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Home , Gustatory hyperhidrosis, Hyperhidrosis

20 Dermatology

Hyperhidrosis is a condition characterised by abnormally increased sweating, in excess of that required for regulation of body . Hyperhidrosis can either be generalised or localised to specifc parts of the body, such as hands, feet and axillae. Hyperhidrosis can be divided into primary or idiopathic, and a secondary type. Te primary type usually starts during adolescence or even earlier, while secondary hyperhidrosis can start at any point in life. Te latter form may be due to a disorder of the or , mellitus, tumours, , , or certain medications. Tis article highlights the clinical features and the treatment options for this condition. Nabil Aly, Consultant Physician, University Hospital Aintree, Liverpool email [email protected]

Epidemiology Hyperhidrosis is sweating in axillae; localised hyperhidrosis, excess of that required for and generalised hyperhidrosis.1,2 normal . It is a Localised hyperhidrosis, unlike People of all ages can be afected condition that usually begins in generalised hyperhidrosis, by hyperhidrosis. Primary either childhood or adolescence usually begins in childhood or hyperhidrosis affects men and can affect any site on the adolescence. Localised unilateral and women equally, and most body. However, the sites most or segmental hyperhidrosis is commonly occurs among people commonly afected are the palms, rare and of unknown origin. aged 25–64 years. Some may soles, and axillae. Excessive The condition usually presents have been affected since early sweating may be primary on the forearm or forehead in childhood, and about 30–50% (idiopathic) or secondary to otherwise healthy individuals, have another family member medication use, certain diseases, without evidence of the typical afflicted, implying a genetic metabolic disorders, or febrile triggering factors found in predisposition.5 Localised illnesses. Hyperhidrosis often essential hyperhidrosis. Unilateral hyperhidrosis, unlike generalised causes great emotional distress hyperhidrosis with accompanying hyperhidrosis, usually begins in and occupational disability contra-lateral anhidrosis is also childhood or adolescence. In a for the patient, regardless of rare.3 Palmar hyperhidrosis is a study of 850 patients with palmar, the form and the extent of the benign functional disorder that axillary, or facial hyperhidrosis, problem. Hyperhidrosis is is a psychological and social 62% of patients reported that difcult to treat efectively. With handicap. sweating began since before the newer treatment modalities is characterised by unilateral they could remember; 33% now available, the patient has hyperhidrosis and flushing, since puberty; and 5% during numerous options and is ofered predominantly induced by heat adulthood.6 In a cross-sectional a better prognosis. or exercise.4 The sympathetic primary care study among 795 defcits are usually limited to the older patients (older than 64 face.4 among older years), 10% reported being Types people could be related to certain bothered by night sweats, 9% systemic conditions and clinical by day sweats, and 8% by hot Hyperhidrosis exists in three forms: assessment is always required flushes.7 All three symptoms emotionally induced hyperhidrosis, to rule out the presence of these were associated with reduced which affects palms, soles, and causes (Box 1). quality of life.7

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less numerous and are found in Box 1: Common causes of night sweats among older patients the axilla and genital regions. Te apoeccrine glands are found only in the adult axilla. Te eccrine Te condition Clinical features type is the one mainly involved Menopause Women would also experience in hyperhidrosis. Hyperhidrosis hot fushes is usually stimulated by emotion Pulmonary tuberculosis (TB) Usually associated with and stress, so it does not occur and during sleep or sedation. While However, atypical presentation is normal sweating is controlled not uncommon primarily by thermoregulation Diabetes mellitus Tis type of hyperhidrosis could and, thus, occurs independently be a manifestation of autonomic of level of consciousness. The dysfunction primary defect in patients with hyperhidrosis may be Medications* Several medications may induce hypothalamic hypersensitivity excessive sweating at night to emotional stimuli from the In general, the drugs listed cerebral cortex.8 Generalised below can be associated with hyperhidrosis may be the hyperhidrosis consequence of autonomic Nights sweats are a symptom of dysregulation, or it may develop certain types of Hodgkin’s disease secondary to a metabolic found in older patients disorder, febrile illness, or Parkinson’s disease Te condition can be associated malignancy. In its localised form, with localised or generalised hyperhidrosis may result from a hyperhidrosis disruption followed by abnormal Mental disorder/stress and depression may cause regeneration of sympathetic night sweats nerves or a localised abnormality in the number or distribution of the eccrine glands, or it may be * These include: Calcitonin, fentanyl, acyclovir, ceftriaxone, levothyroxine, associated with other (usually levodopa and carbidopa, quetiapine, amlodipine, omeprazole, , vascular) abnormalities. When medroxyprogesterone, testosterone, prednisolone and tamoxifen. caused by stress, hyperhidrosis may be generalised or limited to the palms, soles, and forehead.8 Pathophysiology sweat production are mainly controlled by the cerebral cortex, Te pathophysiology underlying anterior hypothalamus and the Aetiology hyperhidrosis is complex and sympathetic nervous system. In not well understood. Tere are addition, there are three types of Hyperhidrosis can be idiopathic two distinct types of sweating: sweat glands: eccrine, apocrine or sometimes secondary to other thermal sweating, which tends and apoeccrine. The eccrine diseases, metabolic disorders, to occur on the trunk and is type is the most numerous type, febrile illnesses, or medication controlled by the hypothalamus predominantly occurring on the use. Use of medications may via the thermo-sensitive preoptic soles of the feet, palms, axilla and afect one or more components sweat centre, and emotional face, and this type is innervated by of human thermoregulation sweating, which is predominately the sympathetic nervous system, and induce hyperhidrosis. on the palms and soles and with acetylcholine as the principle Hyperhidrosis beginning later is regulated by the cerebral neurotransmitter.8 Apocrine in life should prompt a search cortex. Thermoregulation and glands are androgen-dependent, for secondary causes such

