Hyperhidrosis generally is defined as sweating in excess of physiologic requirements. Although it is possible to quantify the level of increased sweating in comparison with the general population, the diagnosis is established by the characteristic history. Patients typically present between the ages of 18 and 25 years and regularly report palmar and plantar sweating since early childhood. Parents may comment on inordinate wetness of the hands and feet during infancy. Sufferers from hyperhidrosis often relate that grade school classmates would refuse to hold their hands because of excessive wetness and that teachers would berate them for submitting wet, ink-smudged assignments. They describe puddles of sweat accumulating on computer and piano keyboards. As patients enter adulthood, their wet hands begin to adversely affect social interactions and influence career choice, causing many to seek treatment.
Sweating is sporadic and occurs both at times of apparent tranquility and at times of obvious tension. Hyperhidrosis is usually worse during the summer months. While the degree of hyperhidrosis varies, sweating is much greater than the dampness normally associated with stress. A dry hand may become soaking wet within minutes. The volar surfaces of the fingers, thenar and hypothenar eminences, and palmar skin folds fill with perspiration (Fig. 121-1). Sweat frequently drips to the floor.
Concomitant plantar hyperhidrosis occurs in all patients with palmar hyperhidrosis. Walking barefoot creates footprints similar to those seen after exiting a shower. The constant moistness ruins footwear. However, despite pedal dampness, fungal infections are rare. Concomitant axillary hyperhidrosis with associated garment staining and odor (bromhidrosis) is present in as many as 50% of patients with palmar and plantar hyperhidrosis.1–4
Sufferers from hyperhidrosis avoid direct or indirect hand contact. A handkerchief or tissue is always available. The habitual wiping of hands on clothing is noticeable. In social situations, sufferers often hold a cold drink in their dominant hand to provide an explanation for the need to wipe their hands before a handshake.
The prevalence of palmar and plantar hyperhidrosis is estimated to be between 0.6% and 1%5 and affects all racial groups. Severe axillary hyperhidrosis affects 1.4% of the population of the United States.6 Patients with classic palmar and plantar hyperhidrosis do not have concomitant illnesses, although generalized hyperhidrosis may be associated with thyrotoxicosis, neurologic diseases, and rare inherited disorders.
As many as 65% of patients who have undergone sympathetic surgery have a familial history of hyperhidrosis.2,7 Analysis of kindred data provided by 49 affected individuals led to the conclusion that the disease allele is present in 5% of the population.7
Thermoregulation is controlled by the autonomic nervous system, and extremity sweating is controlled primarily by the sympathetic component. Sympathetic fibers originating from spinal levels T1-T8 ascend in the sympathetic chain and commonly reach the brachial plexus via the stellate ganglia. However, alternative pathways from the T2 and T3 ganglia that bypass the stellate ganglia have been demonstrated.8 The precise spinal levels responsible for palmar sweating have not been defined. Eccrine sweat glands located in the palm, axilla, and face are stimulated by the release of acetylcholine from postganglionic neurons.
The sympathetic chain descends vertically within the thorax over the rib heads (Fig. 121-2). Rarely, it is found between the medial border of the rib head and the collus longus muscle.9 The sympathetic ganglia are located approximately 2 mm cranial to the midportion of the underlying vertebral body.
The sympathetic chain descends vertically over the rib heads. The sympathetic ganglia lie approximately 2 mm cranial to the midportion of the underlying vertebral body.
Whether hyperhidrosis is emblematic of a global autonomic nervous system dysfunction or representative of a focal abnormality remains unknown. At room temperature, resting palmar sweat production is twice the normal rate.10 The pseudomotor skin response is enhanced as a consequence of shortened nerve recovery time.11 Palmar sweat production in response to stress is greatly increased (Fig. 121-3). Pulmonary function and resting cardiac function in the supine position are normal when compared with unaffected control individuals.12 Plasma catecholamine levels are within normal limits.13 However, peak exercise and resting heart rates in the standing position are increased.12,14 The ultrastructure of hyperhidrotic axillary eccrine glands is normal.15
Abnormal sweat response. Attachment of the measuring device (Skin Moisture Meter SKD 2000, Skinos Co., Ltd., Japan) causes anxiety, and the baseline never reaches normal. The response to the stimulus is many times greater than that in a normal subject. The ordinate is in minutes, and the abscissa is in milliliters of moisture. Upper line: Thenar eminence. Lower line: Forehead (control).
Aluminum chloride hexahydrate 20% anhydrous ethyl alcohol solution (Drysol), a highly concentrated liquid preparation of the active underarm antiperspirant ingredient, may be applied daily to the affected area before bedtime. The hands or feet are covered in plastic wrap to prevent damage to clothing or bedding. Once the desired anhidrosis is obtained, the application frequency is decreased. Side effects include rash and paradoxical hyperhidrosis. Many patients report therapeutic failure, and the efficacy of this treatment has not been assessed in a controlled trial.
