Treating hyperhidrosis

Physiological sweating from cutaneous eccrine glands maintains normothermia and skin hydration. Properly hydrated palmar skin contributes to the effectiveness of normal grip and permits tasks such as turning the pages of the BMJ. Hyperhidrosis is unphysiological and excessive sweating, which squanders water and electrolytes without compensatory cooling from the latent heat or enthalpy of evaporation. It affects about 1% of the United Kingdom population. What help can be offered to patients with this disabling condition?

Hyperhidrosis commonly affects the palms of the hands, the soles of the feet, or the armpits, but in a small number of patients it occurs over the whole body surface. In most patients palmar and/or axillary hyperhidrosis is the major problem, and it is freedom from sweating in the hands or armpits that they seek. In some patients hyperhidrosis affects only the hands or armpits or soles of the feet. Patients with palmar hyperhidrosis have a slippy grip and a cold wet handshake, and their sweat drips into computer keyboards, wets paper, and smudges ink. Exuberant axillary and plantar hyperhidrosis stains and damages clothing and shoes. Eccrine sweat is initially odourless, but patients are embarrassed and inconvenienced by having sodden clothing and damp hands.

Conventional medical therapy with anticholinergic drugs or topical aluminium chloride hexahydrate is inconvenient, unpleasant, and temporary. Patients usually stop using anticholinergic drugs because of a dry mouth, and aluminium chloride hexahydrate often causes skin soreness and irritation. Antiperspirants can provide useful palliation in patients with moderate hyperhidrosis, but in severe cases they are ineffective. Most patients with severe localised hyperhidrosis need to consider either surgery or injections of botulinum toxin.

Eccrine sweat glands are innervated by the sympathetic nervous system. Uniquely, the secretomotor neurotransmitter is acetyl choline not noradrenaline.¹ The sympathetic nerves to the arm arise from spinal cord segments T2-T6 and leave the spinal canal in the corresponding ventral rami to synapse or pass through the 2nd to 6th thoracic sympathetic ganglia. All postganglionic sympathetic fibres to the hand, forearm, and arm except the axilla run with the somatic nerves of the brachial plexus (root origins C5-T1). Consequently, division of the sympathetic trunk between the first and second thoracic ganglia will interrupt all the sympathetic innervation to the arm, comprising preganglionic and post-ganglionic fibres.²

A study of 54 patients treated by thoracoscopic division of the sympathetic trunk with scissors on the 2nd rib and followed up for up to five years showed an initial cure rate of 100% for palmar hyperhidrosis³ and no cases of Horner's syndrome, which can occur with electrocoagulation or diathermy division of the intact sympathetic trunk.⁴ Hyperhidrosis may recur nine to 12 months later from regrowth of preganglionic nerves. Reinnervation can be impeded by inversion of the cephalad and electrocoagulation of the caudad sympathetic trunk after severance.

Thoracoscopic excision or destruction by electrocoagulation of the T2 and T3 sympathetic ganglia is difficult. Unless both ganglia are ablated axillary sweat glands can still be innervated by sympathetic fibres in the 2nd and 3rd intercostal nerves. It is probably for this reason that axillary hyperhidrosis is often not cured by sympathectomy.

Pedal sympathetic denervation requires removal of the 2nd lumbar sympathetic ganglion. In men ejaculatory impotence after bilateral surgery is almost certain. Some surgeons have reserved the operation for women, but this is questionable since genitosexual innervation is analogous in men and women.⁵

For palmar hyperhidrosis alone the treatment of choice is thoracoscopic sympathetic trunkotomy. Patients with both palmar and axillary hyperhidrosis can be treated by thoracoscopic excision of the T2 and T3 sympathetic ganglia. Those with only axillary or plantar hyperhidrosis are best served by topical botulinum toxin injection.

For axillary hyperhidrosis 240 units of botulinum A toxin-haemagglutinin complex (Dysport) per armpit is injected in 12 0.1 ml aliquots subdermally covering the hyperhidrotic area. Pedal hyperhidrosis is more tedious and uncomfortable to treat because of the large surface area and sensitivity of the feet: 24 to 36 subdermal injections of 0.1 ml are required to cover the entire plantar surface of foot and toes.

Botulinum toxin binds to presynaptic nerve membranes and then inhibits release of acetyl choline by disrupting the Ca²⁺ dependent K⁺ evoked release mechanism.⁶ A small before and after study of patients with disabling hyperhidrosis refractory to drug treatment showed that botulinum toxin completely abolished sweating in the injected areas after a delay in onset of two to three days.⁷ The effect lasts for up to 11 months.⁸ Second and third treatments have been of undiminished effectiveness, but antibody formation may reduce long term therapeutic potency. Attempts to use botulinum toxin to treat palmar hyperhidrosis were complicated by paresis of the intrinsic muscles of the hand.⁹ The risk of hand dysfunction is a high price to pay when thoracoscopic sympathetic trunkotomy is a safer alternative. Local toxin diffusion in the axilla or foot is, however, unlikely to produce symptomatic muscle weakness, and we have observed no adverse effects in over 20 patients we have treated.

Thoracoscopic sympathetic trunkotomy and ganglionectomy are safe procedures and operative complications are rare. Deaths and permanent neurological damage from anoxia have occurred when surgeons have unwisely performed immediate consecutive bilateral thoracoscopy rather than two separate operations.¹⁰ The eye signs of Horner's syndrome are produced by deliberate or inadvertent destruction of the first thoracic sympathetic ganglion. This complication is unnecessary and avoidable. Intercostal neuralgia can occur if the sympathetic ganglia are destroyed by electrocoagulation rather than excision.

The incidence of compensatory hyperhidrosis is proportional to the surface area rendered anhidrotic. Compensatory sweating is uncommon after unilateral sympathetic trunkotomy but usual after bilateral T2, T3 ganglionectomy.³ Its occurrence after axillary botulinum toxin injection in a patient with bilateral sympathetic trunkotomy but incomplete ganglionectomy regressed as axillary sweating returned. Post- sympathectomy gustatory sweating has been reported in 28%of patients.¹¹