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as systemic diseases, adverse Box 2: Secondary causes of hyperhidrosis effects of medication use, or metabolic disorders. Secondary Generalised hyperhidrosis causes may include endocrine (an area >100 square cm) diseases such as diabetes • Afecting almost any skin area mellitus, hyperthyroidism, and • Starts at older age .8 In one series, • Symmetry is not very distinctive one third of cases were neurologic • Could be related to secondary causes, including medications in origin, including peripheral and systemic disorders nerve injury, Parkinson disease, reflex sympathetic dystrophy, Localised hyperhidrosis spinal injury, and Arnold-Chiari malformation.9 Other secondary (an area <100 square cm) causes to be considered may • Afects axillae more than hands include , • Starts at early age (<25) and improve later (>50) respiratory disease, and • Usually bilaterally symmetrical psychiatric disease (Box 2). • Tends to cease during sleep Asymmetric hyperhidrosis may • Mainly related to autonomic dysfunction. suggest neurologic disease.9 1. Neurologic or neoplastic diseases Primary hyperhidrosis usually 2. Spontaneous periodic and hyperhidrosis starts during adolescence or even 3. Metabolic disorders or processes: thyrotoxicosis, diabetes before and seems to be inherited mellitus, , gout, pheochromocytoma, as an autosomal dominant genetic menopause trait. Primary hyperhidrosis 4. Febrile illnesses must be distinguished from 5. Medications: , physostigmine, pilocarpine, secondary hyperhidrosis, tricyclic antidepressants, and serotonin reuptake inhibitors. which can start at any point 6. Chronic alcoholism in life. Primary hyperhidrosis 7. Hodgkin disease or tuberculosis (causing nocturnal can be differentiated from hyperhidrosis) secondary type by certain clinical 1) Gustatory stimuli: criteria (Box 3). These criteria • Seen in Frey syndrome, , , diabetic discriminate well between the two neuropathies, herpes zoster , and parotid types (sensitivity: 0.99; specifcity: 2) Eccrine nevus & Blue rubber-bleb nevus 0.82; positive predictive value: 3) Eccrine angiomatous hamartoma* 0.99; negative predictive value: 4) 0.852) and may facilitate 5) POEMS syndrome: Peripheral neuropathy, organomegaly, optimal clinical management.10 endocrinopathy, monoclonal plasma-proliferative disorder, and Essential hyperhidrosis is a skin changes. dermatologic and neurologic 6) disorder characterised by 7) excessive sweating of the eccrine 8) Pre-tibial myxoedema sweat glands.11 It is a disorder of the eccrine sweat glands and is associated with sympathetic * A rare benign malformation characterised by both eccrine and vascular overactivity.12 Essential components, usually frst evident at birth or during early infancy as a hyperhidrosis does not appear to nodule/plaque, usually solitary, involving acral skin and although it be a generalised disorder involving is ofen asymptomatic, it may be associated with , vascular endothelium. Patients , and . note excessive sweating in afected areas, which ultimately prompts

