CLINICAL PRESENTATION

The typical patient gives a history of palmar and plantar sweating since early childhood. Parents may report that excessive wetness of the hands and feet was present during infancy. Patients commonly report having been teased by other children, who would not want to hold their hands, and having been berated by teachers for submitting assignments that were wet and smudged. Puddles are left on computer and piano keyboards. As patients enter adulthood, their wet hands adversely affect social interaction and influence career choice.

Sweating is intermittent and occurs at times of both apparent calm and obvious stress.⁷ Sweating is usually worse during the summer months. Although the degree of hyperhidrosis varies, sweating is much greater than the dampness associated with stress. A dry hand may become soaking wet within minutes. Perspiration forms on the volar surface of the fingers and on the thenar and hypothenar eminences, and it fills the palmar skin folds (Fig. 44-1). Sweat may actually run down the arm and drip to the floor.

Figure 44–1 Typical appearance of palmar hyperhidrosis. Note wetness on the thenar and hypothenar eminences and on the palmar surface of distal phalanges.

Nearly all patients with palmar hyperhidrosis also suffer from plantar hyperhidrosis, the degree and timing of which parallels that manifested in the hands. Patients walking barefoot leave tracks as if they were walking out of the shower. Footwear is ruined by the constant moistness. Open-toe sandals are impossible to wear because the wet feet slip. Despite the frequent moistness, fungal infections are rare. As many as 50% of patients with palmar and plantar hyperhidrosis also suffer from concomitant axillary hyperhidrosis that causes garment staining and odor (bromhidrosis).^1,6,8–13 Isolated axillary hyperhidrosis is a frequent complaint. Severe facial sweating is much less common.

In addition to altering their life style to avoid direct or indirect hand contact, sufferers from hyperhidrosis develop other coping mechanisms. A handkerchief or tissue is always in hand. They frequently wipe their hands on their clothing. In social situations, a cold drink is ever present to provide a reason for their cold wet hand or an excuse for the need to wipe their hand before a handshake.

The diagnosis of hyperhidrosis is based on patient history and physical examination. One expert multispecialty working group defined hyperhidrosis as focal sweating of greater than 6 months’ duration that fulfills at least two of the following criteria: it is bilateral and symmetric, it impairs daily activities, it occurs at least weekly, the age of onset is less than 25 years, there is a family history, and focal sweating ceases during sleep.¹⁴ There are currently no accepted objective definitions of palmar hyperhidrosis, but some have suggested that focal axillary sweat production of greater than 50 to 100 mg/5 min is diagnostic of axillary hyperhidrosis.¹⁴

EPIDEMIOLOGY

The prevalence of palmar and plantar hyperhidrosis was estimated as 0.6% to 1%¹ in a study of Israeli army recruits. Based on a survey of 13,000 college and high school students, investigators from Asia reported a prevalence of 4.6%.¹² A recent survey of 150,000 U.S. households yielded a hyperhidrosis prevalence of 2.8%.¹¹ Generalized hyperhidrosis may be associated with thyrotoxicosis, neurologic diseases, and rare inherited disorders. Patients with classic palmar, plantar, and axillary hyperhidrosis do not have concomitant illnesses.

A familial history of hyperhidrosis has been obtained in as many as 65% of patients who have undergone thoracoscopic sympathectomy.^1,10,12,15 Detailed kindred information provided by 49 affected individuals has led to the conclusion that the disease allele is actually present in 5% of the population, and that having one or two copies of the allele results in hyperhidrosis in 25% of carriers.¹⁵ Investigators have localized hyperhidrosis associated genes to chromosomes 14¹⁶ and 5.¹⁷

AUTONOMIC NERVOUS SYSTEM: ANATOMY AND FUNCTION

The autonomic nervous system is responsible for thermoregulation. Although both the sympathetic and parasympathetic components may contribute to sweating, the sympathetic nervous system primarily controls extremity sweating. Impulses originating in the hypothalamus reach preganglionic fibers located in the lateral horn of the ventral root of the spinal column.¹⁸ These myelinated fibers exit the ventral root and travel a brief distance through the spinal nerve before exiting as the white rami communicantes to join the paravertebral ganglia of the sympathetic chain. The nerve may immediately establish a synapse with an unmyelinated postganglionic fiber, which returns to the spinal nerve as the gray ramus communicantes, or it may ascend a variable distance within the sympathetic chain before synapsing with a postganglionic fiber. The postganglionic nerve often travels a great distance before arriving at its target organ.

The preganglionic sympathetic fibers responsible for sudomotor (sweating) activity in the hand are thought to arise from spinal segments T3 to T6. They converge on the T2 and T3 ganglia, where postganglionic fibers ascend to reach the hand via connections of the stellate ganglia to the brachial plexus.¹⁹ The precise spinal levels responsible for palmar sweating have not been defined, but T2 has been thought to be the common pathway. Release of acetylcholine from the postganglionic neurons stimulates the eccrine sweat glands.

The sympathetic chain descends vertically in the thorax over the rib heads (Fig. 44-2), and rarely it is found between the medial border of the rib head and the longus colli muscle.^20,21 The sympathetic ganglia are located approximately 2 mm cranial to the midportion of the underlying vertebral body.²² For example, the T2 ganglion is located between the heads of the second and third ribs. In addition to the orderly arrangement of the sympathetic nerves, Kuntz identified inconstant sympathetic branches from the second intercostal nerve to the first intercostal nerve (and hence brachial plexus) that bypassed the stellate ganglia.²³ The physiologic function of these nerves is unclear.

