Complications in Patients with Palmar Hyperhidrosis Treated with Transthoracic Endoscopic Sympathectomy

To the Editor: I was pleased to read the article by Lai et al.(7). Based on our experience in the treatment of a large number of patients with palmar hyperhidrosis (PH) (2,4-6), I offer the following comments on a few points regarding the high incidence of compensatory hyperhidrosis (CH), gustatory sweating (GS), and Horner's syndrome (HS) reported in the article by Lai et al. (7) There are several factors that might contribute to the extraordinary high incidence of CH in the report presented by Lai et al.(7). 1) Most of their patients were young and may have inherited a relatively high systemic sudomotor activity in addition to PH. Subsequently, such patients are prone to develop post-operative CH of a severe degree. 2) The humidity of the climate is notoriously high in the authors' geographical area. Hot and highly humid environments make CH worse and even intolerable (4,6). It is interesting that patients from the United States, Canada, and Australia who have received our surgical treatment rarely complain of significant CH. 3) The extent of sympathectomy is greater in the series presented by Lai et al.(7). Since we introduced the application of intraoperative monitoring of palmar skin temperature as an aid to ensure a precise and adequate sympathectomy, we postulated that en bloc ablation of T2 segment, instead of extensive sympathectomy, should be sufficient and adequate for PH (4-6). Subsequently, the incidence and severity of CH became less and less in the later series. It seems there is a correlation between the extent of sympathectomy and the severity of CH. Based on our experience, several possible mechanisms of CH are postulated. One possibility is denervation hypersensitivity of the injured sympathetic stump. The injured tissue distal to the ablated segment becomes hypersensitive to acetylcholine. This can explain why CH may appear very early after sympathectomy but does not develop in those submitted to local excision of the axillary sweat glands. Another possibility is regrowth of preganglionic sympathetic fibers and/or collateral sprouting of sympathetic fibers to the sympathetic trunk distal to the ablated segment. The above two mechanisms can explain the late onset but long-term existence of CH. Fortunately, most patients are able to tolerate CH in time (4-6). Regarding postsympathectomy GS, our experience is different from that of Lai et al. (7) and others (1,6,8). Genuine GS has rarely been encountered in our patients whose T2 sympathetic segments have been clearly identified and then delicately ablated under well-illuminated endoscopic view. Most patients experience a concomitant reduction of their facial sudomotor activity because of part of the facial sympathetic innervation dose from the T2 segment(3). On the other hand, many patients with PH before sympathectomy experience some degree of GS, particularly if provoked by eating hot food. Most postoperative patients neglect the subtle reduction of their facial sweating activity in time. However, when they are asked whether they have felt some facial sweating associated with eating, a substantial percent say yes. This phenomenon is very difficult to differentiate from that existing before sympathectomy. Therefore, genuine GS might rarely occur in patients with PH if a delicate ablation of the T2 sympathetic segment has been performed. However, GS is relatively prone to occur in those patients whose sympathectomy is performed under a more invasive procedure, such as an open dorsal or supraclavicular approach (1,8), or in those patients whose target sympathetic segment could be only partially or inappropriately ablated because of severe adhesions at the apical thorax, leading to an incomplete relief of PH and a high rate of GS. GS may attribute to the regrowth of preganglionic fibers or collateral sprouting of postganglionic fibers to the stellate ganglion. This regrowth or sprouting is presumed to be induced by the irregularly surgically injured sympathetic trunk. The incidence of HS in the series presented by Lai et al.(7) seems particularly high. We have surveyed 9988 patients with PH treated by transthoracic endoscopic sympathectomy from 17 hospitals in our country. The incidence of HS is approximately 1%. We agree that the high incidence may be related to the strong electric current-relayed thermal damage to the sympathetic tissue higher than the T2 segment. Fortunately, this kind of HS is usually mild and transient compared to that resulting from a dorsal or supraclavicular approach in which HS is often more obvious and long-lasting, possibly because of the direct surgical injury to the stellate ganglion. It is very impressive that via a transthoracic endoscopic approach, more than 90% of HS occurred in the left eye. We postulate that there is a slight anatomic difference between the two sides of the upper sympathetic trunk. The left T2 segment sends more sympathetic fibers to the craniofacial region than from right T2 segment; subsequently, ablation of the left T2 segment results in a higher risk of producing HS than that of the right side.