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Video-assisted thoracoscopy has replaced all other approaches to the intrathoracic sympathetic ganglionic chain. Thoracoscopic sympathicotomy is the most common treatment of severe palmar hyperhidrosis, although axillary hyperhidrosis, facial sweating, and facial blushing also have been treated with this modality. In addition, thoracoscopic sympathicotomy has been used to treat the rare patient with vasomotor disorder or chronic pain syndrome of the upper extremities. |
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HYPERHIDROSIS 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. Epidemiology 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 Anatomy and Function 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.
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
Nonoperative Treatment 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. Surgery 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.
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. TECHNIQUE 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.
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 RESULTS 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 Immediate 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. Chronic COMPENSATORY SWEATING 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 CARDIOPULMONARY 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 |
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VASOMOTOR DISORDERS AND PAIN SYNDROMES Microvascular Arterial Disease Ablative surgery of the thoracic sympathetic chain is a technique that has been used for many years to treat upper extremity vascular insufficiency owing to diseases of the microvasculature. However, reports documenting the efficacy of the thoracoscopic approach are few in number. Twenty-eight patients with Raynaud's disease, including seven with digital ulceration, underwent thoracoscopic sympathicotomy after medical therapy failed.39 The sympathetic chain was transected over the T2 to T4 vertebrae using the operative technique previously described for palmar hyperhidrosis. Immediate symptomatic improvement was noted in 93% of patients. All the digital ulcers healed within 1 month of surgery. Eighty-two percent of patients reported recurrence of symptoms within 16 months, although with reduced frequency and severity. Thoracoscopic sympathetic surgery also has been used to treat ischemia of the upper extremity caused by peripheral arterial obstruction. Fifteen patients with atherosclerosis (n = 8), Buerger's disease (n = 4), and ischemia owing to intraarterial drug injection underwent resection of the sympathetic chain from T2-T4.40 Eleven patients had terminal digital necrosis, gangrene, or ulceration. Most patients experienced a decrease in pain, and five patients had complete healing of the skin ulcers. Complex Regional Pain Syndromes The International Association for the Study of Pain created specific definitions for the diagnosis of the complex regional pain syndrome (CRPS).25 Included within CRPS type I is a group of poorly defined disorders, including reflex sympathetic dystrophy, shoulder-hand syndrome, and Sudeck's atrophy (Table 121-1). CRPS type II is initiated by a peripheral nerve injury and is commonly known as causalgia. The clinical course of CRPS has been divided into three stages (Table 121-2). While the pathophysiology of CRPS has not yet been elucidated, a strong relationship to dysfunction of the sympathetic nervous system is well established. Nonoperative treatment of CRPS includes physical therapy, medications, transcutaneous neural stimulation, spinal cord stimulation, and percutaneous sympathetic nerve blocks. There are substantially fewer reports of thoracoscopic sympathetic surgery for this disease than for hyperhidrosis.
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Forty-one patients with CRPS type I of the upper extremity were treated with 46 thoracoscopic sympathectomies.41 The surgical technique was different from that described earlier for treatment of hyperhidrosis. The sympathetic chain was removed from the inferior aspect of the stellate ganglia to the third or fourth thoracic ganglia. Before the sympathetic chain was transected, a clip was placed across the inferior aspect of the stellate ganglia. All patients had previously undergone successful percutaneous bupivacaine sympathetic blocks to document the response to interruption of the sympathetic nervous system. Success was defined as greater than a 50% reduction in the patient's basal pain score that persisted for more than 2 days. Postoperative sympathalgia developed in 24% of patients and consisted of new pain over the scapula. In all but one patient, the pain resolved within 90 days. Three months after surgery, 90% of patients reported a greater than 50% reduction in pain and improved limb motion. By 1 year postoperatively, the pain reduction persisted in only 72% of patients, but most were satisfied with the procedure.
Thoracoscopic sympathectomy of the T2 ganglia was planned in 42 patients with CRPS type II.42 Before surgery, all patients had been treated with a variety of medications. Stellate ganglion blocks (frequently multiple) were performed in all patients, 25 of whom experienced symptomatic improvement. The minimally invasive procedure was completed successfully in 30 patients but was converted to a supraclavicular approach in 12 patients because of dense adhesions or apical pleural thickening. The intraoperative findings that prevented the thoracoscopic approach were attributed to the multiple stellate ganglion injections. Thirty-two patients reported excellent (n = 20) or good (n = 12) results. Response to sympathectomy did not correlate with the response to stellate ganglion injections. Symptomatic improvement correlated with the thoracoscopic approach and performance of the sympathectomy within 3 months of symptom onset. The beneficial effect persisted throughout the 41-month median follow-up.
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SUMMARY Thoracoscopic sympathicotomy is the surgical treatment of choice for patients with severe palmar hyperhidrosis not responsive to medical therapy. The level at which the thoracic chain should be interrupted has not been determined definitely, but the T3-T4 level appears appropriate. Patients must be specifically warned about compensatory sweating that occasionally may be severe. Axillary hyperhidrosis is best treated with Botulinum toxin injections. Thoracoscopic sympathicotomy also provides relief from symptoms of Raynaud's disease and CRPS. |
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CASE HISTORY The patient is a 23-year-old man who has had wet hands and feet since early childhood. He reports that sweating occurs intermittently and unpredictably, although it is worsened by stress. The sweat sometimes drips to the floor and is worse during the summer months. Pedal sweating accompanies the palmar hyperhidrosis but has not been associated with fungal infection. Throughout grammar school and high school, teachers wondered why his papers were always wet and smudged with ink. During his teenage years, he experienced social difficulties because of his wet and cold hands. He is now beginning a career in business and is worried that his palmar hyperhidrosis will interfere with his ability to interact with clients. He has tried Drysol and Drionic without success. A younger brother also has palmar hyperhidrosis. The reminder of his medical history is normal. Physical examination revealed wet hands and feet, with sweat pooling on the volar surface and within the palmar creases. The nonoperative and operative treatments of hyperhidrosis, as well as the potential benefits and complications, were discussed in detail. Included in the informed consent was the possibility of a Horner's syndrome, a pneumothorax that might require a chest tube, and compensatory sweating, which may be severe. Transection of the sympathetic chain versus application of crushing clips also was discussed. He elected to undergo sympathicotomy, which was performed as an outpatient procedure at the T3 and T4 levels. Two weeks after the surgery, he reported dry hands and minimal compensatory sweating. He was elated with his new-found self-confidence. |
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EDITOR'S COMMENT Thoracic sympathicotomy can relieve many benign yet quality of life altering diseases. The equally debilitating complication of compensatory hyperhidrosis warrants a rather cautious approach regarding the extent of sympathicotomy attempted. –LZ |
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REFERENCES
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