Facial Hyperhidrosis Ms Natasha Berridge and Mr Mahesh Kumar discuss the recognition, diagnosis and management of facial hyperhidrosis
Facial hyperhidrosis is a localised variant of hyperhidrosis, a common condition of exaggerated sweat production from the eccrine sweat glands. The condition exists in two variants. Commonly, there is no medical cause identified (nor is it a side effect of medication); hence, it is of primary idiopathic origin. Secondary hyperhidrosis occurs due to an underlying medical cause such as Frey’s syndrome or as a side effect of medication.1-4 Understandably, excessive facial sweating can impact significantly
upon the psychosocial wellbeing of the affected individual and directly affect quality of life.5,6 Aesthetic practitioners tend to have little experience in treating facial hyperhidrosis, unlike more common forms such as axillary and palmoplantar hyperhidrosis. In this article, we will discuss facial hyperhidrosis and review the most up-to-date treatment options available to manage this debilitating condition.
About hyperhidrosis
Hyperhidrosis is a common distressing complaint, affecting approximately 1% of the population in the UK.1,4 It is characterised by excessive sweat production from the eccrine sweat glands, which are distributed over nearly the entirety of the body. Eccrine sweat glands are most densely populated in the axillae, forehead, palms of the hands and soles of the feet.7,8 Conversely, apocrine sweat glands are less numerous and are limited in distribution to the axilla and groin. Eccrine sweat glands open directly onto the skin surface, whereas apocrine sweat glands open onto the hair follicle within the dermis of the skin.2,8 For the majority of people, sweating is a normal physiological process that is essential to regulate ‘normal’ body temperature, otherwise known as ‘thermoregulation’. Thermoregulation is controlled by the sympathetic nervous system within the thoracic region, but is also responsive to emotional and gustatory stimuli.2,8 In hyperhidrosis, the amount of sweat produced is far greater than that required for normal body temperature regulation. It is widely postulated in the literature7,9,10 that this is a consequence of dysfunction of both the sympathetic and parasympathetic nervous systems, rather than actual pathology of the gland itself. Hyperhidrosis may lead to dehydration, electrolyte disturbances, blurred vision (profuse sweating of the face) and recurrent skin infections if not
appropriately treated.6 Primary idiopathic hyperhidrosis, otherwise known as ‘focal’ hyperhidrosis, occurs in very specific body areas such as the axilla, palmoplantar and craniofacial regions. Typically, it occurs symmetrically and often begins in childhood or early adolescence.1,2 Ro and colleagues report an autosomal dominant positive family history in up to 65% of cases11 and genome studies report a possible association with chromosome 14q.12 Distinction must be made from ‘generalised’ hyperhidrosis that affects the whole body and tends to occur in adulthood. Unlike primary hyperhidrosis, sufferers experience sweating whilst sleeping overnight.1,2,10 Secondary hyperhidrosis can be related to medication (e.g. antidepressants), infection, endocrine disorders (e.g. hyperthyroidism,
hyperpituitarism, acromegaly, menopause and pregnancy) and malignancy (e.g. carcinoid syndrome, pheochromocytoma, Hodgkin’s disease).1,2 Special forms of ‘focal’ hyperhidrosis results from central or
peripheral neuronal damage. Frey’s syndrome is a classic example of secondary focal hyperhidrosis and almost exclusively occurs in those who have surgery or, less commonly, trauma to the parotid gland.1
Frey’s syndrome causes ‘gustatory sweating and/or facial flushing’ in the cheek and mandibular regions during mastication, particularly with hot foods types. Authors are yet to fully elucidate the exact
pathophysiology, but it is believed that Frey’s syndrome occurs due to aberrant re-innervation of postganglionic parasympathetic neurons to denervated sweat glands and cutaneous blood vessels.13-16 Gustatory sweating may also be seen in families, known as hereditary gustatory sweating, or can simply occur as part of a compensatory mechanism, causing excess sweating in diabetic patients.1,2,17
Excessive facial sweating is undoubtedly a distressing problematic disorder that has the potential to interfere with leading a normal lifestyle. Various well documented studies2,6,18 have used validated
subjective assessment tools such as the Hyperhidrosis Impact Questionnaire (HHIQ) to demonstrate that quality of life can be greatly affected.19 A 2016 multi-centre study by Bahar et al. using patient-based health questionnaires reported that there is an increased prevalence of anxiety and depression in those patients with hyperhidrosis.18
Diagnosis
A diagnosis of hyperhidrosis is often made clinically and usually no further investigations are required for those who give a classic history of primary or secondary focal hyperhidrosis.9,20 However, it is
important to pay particular attention to the distribution of excessive sweating, as a suspected diagnosis of generalised hyperhidrosis warrants medical investigations to exclude an underlying cause such