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may reveal underlying Box 3: Criteria for the clinical diagnosis of primary (idiopathic) hyperthyroidism or hyperhidrosis thyrotoxicosis ii. Blood glucose levels may reveal diabetes mellitus or Diagnostic criteria favouring primary hyperhidrosis: hypoglycaemia • Excessive sweating of six months or more in duration, iii. Urinary catecholamines with four or more of the following: may reveal a possible 1. Primarily involving eccrine-dense (axillae/palms/soles/ pheochromocytoma craniofacial) sites iv. Uric acid levels may reveal 2. Bilateral and relatively symmetric sweating gout v. Screening test for 3. Cessation of sweating during sleep (absent nocturnally) tuberculosis, such as purifed 4. At least one episode per week protein derivative (PPD) test. 5. Onset at 25 years of age or younger Imaging studies 6. Family history of idiopathic hyperhidrosis (positive family history) Chest radiography may be used to rule out tuberculosis 7. Impairing daily activities. or a neoplastic cause of the hyperhidrosis. them to seek medical attention. physical findings suggestive Palmoplantar hyperhidrosis, of secondary hyperhidrosis. excessive sweating of the palms Management and soles, is observed in persons with chronic alcoholism and Investigation Therapy for hyperhidrosis can be it could be inherited in an challenging for both the patient autosomal dominant manner.13,14 Laboratory tests are not required and the physician. Both topical to make a diagnosis of primary and systemic medications have hyperhidrosis, but they only been used in the treatment of Clinical assessment serve to rule out and work-up hyperhidrosis. Other treatment potential secondary causes of options for hyperhidrosis Diagnosis of this potentially excessive sweating. A number include and embarrassing and socially of specialised tests have been injections. In disabling condition is based on developed that quantify both addition to pharmacological the patient’s history and visible sweat production and the therapy, other treatments signs of sweating. Clinical impact on quality of life, such include surgical sympathectomy, examination may be normal, as starch iodine test. However, surgical excision of the affected but will often reveal obvious they are not required, nor are areas, and subcutaneous areas of focal sweating or they particularly useful in the liposuction. Each modality could skin maceration. The primary clinical setting. The work-up be used effectively. In general, objective of clinical examination for generalised sweating or management of hyperhidrosis is to reveal any evidence of secondary hyperhidrosis can be should follow a gradational underlying chronic illness complicated, and often includes step-wise approach, beginning suggestive of a secondary cause, a number of investigations. first with the least invasive for example lymphadenopathy. therapies and transitioning to The main aims of clinical Laboratory studies progressively more invasive assessment should be: Important laboratory studies in treatments for those patients 1. Identifying anatomical sites the hyperhidrosis workup may who fail. The appropriate with excessive sweating include the following: treatment will differ for each 2. Ensure the absence of i. Thyroid function tests patient, and will depend on the

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Box 4: Terapy options for hyperhidrosis (starting with the least invasive)

Treatment options Afected area Topical Systemic Ionto- Focal Surgery Subcutaneous therapy therapy phoresis Botulinum (ETS liposuction & injections & others) laser therapy

Axillae √ √ √ √ Face/head √ √ √ √ Palms/hands √ √ √ Feet/soles √ √ √ Groin √ Generalised √ location of focal hyperhidrosis, be neutralised with the topical profile may include mydriasis, the severity and patient tolerance application of baking soda.16 blurring of vision, dry mouth and (Box 4). Aluminum chloride (frequently eyes, difculty with micturition, used in antiperspirants) is and constipation. However, thought to obstruct sweat pores other systemic medications, such Pharmacolological and induce of secretory as sedatives and tranquilisers, therapy cells within the sweat glands. indomethacin, and calcium The only contraindication to channel blockers, may be Topical medications this treatment is documented beneficial in the treatment of Topical agents for hyperhidrosis hypersensitivity, and aluminum palmo-plantar hyperhidrosis. therapy include topical chloride should not be used on , boric acid, 2-5% irritated, broken, or recently Other therapies tannic acid solutions, resorcinol, shaven skin. In addition, axillary potassium permanganate, hyperhidrosis may be treated Iontophoresis , glutaraldehyde, with aluminium chloride gel, Iontophoresis consists of passing a and methenamine.15 All of these although the gel may cause mild direct current across the skin.20 Te agents are limited by staining, cutaneous irritation.17 exact mechanism of action remains contact sensitisation, irritancy, under debate.21,22 In palmo-plantar or limited efectiveness. Because Systemic medications hyperhidrosis, the daily treatment of the limitations of other Systemic agents used to of each palm or sole for 30 minutes agents, Drysol, a 20% aluminum treat hyperhidrosis include at 15-20mA with tap water chloride hexahydrate in absolute medications, iontophoresis is efective.23 Intact anhydrous ethyl alcohol, is more such as , skin can endure 0.2-mA/cm2 commonly used as the frst-line glycopyrrolate, , and galvanic current without negative topical agent.16 Drysol should benztropine. These agents are consequences, and as much as 20– be applied nightly on dry skin efective because the preglandular 25mA per palm may be tolerated.23 until a positive result is obtained, neurotransmitter for sweat Numerous agents have been afer which the intervals between secretion is acetylcholine; used in iontophoresis to induce applications may be lengthened. although the sympathetic nervous hypohidrosis, including tap water To minimise irritation, the system innervates the eccrine and anticholinergics; however, remainder of the medication sweat glands.18,19 However, the treatment with anticholinergic should be washed of when the use of anticholinergics is limited iontophoresis is more effective patient awakes, and the area may because their than tap water iontophoresis.24

