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Hyperhidrosis is the pathologic condition of sweating in excess of physiologic requirements for thermoregulation. This excess sweating can be quantified in comparison with the general populace, but patients usually present with a typical history. The typical hyperhidrosis patient is young, between 18 and 25 years old and has had palmar and plantar sweating since early childhood. Parents may recall inordinate wetness of the hands and feet during infancy. Patients may recall grade school classmates refusing to hold their hands because of excessive wetness or teachers scolding them for submitting wet, smudged assignments. Puddles of sweat can accumulate on computer and piano keyboards. Entering adulthood, wet hands adversely affect social interaction and influence career choice.
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Sweating is sporadic, occurs during periods of stress or calm, and is usually worse during the summer. Although the degree of hyperhidrosis varies, the sweating is much greater than the dampness associated with stress. Within minutes, a dry hand can become soaked, with sweat dripping to the floor. The volar surface of the fingers, thenar and hypothenar eminences, and palmar skin folds fill with perspiration (Fig. 146-1).
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Hyperhidrosis sufferers avoid direct or indirect hand contact and have a handkerchief or tissue always available. Characteristic wiping of the hands on their clothing is noticeable. The damp hands are disguised in social situations by a cold drink held in the right hand. This provides an explanation for the dampness and the need to wipe the hand prior to a handshake.
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Concomitant plantar hyperhidrosis occurs in nearly all patients with palmar hyperhidrosis. When walking barefoot, wet footprints are created which are similar to those seen after exiting a shower. Though fungal infections are rare, the constant moistness ruins footwear. 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
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The prevalence of palmar and plantar hyperhidrosis is estimated to be 0.6% to 1% and affects all racial groups.5 Severe axillary hyperhidrosis affects 1.4% of the United States population.6 Patients with classic palmar and plantar hyperhidrosis do not have concomitant illnesses. In contrast, generalized hyperhidrosis, which is treated medically, may be associated with thyrotoxicosis, obesity, neurologic diseases, and rare inherited disorders.
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Up to 65% of patients who have undergone sympathetic surgery have a familial history of hyperhidrosis.2,7 In one study, analysis of the kindred data of 49 affected individuals led to the conclusion that the disease allele is present in 5% of the population.7 One study of 11 families mapped a locus for primary palmar hyperhidrosis to chromosome 14.8
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Overall, thermoregulation is controlled by the autonomic nervous system with the sympathetic system primarily in control of extremity sweating. Sympathetic fibers originating from spinal levels T1 to T8 ascend in the sympathetic chain and commonly reach the brachial plexus via the stellate ganglia. However, alternate pathways from the T2 and T3 ganglia that bypass the stellate ganglia have been demonstrated.9 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 release of acetylcholine from postganglionic neurons.
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The sympathetic chain descends vertically within the thorax over the rib heads (Fig. 146-2). Rarely, it is found between the medial border of the rib head and the collus longus muscle.10 The sympathetic ganglia are located approximately 2 mm cranial to the midportion of the underlying vertebral body.
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Whether hyperhidrosis is emblematic of a global autonomic nervous system dysfunction or it represents a focal abnormality remains unknown. Room temperature resting palmar sweat production is twice normal.11 The sudomotor skin response is enhanced as a result of shortened nerve recovery time.12 Palmar sweat production in response to stress is greatly increased (Fig. 146-3). Pulmonary function and resting cardiac function in the supine position are normal when compared with unaffected controls.13 Plasma catecholamine levels are within normal limits.14 However, peak exercise heart rate and resting heart rate in the standing position are increased.13,15 The ultrastructure of hyperhidrotic axillary eccrine glands is normal.16
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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 prior to sleep. The effect may be from blockage of the sweat gland ducts or by atrophy of the secretory cells. The hands or feet are covered in plastic wrap to prevent damage to clothing or bedding. Once the desired anhidrosis is obtained, application frequency is decreased but must be continued for lasting effect. Side effects include rash and paradoxical hyperhidrosis. Many patients report therapeutic failure as efficacy in palmar hyperhidrosis has not been assessed in a controlled trial. A randomized trial compared botulinum toxin A to a topical 20% aluminum chloride administration in patients with axillary hyperhidrosis and showed greater effectiveness in the botulinum toxin group, although the study was only 12 weeks in duration.17
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Botulinum Toxin A (Botox®) stops sweat production by blocking the release of acetylcholine from the postganglionic nerve end. Randomized trials have demonstrated efficacy of this treatment for both palmar and axillary hyperhidrosis.18,19 Median duration of sweat control varies between 6 and 9 months. Each treatment session involves multiple injections as well. Weakness of the intrinsic muscles of the hand has been reported in 25% to 60% of patients. Botulinum Toxin A injections may represent the treatment of choice for axillary hyperhidrosis.