as medication or disease. Routinely in our clinical practice, we use the well-established Minor’s Starch Iodine test, a useful diagnostic test to objectively evaluate the exact location of excess sweat production
in the facial region.4,10,14 We apply a coating of aqueous povidone-iodine solution to the facial skin, allow it to dry for 10 minutes, then uniformly powder a layer of corn starch over the iodine. To stimulate
sweating, our patients are either placed in a warm room or given a strong gustatory stimulus (such as lemon drops) depending on whether primary focal hyperhidrosis or Frey’s syndrome is
suspected, respectively. After approximately 10-15 minutes, the onset of sweating is highlighted by a blue/violet discolouration as a result of the interaction between iodine and starch (Figure 1). Other
quantitative tests are available, such as sudometry and gravimetry which are commonly used as part of research or clinical trials to determine the exact amount of sweat produced in a defined period
of time (e.g. mg/mL).6,10 Additionally, there are numerous patient-based assessment scales
used to quantify the severity of symptoms.2 Specifically, Solish and colleagues demonstrated that the Hyperhidrosis Disease Severity Scale (HDSS) is a quick and easy method of grading disease severity
the into mild, moderate and severe based upon how sweating interferes with activities of daily living (Table 1).21
Treatment Options
There are a number of treatment options currently available that are clinically effective in reducing the amount of sweat produced in hyperhidrosis. In addition to lifestyle modifications, treatments are
typically categorised into non-surgical (topical agents, iontophoresis, oral medications, botulinum toxin A injections) and surgical techniques (such as endoscopic thoracic sympathectomy and surgical excision of eccrine sweat glands). 3,4,7,9,10,13,14,16,22-25 All of these interventions vary in their effect (temporary
versus permanent), associated risks and clinical efficacy dependent upon body site treated. In this article, we will specifically review non-surgical and minimally invasive treatments which are commonly used
for facial hyperhidrosis, while an extended online version of this article will also discuss the surgical interventions.
Non-surgical options
Topicals
In a recent literature review, authors documented that topical antiperspirants, which contain aluminium salts (usually 20% aluminium chloride in absolute anhydrous ethyl alcohol) are often first-line
treatment in the management of hyperhidrosis because of the ease of use, cost-effectiveness and good safety profile.8 A small study of 15 patients with axillary hyperhidrosis treated with topical antiperspirants demonstrated that long-term use leads to obstruction of the distal eccrine sweat gland ducts, causing structural and functional damage, with an overall reduction in sweat production.26 Most patients achieve satisfactory results with antiperspirant therapy for axillary hyperhidrosis, although the effects are short-lived and temporary.9,10 Patient compliance is imperative for maintenance of long-term success, although in the facial area this may be challenging. Adverse events are limited, but irritation
to the skin or eyes and/or allergic hypersensitivity to the aluminium salts is commonly reported.2,4,9,22 Various studies have demonstrated that topical anti-cholinergic ointments such as glycopyrrolate and
oxybutynin are highly effective agents used in the treatment of facial hyperhidrosis.24,27 These agents reduce excessive facial sweating by competitively binding to postsynaptic acetylcholine receptors near eccrine sweat glands.2,9,28 In a 2008 study by Wo et al., of 25 patients treated with 2% topical glycopyrrolate for facial hyperhidrosis at least 96% were satisfied with its therapeutic effect.27 We commence treatment with 0.5% topical glycopyrrolate, dose titrating to a maximum of 2%, dependent upon symptom control. Patients are advised to apply the ointment to the affected facial area at night and warned to avoid inadvertent application to the mucous membranes of the mouth, nose or eyes. Inappropriate absorption of glycopyrrolate can lead to problematic dry eyes, blurred vision and dry mouth.9,27
Systemics
Anticholinergic agents, such as glycopyrrolate, may also be used systemically in the treatment of hyperhidrosis. In a 2017 literature review, the authors conclude that oral anticholinergics are an effective
potential treatment alternative for hyperhidrosis.9 Unfortunately, their use in most patients is limited by their intolerable systemic side effects which include dizziness, blurred vision, dry mouth/eyes, constipation and heart rhythm disturbances.2,9,10
Botulinum toxin A injections
Iontophoresis has been shown to be an effective treatment for focal hyperhidrosis, particularly of the palms and soles if regularly used.29 The exact mechanism of action by which iontophoresis reduces sweat production is not fully elucidated, although it’s postulated that ionised particles either physically block or prevent sympathetic mediated regulation of the eccrine sweat glands.9,4,28 In facial hyperhidrosis, iontophoresis is delivered via the patient wearing a well-fitting mask