Iontophoresis has been reported to control palmar hyperhidrosis in 82% of 112 patients who underwent eight daily 15-minute treatments.16 In this study, the hands or feet were placed in a tap water solution through which an electric current flowed (Drionic). Anhidrosis is thought to result from the electrically induced precipitation of salts in the sweat ducts. The mean remission in this study was 35 days. Undesirable effects included tingling, erythema, and vesicle formation.
Botulinum toxin A (Botox) stops sweat production by blocking the release of acetylcholine from the postganglionic nerve end. Randomized trials have demonstrated the efficacy of this treatment for both palmar and axillary hyperhidrosis.17,18 Median duration of sweat control ranges from 6 to 9 months. Weakness of the intrinsic muscles of the hand has been reported in 25–60% of patients. Botulinum toxin A injections may represent the treatment of choice for axillary hyperhidrosis.
Oral anticholinergic medications such as glycopyrrolate and oxybutynin have the theoretical ability to block stimulation of the sweat gland caused by the release of acetylcholine. However, the efficacy of this treatment has not been documented. Common side effects include dry mouth, blurry vision, and constipation.
Interruption of sympathetic innervation can be achieved by transecting the sympathetic chain, crushing the sympathetic chain with clips, or transecting the rami communicantes. It is not necessary to resect the ganglia itself. The thoracic level(s) necessary to achieve the desired anhidrosis while minimizing systemic side effects is not known precisely. Palmar hyperhidrosis commonly has been treated by transecting the sympathetic chain over the second (T2) and third ribs (T3) and, if concomitant axillary hyperhidrosis is present, additional transection over the fourth rib (T4).1,2,4,19,20 In the absence of palmar hyperhidrosis, axillary sweating has been treated by transecting the sympathetic chain at the T3-T4 level. To decrease the side effects of surgery, many surgeons now perform a more distal sympathicotomy at T3-T4 or limit the sympathicotomy to T3 alone.2,19 More recently, transection at the T4 and T5 levels has been reported.3,21 Correct identification of the anatomic level is imperative.
Generally, the second rib is the most proximal rib that can be seen within the thorax. It can be identified reliably by a vertical descending arterial branch that originates from the subclavian artery (Fig. 121-4). This vessel forms the second intercostal artery and crosses the rib 1 cm lateral to the sympathetic chain.22 The first intercostal space is covered by a fat pad, and the first rib is rarely visible from within the thorax. Additional landmarks are the azygos vein, which lies at the level of the right fifth interspace, and the aortic arch, which reaches to the left fourth interspace. The rib number can be determined with certainty by obtaining an intraoperative x-ray after a metallic marker has been introduced into the chest and placed over a rib.
The descending arterial vessel crosses the right second rib lateral to the sympathetic chain.
Outpatient bilateral endoscopic thoracic sympathicotomy is currently the operation of choice for the surgical treatment of palmar hyperhidrosis. Results are uniformly excellent. Virtually all patients will have dry, warm hands after the procedure. Axillary and facial sweating also may be treated in a similar fashion, although the outcomes are not as uniform. The details of the operation are determined by the level at which the sympathetic chain is clipped or transected.
General anesthesia is induced with a single-lumen endotracheal tube. The patient remains supine with the arms are abducted 90 degrees. The head of the operating table is elevated, or the table is flexed into the semi-Fowler's position. A 1-cm incision is made over the third interspace in the anterior axillary line lateral to the pectoralis major muscle (Fig. 121-5). CO2 gas (600–1200 mL) is insufflated via a Veress needle, and a 10-mm trocar is introduced under direct vision (VISIPORT*PLUS, Autosuture, Mansfield MA). The operating thoracoscope (Karl Storz 26037 AA, Tuttlingen Germany) is inserted, and the sympathetic chain is visualized (Fig. 121-6). A cautery device is introduced via the operating thoracoscope.
The patient is placed in the supine position with both arms perpendicular to the torso. A 1-cm incision is made lateral to the pectoralis major muscle at the level of the axillary hairline.
Thoracoscopic view of the sympathetic chain.
Palmar hyperhidrosis and concomitant axillary hyperhidrosis are treated by transecting the sympathetic chain at the T3-T4 level. Isolated axillary hyperhidrosis also may be treated by transecting the sympathetic chain at T3-T4, although Botox injection may be a better alternative. Craniofacial hyperhidrosis is treated by transecting the sympathetic chain at the T2 level.23
Hemorrhage can occur from venous branches that occasionally cross the sympathetic chain. Rarely, injury to a major arterial or venous vessel is caused by misplacement of the trocar or cautery. In addition, the intercostal vasculature can be injured while placing the trocar. Hemostasis is ascertained, and the lung is inflated under direct vision as the trocar is withdrawn. The wound is closed, and the identical procedure is repeated in the contralateral thorax. A postoperative chest x-ray frequently demonstrates small apical pneumothoraces. Chest tubes are not required. When awake and comfortable, the patient is discharged.