Figure 44–2 Left sympathetic chain.

Whether hyperhidrosis represents focal dysfunction of the autonomic nervous system or is emblematic of a more global abnormality remains unknown. Resting palmar sweat production at room temperature is twice normal (Fig. 44-3).²⁴ The sudomotor skin response is enhanced as a result of shortened nerve recovery time.²⁵ Abnormal sensory processing is suggested by a decrease in spatial discrimination thresholds that did not improve under conditions of sensory deprivation.²⁶ These findings (i.e., the absence of plastic cortical somatocellular changes) suggest a lack of inhibition of the hypothalamus. Palmar sweat production in response to stress is greatly increased (see Fig. 44-3). When compared with the responses in unaffected controls, pulmonary function and resting cardiac function in the supine position are normal.^27–30 Circulating plasma catecholamine levels are within normal limits.³¹ However, peak exercise heart rate and resting heart rate in the standing position are increased.^27,28 Other investigators have suggested that concomitant abnormalities of the parasympathetic system contribute to hyperhidrosis.^32,33

Figure 44–3 A, Normal sweat response. After attachment of the measuring device (Skin Moisture Meter SKD 2000, Skinos, Ltd, Japan), the patient reaches baseline. Sweating increases as autonomic stimulation begins. The subject does not return to baseline. B, Abnormal sweat response. Attachment of the measuring device causes anxiety and the baseline never reaches normal. The response to the stimulus is many times greater than in the normal subject. In both A and B: Upper line, thenar eminence; lower line, forehead.

TREATMENT

Surgical

The goal of surgery is to interdict the sympathetic nerve innervation to the hand, axilla, or face. Disruption of the sympathetic chain can be accomplished by transection, by resection of ganglia, or by application of clips. The thoracic level at which interruption is necessary to achieve the desired anhidrosis while simultaneously minimizing systemic side effects is not precisely known and remains controversial. Interpretation of the voluminous literature is complicated by a plethora of inconsistent terms used to describe the operative procedures. For example, sympathectomy has been employed to describe both transection of the sympathetic chain and actual removal or ablation of the ganglion. The following recently proposed definitions seem reasonable⁴⁰:

• Sympathectomy: removal or ablation of a sympathetic ganglion, accompanied by transection of the sympathetic chain above and below the ganglion

• Sympathicotomy: transection of the sympathetic chain at the indicated level

• Clipping: application of a clip at a specific level

• Blocking: placement of clips above and below the cited ganglion

Traditionally, palmar hyperhidrosis has been treated by transecting the sympathetic chain over the second and third ribs. If concomitant axillary hyperhidrosis was present, the sympathetic chain was also transected over the fourth rib. In the absence of palmar hyperhidrosis, axillary sweating was treated by transecting the sympathetic chain over the third and fourth ribs. Some authors believe that palmar hyperhidrosis can be effectively treated by limiting the transection to the level of the third rib.⁴¹ Others have demonstrated equivalent results by transecting or clipping the sympathetic chain at T3-4.^10,42 Yet other surgeons have reported success with T4-5 sympathicotomy.⁴³

Four phase III trials have been performed, three comparing different levels for palmar hyperhidrosis and one for isolated axillary hyperhidrosis. Sixty patients with palmar hyperhidrosis were randomized to either T2-3 or T3-4 sympathicotomy.⁴⁴ The single patient who did not experience complete resolution of symptoms was in the T3-4 group. However, the patients in the T3-4 group reported less severe compensatory sweating. In a second study, 232 patients were randomized to either T3 sympathicotomy or T2-to-T4 sympathicotomy.⁴¹ All patients had resolution of symptoms, but patients in the T3 cohort had fewer instances of severe compensatory sweating and were more likely to be satisfied with the results of surgery. Finally, 25 patients underwent unilateral ablation of the T2 ganglion and contralateral ablation of the T2-3 ganglia.⁴⁵ The procedures were equally effective. Compensatory sweating was mild and did not differ between the two sides. Sixty-two patients with isolated axillary hyperhidrosis were randomly assigned to either T3-4 or T4 sympathectomy.⁴⁶ All patients reported resolution of symptoms. However, the T4 cohort had a lower incidence of compensatory sweating (57% versus 91%).

Regardless of the surgical technique, correct identification of the anatomic level is crucial. The second rib is generally the most proximal rib that can be seen in the thorax and can be reliably identified by a vertical, descending arterial branch that crosses the rib 1 cm lateral to the sympathetic chain.⁴⁷ This arterial branch originates from the subclavian artery and forms the second intercostal artery (Fig. 44-4A). The first intercostal space is covered by a fat pad, and the first rib is generally not visible from within the thorax. Additional landmarks are the azygos vein, which lies at the level of the fifth interspace, and the aortic arch, which reaches to the fourth interspace. The rib number can be determined with certainty by obtaining an intraoperative radiograph after a metallic marker has been introduced into the chest and placed over a rib.

Figure 44–4 A, Descending vessels crossing the right second rib lateral to the sympathetic chain. B, After transection of the sympathetic chain, its proximal and distal stumps are visible.

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