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In one study, iontophoresis was reported to control palmar hyperhidrosis in 82% of 112 patients who underwent daily 15-minute treatment over 8 days.20 This treatment involves placing the hands or feet in a tap water solution through which electric current flows (Drionic®). Anhidrosis is thought to result from electrically induced precipitation of salts in the sweat ducts. The mean remission was 35 days. Tingling, erythema, and vesicle formation were undesirable side effects.
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Oral anticholinergic medications such as glycopyrrolate and oxybutynin have the theoretic ability to block the stimulation of the sweat gland caused by the release of acetylcholine. One hundred and eighty consecutive patients at a single institution were treated with escalating doses of oxybutynin to a maximum of 10 mg per day. Patients were evaluated over a 12-week treatment period, with 80% experiencing improvement in their symptoms and with almost 75% having a quality of life improvement over the 12 weeks. Dry mouth was the most common symptom (70.5%), with 28.7% having severe symptoms. Sixty-eight percent of patients had little to no dry mouth. Very few had other symptoms, including headache (3.6%) and urinary retention (2.8%). One weakness of this study was that 22% of patients were lost to follow-up, leaving open the possibility of a higher failure rate.21
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Interruption of sympathetic innervation may be achieved by transection of the sympathetic chain, crushing the sympathetic chain with clips, or transection of the rami communicante. Resection of ganglia is not necessary, and in fact, it may be difficult to locate the ganglia because of frequent anatomic variability and the presence of mediastinal fat. Recently, the Society of Thoracic Surgeons (STS) and the International Society on Sympathetic Surgery copublished a consensus opinion regarding hyperhidrosis, recommending a uniform rib-oriented nomenclature for hyperhidrosis surgery (Table 146-1).22 Cauterization at the third rib would be referred to as “cauterized R3, top.”22 A clipped chain at the fourth rib would be “clipped R4, top.”
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The thoracic level(s) necessary to achieve the desired anhidrosis while minimizing systemic side effects is not known precisely. Palmar hyperhidrosis has been treated by transecting the sympathetic chain individually over the second (T2), third (T3), or fourth rib (T4) or some combination thereof.1,2,4,23– 30 During the past decade, several randomized controlled trials have evaluated the optimal levels at which to interrupt the sympathetic chain in order to control palmar hyperhidrosis and minimize morbidity.25–29 The STS expert consensus document reviewed multiple randomized controlled trials, as well as prospective and retrospective studies. For isolated palmar hyperhidrosis, the STS expert consensus group recommends a top of the third rib (R3) or fourth rib (R4) sympathectomy.8 This recommendation is largely based on two studies: one, a randomized controlled trial of 141 consecutive patients randomized to a cauterized, top R3 or cauterized, top R4 treatment,29 and the other a larger, retrospective study which compared R4 to R3 and R2 operations.30 Each study showed very good efficacy in all the groups, but slightly increased wetness in the palms in the R4 groups, although with decreased compensatory hyperhidrosis and decreased incidence of overly dry palms.29,30 The Expert Consensus Group also makes recommendations regarding other levels of hyperhidrosis. It states that palmar-axillary or axillary sweating can be treated by transecting the sympathetic chain at the R5 level alone or the combined R4 to R5 levels.22 These recommendations for a uniform nomenclature and levels of interruption were made with the goal of allowing for improved analysis of techniques and outcomes with a view towards the creation of robust evidence-based guidelines.22 Each specific recommendation for treatment is based on a few small, single-institution studies and should be evaluated by each surgeon in the light of his or her own experience as well. In general, transecting more levels yields more compensatory hyperhidrosis.31
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Correct identification of the anatomic level is imperative. The second rib is generally the most proximal rib that can be seen within the thorax. It can be reliably identified by a vertical descending arterial branch that originates from the subclavian artery. This vessel forms the second intercostal artery (Fig. 146-4) and crosses the rib 1 cm lateral to the sympathetic chain.32 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.
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Outpatient bilateral endoscopic thoracic sympathectomy is currently the operation of choice for the surgical treatment of palmar hyperhidrosis. Results are uniformly excellent and virtually all patients will have dry warm hands. Axillary and facial sweating may also be treated in a similar fashion, also with good results. The details of the operation are determined by the level at which the sympathetic chain is clipped or transected.
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General anesthesia is induced with a single lumen endotracheal tube. The patient remains supine and the arms are abducted 90 degrees. The head of the operating table is elevated or the table is flexed into the semi-Fowler position. A 1-cm incision is made over the third interspace in the anterior axillary line lateral to the pectoralis major muscle (Fig. 146-5). CO2 gas (600–1200 cc) is insufflated via a Veress needle and a 10 mm trochar is introduced under direct vision (VISIPORT*PLUS, Autosuture). The operating thoracoscopic (Karl Storz 26037 AA) is inserted and the sympathetic chain visualized (Fig. 146-6). A cautery device is introduced via the operating thoracoscope.