which is soaked most commonly in tap water (although other solutions have been tried such as glycopyrrolate) to allow ionised particles to cross the normal skin barrier.30 Treatment regimes vary upon body site (axilla versus face), however, initially it occurs every few days, lasting up to 30 minutes per session until the desired effect is achieved. Thereafter, to maintain results, ‘top-up’ treatment sessions should occur once weekly. Iontophoresis is a relatively safe procedure. However, it has been associated with adverse reactions such as skin erythema, a burning sensation and skin vesicles.9,10,31
Despite its well documented use and license in the UK for axillary hyperhidrosis, botulinum toxin A (BoNT-A) has also been used to treat hyperhidrosis in other body regions such as the face.1,2,4,7,9,10,21,23,24 It is also the treatment of choice for patients with extensive gustatory sweating.13-17,25 BoNT-A is a neurotoxin derived from the anaerobic bacterium Clostridium botulinum and it specifically targets cholinergic nerve endings, which regulate eccrine sweat gland activity in sweat production. This causes a temporary and reversible local chemodenervation by the blockade of acetylcholine release, leading to the desired clinical effect of reduced sweat production at the site of injection. Over time, the formation of new receptors lead to the production of sweat, and hence the ‘wearing off’ effect of BonT-A.22,23 Over the years, BoNT-A has become one of the mainstay treatments for facial hyperhidrosis as it is considered extremely effective and safe when performed by an appropriately skilled clinician. One study demonstrated that BoNT-A for the treatment of primary focal
hyperhidrosis of the axilla, palms and forehead is associated with high levels of patient satisfaction, as evidenced by the modified Dermatology Life Quality Index scale.32 Additionally, BoNT-A provides effective relief of symptoms for up to four to six months as demonstrated in numerous published studies.24,32,33 In our clinical practice, we use onabotulinum toxin A 100IU, which is reconstituted with 4mL of normal saline yielding a solution concentration of 2.5IU/0.1mL. Patients are treated in the outpatient setting. Following identification of the affected facial skin with Minor’s Starch Iodine test, the skin is bordered and divided into 1x1cm squares with a waterproof marking pen (Figure 2). We
administer 2.5IU/0.1mL of toxin into each square, ensuring even superficial intradermal distribution of the toxin diffusion in order to minimise the potential for adverse effects. In our experience, results can usually be observed within one week and last for almost six months, therefore we typically follow-up our patients at two weeks and four months post-injection. Documented complications are rare, however, injection site pain and post procedural bruising are common. In our experience, topical anaesthesia or a nerve block injection, dependent upon the area of facial skin affected, may minimise discomfort during treatment. Furthermore, inadequate injection technique and local over-dosage may result in unwanted, aesthetic
less satisfactory paralysis of the treated mimetic muscles (especially if treatment is performed in the central area of the face). We therefore recommend that hyperhidrosis treatment of central facial areas only be performed by experienced aesthetic practitioners.
Summary
Facial hyperhidrosis (including Frey’s syndrome) is not as common as other forms of hyperhidrosis (axillary, palmoplantar). Without doubt, it can be socially debilitating, severely impacting upon activities of daily living and overall quality of life. Many sufferers will attempt to modify their lifestyle to camouflage or live with the condition, often seeking medical advice and/or treatment long after the onset of symptoms. Our article highlights the current available treatment options that have achieved clinical success and patient acceptance. In our opinion, BoNT-A has revolutionised the management of facial
hyperhidrosis. We feel it is important to raise awareness so that aesthetic practitioners are able to recognise and potentially treat facial hyperhidrosis in their clinical practice.
Acknowledgements: We would like to thank consultant maxillofacial surgeon Mr Michael Amin, for providing the clinical photographs used in this article.
Ms Natasha Berridge is a maxillofacial surgeon with a specialist interest in facial aesthetics and surgical dermatology. A fellow of the Royal College of Surgeons and member of the Faculty of Dental Surgery, Ms Berridge has years of experience in treating facial hyperhidrosis and other maxillofacial conditions with botulinum toxin.
Mr Mahesh Kumar is a maxillofacial and reconstructive surgeon with more than 15 years’ experience as a NHS consultant in treating head and neck oncology, surgical dermatology and aesthetic facial surgery. Figure 2: Following identification of the affected facial skin with Minor’s Starch Iodine Test, the area is bordered and divided into 1x1cm squares to aid intradermal injection of toxin.
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