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Botulinum toxin hyperhidrosis.33,34,35 Two surgical Subcutaneous liposuction is Botulinum toxin injections approaches are available: an open another means of removing the are effective because of their approach and a newer endoscopic eccrine sweat glands responsible anticholinergic effects at the approach, such as endoscopic for axillary hyperhidrosis. neuromuscular junction and in thoracic sympathectomy (ETS). Compared with classic surgical the postganglionic sympathetic The endoscopic approach has excision, this modality results in nerves in the sweat become favored because of less disruption to the overlying glands.25,26,27 Adverse effects its improvements in terms of skin, resulting in smaller surgical of intradermal injections of complications, surgical scars, scars and a diminished area of botulinum A toxin may result and surgical times. In palmar .39 from diffusion into underlying hyperhidrosis, a survey showed Laser treatment of axillary muscles.28,29 Treatment of axillary thoracoscopic sympathectomy hyperhidrosis using the 1064-nm hyperhidrosis with botulinum to be minimally invasive and Nd-YAG laser was found to be toxin type A reconstituted in to improve the patient’s quality efective and safe as well.40 lidocaine was associated with of life, even if compensatory less pain (from the injection) hyperhidrosis occurs.36 Numerous when compared with the one complications are associated Conclusion reconstituted in normal saline.30 with the endoscopic treatment The results were the same in option; including compensatory Hyperhidrosis is a condition the two groups, thus, lidocaine- sweating (induction of sweating in which excess sweating reconstituted botulinum toxin in previously unafected areas of affects various parts or the A may be preferable for treating the body), gustatory sweating, whole body. The condition axillary hyperhidrosis. In cases pneumothorax, intercostal usually is idiopathic and can be with palmar hyperhidrosis, neuralgia, Horner syndrome, secondary to various disorders or multiple (50) subepidermal recurrence of hyperhidrosis, and medications use. Hyperhidrosis injections result in anhydrosis the sequelae of using general beginning later in life should lasting 4–12 months, and each anesthetic. Topical glycopyrrolate prompt a search for secondary injection produces an area of application may be efective and causes, including systemic anhydrosis approximately 1.2cm safe for the treatment of excessive diseases and adverse effects of in diameter.31 Te only adverse facial sweating in primary certain medications. Treatment effect is mild transient thumb craniofacial and secondary options for hyperhidrosis that resolves within following include topical agents, three weeks. sympathectomy.37 Lumbar iontophoresis and botulinum sympathectomy is a relatively new toxin injections. In addition procedure aimed at those patients to pharmacologic therapy, Surgical treatment for whom ETS has not relieved endoscopic sympathectomy and excessive plantar sweating. The surgical excision of the afected Sympathectomy success rate is about 90% and the areas have been used. However, Sympathectomy has been used as operation should be carried out the condition is difcult to treat a permanent efective treatment only if patients first have tried efectively and a logical approach for almost 90 years. It is usually other conservative measures.38 must be taken to individualise reserved for the fnal treatment therapy based on the degree of option.32 Sympathectomy Other surgical techniques functional impairment. involves the surgical destruction Surgical excision of the afected of the ganglia responsible area identifed using iodine starch Conflict of interest: none for hyperhidrosis, T2 and T3 testing, removes the appropriate declared thoracic ganglia in palmar sweat glands, thereby eliminating hyperhidrosis, T4 thoracic sweating. This technique is References available on online ganglia in axillary hyperhidrosis, particularly useful in axillary version at www.gmjournal. and T1 thoracic ganglia in facial hyperhidrosis. co.uk

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