5.2 Issues in technique
5.2.3 Limited ganglionectomy: a prospective evaluation
Primary hyperhidrosis, particularly of the palms, causes much psychosocial trauma and sometimes physical discomfort; on occasions this condition may compromise an individuals vocation. It is therefore not surprising that the palmar component of primary hyperhidrosis is what drives the patient to seek treatment. By contrast axillary hyperhidrosis, even though it occurred in just under 60% of our patients, was rarely troublesome to the extent that specific treatment was requested. Likewise plantar hyperhidrosis - evident in nearly 90% of our patients - was largely tolerable, even though longstanding plantar hyperhidrosis predisposes to blistering, infections, bromhidrosis and rotting of shoes and socks (Moran and Brady, 1991 ).
Surgical sympathectomy, by various approaches, has long been acknowledged as offering the most effective and enduring treatment of hyperhidrosis.
Minimal Access Surgery, using the thoracoscopic approach, has gone a long way to diminishing the morbidity associated with open syrnpathectomy (Byrne et al., 1990;
Kux, 1978; Singh et al., 1996; Edmonson et al., 1991 ). Notwithstanding this, there are two problems associated with sympathectomy undertaken for hyperhidrosis that persists during the thoracoscopic era. These relate to the problem of compensatory hyperhidrosis and the appropriate management of axillary hyperhidrosis. We suggest that these issues are related to the extent of the syrnpathectomy undertaken for upper limb hyperhidrosis.
Compensatory hyperhidrosis is recognized as an unpredictable but potentially devastating effect of thoracic syrnpathectomy. The reported incidence of compensatory hyperhidrosis ranges from 22-81 % (O' Riordain et al., 1993; Hsu et al., 1994 ). This wide range probably reflects the varying extent of the sympathectomy undertaken for upper limb hyperhidrosis. In addition most series fail to quantify the degree or severity of the compensatory hyperhidrosis.
The mechanisms responsible for compensatory hyperhidrosis are unclear. Whereas the original hyperhidrotic state may be induced by emotions, amongst other factors, compensatory hyperhidrosis tends to be largely a heat regulated phenomenon.
Following upper limb sympathectomy nearly 40% of the total sweat gland function is lost; it is therefore not surprising that the residual truncal sweat glands show unusually increased activity, thereby producing compensatory hyperhidrosis. Thus, the greater the
151
number of sweat glands excluded from thermoregulatory control, the greater the chance of compensatory hyperhidrosis. However, other factors may yet be involved because compensatory hyperhidrosis may occur even in an air-conditioned environment (Shelley and Florence, 1 960; Andrews and Rennie, 1997).
The surgical technique of clipping the sympathetic chain and removing these clips on the development of compensatory hyperhidrosis is an interesting option that merits further evaluation. The preliminary results reported by Lin (1998) suggests that this approach may prove to be invaluable in the management of this difficult problem.
Notwithstanding this, reducing the extent of the sympathetic ganglionectomy has been associated with a lower incidence of compensatory hyperhidrosis. An incidence of compensatory hyperhidrosis of up to 64% has been reported when the ganglionectomy is extended up to the 5th or 6th thoracic ganglion. By contrast, limiting the extent of the ganglionectomy to the 2nd thoracic ganglion has been associated with a reduction in compensatory hyperhidrosis to between 22 - 24%. Hederman (1994) has reported a 24% incidence with electrocautery of the 2nd thoracic ganglion. O'Riordain (1993) has reported a 22% incidence of compensatory hyperhidrosis following precise excision from below the stellate ganglion to above the 3rd ganglion, effectively removing the 2nd ganglion and the adjacent interganglionic segment. The anatomical basis for a successful upper limb sympathectomy with a 2nd thoracic ganglionectomy was described by Hyndman and Wolkin, but clearly was not widely appreciated (Hyndman and Wolkin, 1942).
In this series the overall compensatory hyperhidrosis rate is 20% (11 patients); if the 4 patients assessed to have moderate, tolerable compensatory hyperhidrosis are excluded that rate of severe compensatory hyperhidrosis is 12.6% (7 patients).
Assessment of compensatory hyperhidrosis is based on subjectivity, rather than on objective sweat production analysis. It is suggested that compensatory hyperhidrosis rates may be significantly reduced by a meticulous dissection and resection of only the 2nd thoracic ganglion. Diathermy application on the sympathetic chain should be avoided as this may cause a coagulative necrosis proximal and distal to the 2nd thoracic ganglion, thereby effectively extending the extent of the ganglionectomy. For similar reasons traction should not be applied on the chain. These technical considerations are probably the basis for the absence of facial anhidrosis and gustatory sweating in this series.
Accurate localization of the 2nd thoracic ganglion is crucial and is afforded by dissection of the pleura off the chain and a thorough appreciation of the anatomy of the thoracic sympathetic chain. However, compensatory hyperhidrosis remains largely unpredictable; when severe this side-effect surplants the presenting palmar hyperhidrosis. In this series 3 of the 7 patients with severe compensatory hyperhidrosis regretted undergoing the procedure (even though their palms were now anhydrotic). A variety of non-surgical measures such as topical agents (aluminium chloride, tanning agents, glutaraldehyde), iontophoresis (electric coagulation of the eccrine sweat glands) and systemic anticholinergic agents have been used, invariably, without much success.
For these reasons it behoves the attendant surgeon to fully counsel the patient about this potential side-effect (Andrews and Rennie, 1997).
Because axillary hyperhidrosis often occurs concomitantly with palmar hyperhidrosis, the traditional approach has been to perform an extended sympathectomy (up to the 5th - 6th thoracic ganglion) in an endeavour to effect axillary anhidrosis. The anatomical basis for this approach is unclear. The potentially devastating effects of an extended sympathectomy have been mentioned; furthermore it has been reported that extensive ganglionectomy does not guarantee a successful outcome for axillary hyperhidrosis (Bretteville, 1973). Clearly a balanced approach is necessary. We suggest that extensive sympathectomy should not be undertaken for concomitant axillary hyperhidrosis, particularly as axillary hyperhidrosis is rarely a presenting factor.
Rather, we recommend a limited 2nd thoracic ganglionectomy be offered. This was associated with an 80% success rate for axillary hyperhidrosis and a disabling compensatory hyperhidrosis rate of 12.6% in our series. In those patients troubled with persistent axillary hyperhidrosis excision of the axillary sweat glands is probably the best option. To date none of our patients have qualified for this procedure which entails excision of an ellipse of skin with careful undermining above and below to remove the deeper layer containing the sweat glands. Siting of the incision is important to avoid an unsatisfactory scar that may restrict arm movement following excision (Hurley and Shelley, 1966).
Plantar hyperhidrosis occurred in 49 patients (89%) but was never a prime complaint;
the anatomical basis for the successful treatment of plantar hyperhidrosis by 2nd thoracic ganglionic (in over 80% of the patients) is unclear. The successful treatment of plantar hyperhidrosis following thoracic ganglionectomy should be regarded as a bonus and, as such, should not be guaranteed to the patient.
Our experience with this procedure suggests that for primary hyperhidrosis thoracoscopic sympathectomy maybe performed on a day care basis and that a limited 2nd thoracic ganglionectomy is adequate to treat palmar hyperhidrosis. Furthermore, this approach may cure axillary hyperhidrosis and more importantly, decrease the incidence of debilitating compensatory hyperhidrosis.