Time- and posture-specific management of severe supine hypertension and neurogenic orthostatic hypotension in diabetic autonomic neuropathy: A case report

RATIONALE: Coexistence of neurogenic orthostatic hypotension with supine or nocturnal hypertension creates a therapeutic challenge because treatment of either component may aggravate the other. This case illustrates a clinical management framework based on characterization of the full hemodynamic phenotype, repeated reassessment, and treatment adaptation according to posture and time of day, integrating postural blood pressure (BP) responses, 24-hour BP monitoring, symptoms, functional status, comorbidities, and safety findings. PATIENT CONCERNS: A 63-year-old man with hypertension and insulin-treated type 2 diabetes presented with orthostatic dizziness and presyncope. Antihypertensive therapy was intensified for elevated seated BP. After intensification, upright tolerance worsened, with recurrent syncope, a rib fracture, and loss of functional independence. Symptoms remained disabling despite antihypertensive withdrawal and nonpharmacological measures. DIAGNOSES: Supine-to-seated-to-standing assessment showed a BP fall from 197/99 mm Hg supine to 122/81 mm Hg seated and 79/56 mm Hg standing, with presyncope and heart rate increasing from 72 to 86 beats/min. Supine measurements and 24-hour BP monitoring documented severe supine and nocturnal hypertension, reverse dipping, and mean asleep BP 203/107 mm Hg. Autonomic testing demonstrated combined cardiovagal and adrenergic dysfunction, supporting neurogenic orthostatic hypotension due to diabetic autonomic neuropathy. INTERVENTIONS: Management was tailored to upright and recumbent periods. A removable transdermal nitroglycerin patch was used overnight. Nonpharmacological measures included repeated encouragement to increase fluid intake, but daily intake generally remained below 2 L. Clinical assessment suggested relative volume depletion. Low-dose morning fludrocortisone was introduced cautiously despite severe supine/nocturnal hypertension. After upright tolerance improved, morning lercanidipine was added. Subsequent 24-hour BP monitoring showed a more balanced profile. OUTCOMES: Orthostatic symptoms and upright tolerance improved. No further syncope or falls occurred, and functional independence improved. Later 24-hour BP monitoring showed reduced nocturnal predominance, with mean awake/asleep BP 164/86 and 165/89 mm Hg, respectively. Mild peripheral edema was managed with intermittent torasemide. LESSONS: This case illustrates how integrating postural BP responses with 24-hour BP patterns can identify competing hemodynamic phenotypes that may require different management during upright and recumbent periods. Repeated reassessment and individualized treatment adaptation according to the documented BP pattern and clinical context may help balance competing risks of upright hypoperfusion and supine/nocturnal hypertension.