Adequate exposure of the sympathetic chain can be achieved with single-lung ventilation or intermittent apnea instead of CO2 gas. The Harmonic scalpel may be used in place of electrocautery. Two 5-mm port sites are required to place crushing clips, the first for the thoracoscope and the second for the automatic clip applier. Smaller incisions have been described by investigators who have access to millimeter-diameter scopes and cautery instruments.24 Intraoperative palmar skin temperature monitoring provides documentation of successful operation25 and usually increases by 1.7°C–2.6°C.26
Palmar hyperhidrosis is cured in virtually all patients who undergo endoscopic thoracic sympathicotomy.1–4,19,20 The recurrence rate in the first several years after operation is 1-3%.1,2,4,20 Quality-of-life questionnaires consistently demonstrate that more than 90% of patients are satisfied with the results.1–4 Surgical treatment for axillary and craniofacial hyperhidrosis is somewhat less successful. Compensatory sweating and recurrence are common reasons for dissatisfaction.
Interruption of the upper thoracic ganglia often produces a decrease in plantar sweating. The anatomic basis for this unexpected response is unexplained, but an increase in plantar skin temperature and decrease in sympathetic skin response have been documented.27
Surgical errors are responsible for early treatment failure. Analysis of 36 patients who underwent reoperation after experiencing resweating within 1 month of operation demonstrated an intact sympathetic chain (11%), incomplete transection (17%), partial regrowth (17%), incorrect ganglia level (11%), slipped clip (30%), and unknown (14%).28 Some of these failures likely resulted from poor visualization of the sympathetic chain owing to pulmonary-chest wall adhesions, overlying vessels, and misidentification of the sympathetic chain.28,29 The role of the Kuntz nerves is controversial. Late failures presumably are due to nerve regeneration. Endoscopic reoperation is feasible. However, the surgeon must be familiar with the distorted intrathoracic anatomy and be prepared to perform a thoracotomy.28,29
Complications and Sequelae
Incisional and retrosternal pain exacerbated by cough or deep breathing are the principal postoperative complaints. Narcotic analgesics generally are necessary for the first 48 hours. Patients commonly return to work or school within 3–7 days. Anhidrosis of the upper chest and face is expected.
Injury to either intrathoracic or extrathoracic structures can result in delayed postoperative hemorrhage. Significant chest wall bleeding may drain into the pleural space without providing external evidence of hemorrhage. In the presence of unexplained hypotension, a repeat chest x-ray and hematocrit are necessary.
Horner's syndrome (i.e., ptosis, miosis, and anhidrosis) occurs in fewer than 1% of patients and results from damage to the sympathetic nerves that pass through the stellate ganglia.1,2,30 Misidentification of the nerve level or proximal transmission of cautery heat is the presumed mechanism of injury. Ptosis is immediate and frequently permanent.
After proximal thoracic sympathicotomy, as many as 75% of patients develop abnormal sweating in previously unaffected regions of the torso.1–4,19–21,31 This “compensatory sweating” is usually no more than an annoyance. However, as many as 3% of patients are affected by sweating of the chest, thighs, and legs equal in severity to the original palmar sweating. While the cause of this most serious of sequela of thoracic sympathicotomy remains obscure, a body mass index of greater than 30 has been found to correlate with increased severity of compensatory sweating.32 Gustatory sweating has been reported in as many as 73% of patients.1–4,19,20,31
Transection of the rami communicantes, while leaving the sympathetic chain intact in the hope of decreasing compensatory sweating, resulted in an increased incidence of recurrent palmar sweating and no change in the occurrence of compensatory sweating.33,34 Similarly, limiting the sympathicotomy to the T2 ganglia appears to have no demonstrable affect on the occurrence of compensatory sweating17,22,27,35,36 when compared with interruption of both T2 and T3.31
Interruption of the T2 ganglia is not necessary to achieve dry palms. Twenty-eight patients who underwent interruption of only the T3 ganglia achieved dry hands, and none developed compensatory sweating.37 Other investigators reporting on interruption of the T4 ganglia noted that compensatory sweating was rare and mild, with only one patient reporting persistent palmar sweating.1,38
Currently, sympathicotomy at T3 and T4 is the most commonly performed procedure. However, if success with a more caudal sympathicotomy is confirmed, the current understanding of upper extremity sympathetic innervation and activity will require reassessment. Although sympathetic fibers from the T2 and T3 spinal levels contribute fibers to the upper extremity, palmar sweating may be determined by sympathetic input originating distal to T4. Interruption at the T4 level would eliminate palmar sweating while leaving the remaining upper extremity sympathetic innervation intact without the need for thermoregulatory compensation.21
Sympathetic fibers to the heart pass through the upper thoracic ganglia. After T2 sympathicotomy, the heart rate at rest and with peak exercise is reduced 13% and 7%, respectively.31 Exercise capacity and the cardiorespiratory response to exercise remain unchanged.12
Prevention and Treatment of Complications
Interruption of the sympathetic chain by application of nerve-compressing clips was devised as a potentially reversible procedure to ameliorate the symptoms of patients suffering from severe compensatory sweating. Hyperhidrosis is controlled as effectively as with sympathicotomy.2,35 As many as 60% of patients note return of palmar sweating and decrease of compensatory sweating following clip removal.2,35 Reconstruction of the transected sympathetic chain with a sural nerve graft has been reported.36