Key result
Postural hypotension in diabetic autonomic neuropathy is driven by a blunted catecholamine response and treated with hydration, salt, and fludrocortisone, though patients have a poorer prognosis.
This review highlights that postural hypotension in diabetic autonomic neuropathy is driven by blunted catecholamine responses and impaired vascular resistance, carrying a poorer prognosis despite available treatments like fludrocortisone.
Alerts clinicians to poorer prognosis in diabetic autonomic neuropathy; leaves open need for prospective treatment trials.
Postural hypotension is uncommon in diabetes but can occur secondary to autonomic neuropathy. Symptoms are rare and include dizziness, weakness, blurred vision, tiredness, and loss of consciousness. The pathophysiology of postural hypotension is not clear, but changes in intravascular volume, heart rate, cardiac output, and splanchnic vascular resistance are similar in patients and controls. The main factors producing hypotension are a blunted catecholamine response to standing, and failure of lower limb vascular resistance to increase adequately. Treatment for symptomatic postural hypotension includes avoidance of dehydration, adequate salt intake, and fludrocortisone. Other treatments are reviewed but are less helpful. Patients with postural hypotension have intermittent symptoms over the years but rarely become severely disabled. They have a poorer prognosis than patients with symptomatic autonomic neuropathy without postural hypotension.
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Purewal et al. (1995) conducted a review in Postural Hypotension in Diabetic Autonomic Neuropathy. Postural hypotension treatments (hydration, salt, fludrocortisone) was evaluated. Postural hypotension in diabetic autonomic neuropathy is driven by a blunted catecholamine response and treated with hydration, salt, and fludrocortisone, though patients have a poorer prognosis.
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