Evidence-based treatment of neurogenic orthostatic hypotension and related symptoms

Sabine Eschlböck, Gregor Wenning, Alessandra Fanciulli, Sabine Eschlböck, Gregor Wenning, Alessandra Fanciulli

Abstract

Neurogenic orthostatic hypotension, postprandial hypotension and exercise-induced hypotension are common features of cardiovascular autonomic failure. Despite the serious impact on patient's quality of life, evidence-based guidelines for non-pharmacological and pharmacological management are lacking at present. Here, we provide a systematic review of the literature on therapeutic options for neurogenic orthostatic hypotension and related symptoms with evidence-based recommendations according to the Grading of Recommendations Assessment, Development and Evaluation (GRADE). Patient's education and non-pharmacological measures remain essential, with strong recommendation for use of abdominal binders. Based on quality of evidence and safety issues, midodrine and droxidopa reach a strong recommendation level for pharmacological treatment of neurogenic orthostatic hypotension. In selected cases, a range of alternative agents can be considered (fludrocortisone, pyridostigmine, yohimbine, atomoxetine, fluoxetine, ergot alkaloids, ephedrine, phenylpropanolamine, octreotide, indomethacin, ibuprofen, caffeine, methylphenidate and desmopressin), though recommendation strength is weak and quality of evidence is low (atomoxetine, octreotide) or very low (fludrocortisone, pyridostigmine, yohimbine, fluoxetine, ergot alkaloids, ephedrine, phenylpropanolamine, indomethacin, ibuprofen, caffeine, methylphenidate and desmopressin). In case of severe postprandial hypotension, acarbose and octreotide are recommended (strong recommendation, moderate level of evidence). Alternatively, voglibose or caffeine, for which a weak recommendation is available, may be useful.

Keywords: Evidence-based treatment; Grade; Neurogenic orthostatic hypotension; Postprandial hypotension; Syncope.

Conflict of interest statement

Academic work, no external financial support allotted. The authors declare no conflicts of interest.

Figures

Fig. 1
Fig. 1
Primary and secondary causes of nOH according to the site of lesion—schematic representation. AAG autoimmune autonomic ganglionopathy, AAN autoimmune autonomic neuropathy, ADLD autosomal dominant leukodystrophy, CRF chronic renal failure, DBH deficiency dopamine-β-hydroxylase deficiency, DM diabetes mellitus, FD familial dysautonomia (=hereditary sensory and autonomic neuropathy type III, Riley-Day syndrome), LBD Lewy-body dementia, MS multiple sclerosis, MSA multiple system atrophy, nOH neurogenic orthostatic hypotension, PAF pure autonomic failure, PD Parkinson’s disease

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