Partial pulmonary sympathetic denervation by thoracoscopic D2–D3 sympathicolysis for essential hyperhidrosis: effect on the pulmonary diffusion capacity

Abstract

In patients with essential hyperhidrosis (EH), a pathological condition characterized by increased activity of the upper dorsal sympathetic ganglia D 2–D 3, anatomical interruption at the D 2–D 3 level by thoracoscopic sympathicolysis (TS) is a safe and effective treatment. The D 2 and D 3 ganglia, however, are also in the pathway of sympathetic lung innervation, which may influence the pulmonary diffusion capacity for carbon monoxide (expressed as transfer factor for and as transfer coefficient for CO: KCO). We therefore studied the effect of TS on T lCO and KCO in 50 EH patients: compared with pre-operative values, both T lCO (−6·7%, P<0·001) and KCO (-4·2%, P=0·002) were significantly decreased at 6 weeks after bilateral TS, an effect which was independent of the smoking status of the patients. In order to explain this phenomenon, the following pharmacological interventions were studied: (1) oral β 1+2-adrenoreceptor blockade with propranolol caused a comparable decrease of T lCO (−6·3%) and KCO (−7·5%) in matched normal subjects, but had no effect on T lCO and KCO in EH patients prior to TS; and (2) subsequent inhalation of the β 2-adrenoreceptor agonist salbutamol in a dosage suspected to cause alveolar β-receptor stimulation had no effect on T lCO and KCO, neither in the normal subjects, nor in EH patients (before and after TS). Although the exact mechanism of the TS-induced decrease in T lCO and KCO remains speculative, these findings suggest that they may be related to a β 1-adrenoreceptor-mediated change in pulmonary capillary membrane permeability, although TS-induced changes in pulmonary blood flow or an interplay of both mechanisms cannot be excluded.