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

AbstractIn patients with essential hyperhidrosis (EH), a pathological condition characterized by increased activity of the upper dorsal sympathetic ganglia D2–D3, anatomical interruption at the D2–D3 level by thoracoscopic sympathicolysis (TS) is a safe and effective treatment. The D2 and D3 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 TlCO and KCO in 50 EH patients: compared with pre-operative values, both TlCO (−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 β1+2-adrenoreceptor blockade with propranolol caused a comparable decrease of TlCO (−6·3%) and KCO (−7·5%) in matched normal subjects, but had no effect on TlCO and KCO in EH patients prior to TS; and (2) subsequent inhalation of the β2-adrenoreceptor agonist salbutamol in a dosage suspected to cause alveolar β-receptor stimulation had no effect on TlCO 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 TlCO and KCO remains speculative, these findings suggest that they may be related to a β1-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