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Palmar hyperhidrosis is treated by clipping or transection at R3 or R4, whereas palmar hyperhidrosis and concomitant axillary hyperhidrosis can be treated by transecting the sympathetic chain at the R5 level alone or the combined R4 to R5 level. Isolated axillary hyperhidrosis may also be treated by transecting the sympathetic chain at T3 to T4, though subcutaneous axillary Botox® injection is another alternative. Craniofacial hyperhidrosis is treated by transecting the sympathetic chain at the T2 level.33
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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 trochar or cautery. In addition, the intercostal vasculature can be injured while placing the trochar. Hemostasis is ascertained and the lung inflated under direct vision as the trochar is withdrawn. The wound is closed and the identical procedure 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.
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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 employed 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.34 Intraoperative palmar skin temperature monitoring provides documentation of successful operation35 and the temperature usually increases by 1.7°C to 2.6°C.36
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Results of Endoscopic Thoracic Sympathectomy
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Palmar hyperhidrosis is cured in virtually all patients who undergo endoscopic thoracic sympathectomy.1–4,23– 29,37 Recurrence during the next few years is reported as 1% to 3%.1,2,4,24 Quality of life questionnaires consistently demonstrates that >90% of patients are satisfied with the results.1–4 Compensatory sweating and recurrence are common reasons for dissatisfaction.
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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 the sympathetic skin responses has been documented.38
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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%).38 Some of these failures likely resulted from poor visualization of the sympathetic chain due to pulmonary–chest wall adhesions, overlying vessels, and misidentification of the sympathetic chain.39,40 The role of the Kuntz nerves is controversial. Late failures are presumably due to nerve regeneration. Endoscopic reoperation is feasible, though the surgeon must be familiar with distorted intrathoracic anatomy and be prepared to perform a thoracotomy.39,40
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Complications and Sequelae of Surgery
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Incisional and retrosternal pain exacerbated by cough or deep breathing are the principle postoperative complaints. Narcotic analgesics are generally necessary for the first 48 hours. Patients commonly return to work or school within 3 to 7 days. Anhidrosis of the upper chest and face is expected.
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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.
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Horner syndrome (ptosis, miosis, and anhidrosis) occurs in <1% of patients and results from damage to the sympathetic nerves that pass through the stellate ganglia.1,2,41 As the optics and collective experience with the procedure has evolved, this has become an exceedingly rare complication. Misidentification of the nerve level or proximal transmission of cautery heat is the presumed mechanism of injury. Ptosis is immediate and frequently permanent.
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Compensatory Sweating Following proximal thoracic sympathectomy, up to 100% of patients can develop abnormal sweating in previously unaffected regions of the body, depending on the level or levels of sympathetic interruption.1–4,23–29,42,43 The “compensatory sweating” is usually no more than an annoyance and all of these studies had very high rates of patient satisfaction. However, as many as 10% of patients are affected by severe compensatory sweating of the chest, thighs, and legs, which can be equal in severity to the original palmar sweating.26–30 The cause of this most serious of sequela of thoracic sympathectomy remains obscure. A body mass index (BMI) >30 correlated with an increased severity of compensatory sweating in one study44 and another large retrospective study showed an increase in severity with increasing BMI.30 Gustatory sweating has been reported in as many as 73% of patients.1–4,23–30,43
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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.45,46
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Interruption of the T2 ganglia is not necessary to achieve dry palms and indeed, appears to increase compensatory hidrosis.26,28,30 Two randomized, controlled trials showed interruption of only the T3 ganglia achieved dry hands with improved compensatory sweating compared to either the T2 or T2 to T4 levels.26,28 Other trials, one a randomized controlled trial and another a large retrospective trial, reported on the interruption of the T4 ganglion. Compensatory sweating was less frequent and more often less severe compared to treatments at the T3 or T2 ganglia.29,30 These studies and others have led to the STS recommendation for interruption at the R3 or R4 level for palmar hyperhidrosis.
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Cardiopulmonary Sympathetic fibers to the heart pass through the upper thoracic ganglia. Following T2 sympathectomy, the resting heart rate at rest and with peak exercise is reduced 13% and 7%, respectively.43 Exercise capacity and the cardio-respiratory response to exercise remain unchanged.12
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Prevention and Treatment of Complications
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Interruption of the sympathetic chain by application of nerve compressing clips was devised as a potentially reversible procedure in order to ameliorate the symptoms of patients suffering from severe compensatory sweating. Hyperhidrosis is controlled as effectively as with sympathectomy.2,47 As many as 60% of patients note return of palmar sweating and decrease of compensatory sweating following clip removal.2,47 Reconstruction of the transected sympathetic chain with a sural nerve graft has been reported.48 Given the high percentage of patients that will persist with compensatory sweating, the STS Expert Consensus Document suggests that patients be advised to consider a procedure with clips irreversible.22