute period of supine rest, one or both of the following is present: at least a 20 mm Hg-fall in systolic pressure or at least a 10 mm Hg-fall in diastolic pressure.²⁰ Soysal et al demonstrated that such a drop in BP, measured one minute after standing, is adequate and effective for diagnosing orthostatic hypotension in the elderly.²¹

Nonpharmacologic management. Recognition and removal of medications that can exacerbate orthostatic hypotension is the first step in managing the condition. Such medications include diuretics, beta-blockers, alpha adrenergic blockers, vasodilators, antipsychotics, antidepressants (SSRIs, trazodone, monoamine oxidase inhibitors, and tricyclic antidepressants), phosphodiesterase inhibitors, narcotics, and antiparkinsonian medications.²²

The most common causes of orthostatic hypotension are not neurologic in origin, but rather involve medications, hypovolemia, and impaired autonomic reflexes.

Lifestyle interventions, such as having the patient arise slowly and maintain good hydration, can be helpful. Eating smaller, more frequent meals may also help if the orthostatic hypotension is triggered postprandially. Compressive stockings can help limit venous pooling in the lower extremities and improve venous return. Tensing the legs by crossing them while standing on both feet has been shown to increase cardiac output and BP.²³ An aerobic exercise regimen of walking or stair climbing 30 to 45 minutes/day 3 days/week for 6 months was shown to eliminate symptoms of orthostasis on tilt table testing in elderly patients with cardiac deconditioning, as opposed to chronic autonomic failure.²⁴

The reduction in central blood volume associated with autonomic insufficiency (due to increased urinary sodium and water excretion) can be lessened by increasing sodium and water intake.^25-27

Pharmacotherapy. Fludrocortisone acetate, a synthetic mineralocorticoid, is the medication of first choice for most patients with orthostatic hypotension whose symptoms are not adequately controlled using nonpharmacologic measures,²⁸ but keep in mind that treating orthostatic hypotension with fludrocortisones is an off-label use of the medication.

Monitor patients taking fludrocortisone for worsened supine hypertension and edema. Also, check their serum potassium levels one to 2 weeks after initiation of therapy and after dose increases. Frequent home monitoring of BP in sitting, standing, and supine positions may be helpful in assessing response to therapy.

If the patient remains symptomatic despite therapy with fludrocortisone, consider adding an alpha-1 adrenergic agonist, such as midodrine. Avoid prescribing midodrine, however, for patients with advanced cardiovascular disease, urinary retention, or uncontrolled hypertension.²⁹