Autonomic neuropathy as post-acute sequela of SARS-CoV-2 infection: a case report

Abstract

Symptoms of autonomic dysfunction, particularly those of orthostatic intolerance, continue to represent a major component of the currently recognized post-acute sequelae of SARS-CoV-2 infections. Different pathophysiologic mechanisms can be involved in the development of orthostatic intolerance including hypovolemia due to gastrointestinal dysfunction, fatigue-associated deconditioning, and hyperadrenergic state due to pandemic-related anxiety. Additionally, there has been a well-established association of a common primary autonomic disorder like postural orthostatic tachycardia syndrome, a subtype of orthostatic intolerance, with antecedent viral infections. Here we report a case of neuropathic type postural orthostatic tachycardia syndrome as a form of autonomic neuropathy that developed following COVID-19 infection.

Keywords: Autonomic neuropathy; COVID-19; Orthostatic intolerance; Postural orthostatic tachycardia syndrome; Small fiber neuropathy; Valsalva maneuver.

Fig. 1

A quantitative sudomotor axonal reflex test showing reduced sweat outputs in the forearm (red) and foot (yellow) sites, while it is normal in the proximal and distal leg sites (blue and green curves, respectively). B Blood pressure response to Valsalva maneuver showing diminished late phase II with normal heart rate response. C Orthostatic tachycardiac response to head-up tilt table test (upper panel) with no significant change in blood pressure (lower panel)

Fig. 2

Skin punch biopsy sections immunohistochemically stained with PGP 9.5 showing normal epidermal nerve fiber densities at the ankle (A) and thigh (B) sites. C Hematoxylin and eosin–stained section from the thigh site showing a small mononuclear cellular infiltrate surrounding a dermal small blood vessel (arrow)