Over the past decade or so, several procedure-specific Enhanced Recovery After Surgery (ERAS) programs have been documented to have beneficial effects, including reduced length of stay (and fewer medical complications) without increasing hospital readmission rates. Early mobilization has been a key element in the multimodal concept of fast-track surgery and ERAS programs, with subsequent positive effects on pulmonary and thromboembolic complications and avoidance of loss of muscle function through immobility. Although postoperative orthostatic intolerance (OI), characterized by symptoms of dizziness, nausea, vomiting, blurred vision, or syncope during sitting or standing, 1 is a well-known clinical problem that can delay early mobilization, relatively few data are available on its mechanism and possible treatment. Consequently, the aim of this freestanding editorial is to provide an update and perspective on the current knowledge regarding the pathogenesis and mechanisms of OI and potential future treatment strategies.
Prevalence and mechanismsAlthough reports have indicated that OI was not a problem after relatively minor surgery (e.g., mastectomy), 2 prospective studies of major surgery have reported that OI is a common problem during early postoperative mobilization, with a prevalence of 42-50%.
3,4Retrospective studies with less well-defined mobilization protocols have reported an OI prevalence in the range of 12-60% across surgical procedures.
5-7The few existing studies with detailed recordings of hemodynamic changes during early postoperative mobilization and with a preoperative control-i.e., in prostatectomy and total hip arthroplasty (THA)-suggest that orthostatic hypotension (OH) with a concomitant decrease in cerebral perfusion is the main mechanism for the OI symptoms experienced in most cases. 3,4,8 Furthermore, the results from these studies suggest that OH is caused by a postoperative attenuated postural vasopressor response during early mobilization. Thus, in both prostatectomy and THA patients, the normal increase in total peripheral resistance during postural change was impaired compared with a preoperative evaluation.3,4 In a separate study in 42 prostatectomy patients, norepinephrine concentrations were measured during early mobilization, and the increase in norepinephrine during transition from supine to standing was impaired during early postoperative mobilization in OI patients. This suggests an attenuated vasopressor response compared with preoperative levels. Finally, a secondary analysis of heart rate variability between pre-and early postoperative mobilization in 23 THA patients found autonomic dysregulation during early mobilization. When compared with the preoperative evaluation, there was a paradoxical shift towards increased vagal activity with movement from the supine to the standing position in OI patients six and 24 hr postoperatively.9 Thus, a state of impaired cardiovascular regulation and autonomic dysfunction may be present in the early postoperative period with undesirable ...