hiperhidroza

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exacerbation of palmar sweating with use of hand lotion

severe facial sweating

severe axillary sweating

generalised sweating

History & exam details

Diagnostic tests

Tests to consider

starch-iodine test

gravimetry

thyroid function test

metabolic panel

24-hour urine collection for catecholamines, metanephrines, normetanephrines

serum free metanephrines, normetanephrines

urine 5-hydroxyindoleacetic acid

urine drug screen

chest x-ray

CT scans

Diagnostic tests details

Treatment details

Acute

primary: axillary hyperhidrosis

topical aluminium chloride

short-term anticholinergics

botulinum toxin type A


local sweat gland excision


endoscopic thoracoscopic sympathectomy (ETS)


primary: palmar hyperhidrosis



iontophoresis

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primary: plantar hyperhidrosis

supportive care


topical aluminium chloride with supportive care


iontophoresis with supportive care


primary: craniofacial hyperhidrosis





secondary hyperhidrosis

treatment of underlying condition


Treatment details

Summary An excess sweating condition beyond physiological need.

Classified as primary and of unknown cause (idiopathic), or secondary due to an underlying condition

(usually an infectious, endocrine, or neurological disorder).

Primary hyperhidrosis may also be described as palmar, plantar, axillary, and craniofacial, each of which

has its own clinical characteristics. Patients may have a combination of anatomical areas affected.

Primary hyperhidrosis occurs in both adults and children, commonly starting in early childhood or at

puberty.

Treatment options for primary hyperhidrosis include medical and surgical treatments. Medical treatments

include topical aluminium chloride, oral anticholinergic agents, iontophoresis, and botulinum type A injections.

Surgical treatments include direct axillary sweat gland removal and thoracoscopic sympathectomy.

DefinitionA condition of excess sweating, beyond physiological need, which isfrequently disabling for the patient, professionally and socially. It can beclassified as primary and of unknown cause (idiopathic), or secondary due to
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an underlying condition (usually an infectious, endocrine, or neurologicaldisorder). Primary hyperhidrosis may also be described as palmar, plantar,axillary, or craniofacial, each of which has its own clinical characteristics.Patients may have a combination of anatomical areas affected.

EpidemiologyHyperhidrosis has a prevalence range of approximately 2% to 4% worldwide,without an obvious gender predisposition.[1] [2] Global differences areapparent. One study estimated the prevalence of hyperhidrosis in the US at2.9%, with approximately half (1.4%) of these people having the axillaryvariety.[2] In the Asian population there is a disproportionately high incidenceof the palmar variety, with up to a 5% prevalence in certain areas ofChina.[3]Approximately 50% of patients with palmar hyperhidrosis have afamily history of the disorder.

Primary hyperhidrosis has a bimodal onset commonly starting in earlychildhood or at puberty.[1] [4] [5]Of patients with severe hyperhidrosis presenting for surgery, most havepalmoplantar hyperhidrosis, 15% to 20% have combined palmar-axillaryhyperhidrosis, 5% to 10% have isolated axillary hyperhidrosis, and less than5% have craniofacial hyperhidrosis.[6]

AetiologyThermoregulation and sweating are controlled by complex neurological

pathways involving the cerebral cortex, hypothalamus, and sympatheticnervous system.[4] The precise aetiology of primary hyperhidrosis is notentirely clear, but it is likely to be a result of overreactivity or hyperexcitabilityof the neurological circuits causing sweating. Although the simplestexplanation is hyperactivity of the sympathetic nervous system, it is likely tobe more complex, involving interactions between the sympathetic system, theparasympathetic system, and higher centres.
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Schematic drawing showing the

relationship of the central nervous system to the sympathetic ganglia and peripheral

and visceral targetsFrom the personal collection of Fritz Baumgartner, MD

The strong familial pattern of palmar hyperhidrosis suggests a hereditarypredisposition.[7]The disorder appears to be an autosomal dominant traitwith variable penetrance, and estimates are that a child born to a parent withthe classic pattern has a 1 in 4 chance of having the disorder as well, but witha wide range of expression. Genetic analysis has mapped the palmar varietyto chromosome 14.[8] However, the genetic locus for the axillary or facialsubsets of hyperhidrosis is not clear.[7] [8] Secondary hyperhidrosis is due to

an organic aetiology, such as an endocrine, a neoplastic, or an infectiouscause.

PathophysiologyHumans have approximately 3 million sweat glands distributed over the bodysurface, with a higher concentration on the palms, forehead, soles, andaxillae.[4] [9] Of the 3 types of sweat glands, the eccrine type is the mostprevalent and clinically most significantly relevant to hyperhidrosissyndromes. Apocrine and apoeccrine sweats are less significant but may also

be involved in axillary sweating. Patients with hyperhidrosis do not have anyabnormalities in the number or histology of the eccrine sweat glands, nor isthere any apparent histological abnormality of the sympathetic nervous fibresor ganglia in affected patients. The pathophysiology involves a more elusiveand complex hyperexcitability of the neurological pathways, which is likely toinvolve cortical, hypothalamic, and autonomic nervous system interactions.The pathophysiology of secondary hyperhidrosis involves the systemic and
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neurological effects of organic disorders and ultimately their effect onthermoregulatory centres in the hypothalamus.

Classification

Primary hyperhidrosis

Palmoplantar hyperhidrosis

Excessive hand sweating (palmar hyperhidrosis) to the point of dripping or near dripping. The soles of

the feet may be equally affected (plantar hyperhidrosis).

Axillary hyperhidrosis

Excessive underarm sweating that is not synonymous with underarm malodour. It is much more varied

in severity, aetiology, and patient impact than palmar or plantar hyperhidrosis.

Craniofacial hyperhidrosis

Excessive head sweating, primarily of the face. It can be disabling for patients in its severe form.

Secondary hyperhidrosis

Excess sweating due to specific pathologies, including endocrine, infectious,neoplastic, cardiovascular, drug, or toxicological causes. It can also resultfrom a neurological injury. Because these disorders are readily suspectedfollowing a thorough history and physical exam, it is usually a simple matter

to distinguish secondary from primary hyperhidrosis.

Secondary preventionPreventative measures to help patients with hyperhidrosis (e.g., relaxationtechniques or psychotherapy) are usually ineffective because the disorderhas an organic, physiological, rather than psychological cause.

History & examinationKey diagnostic factorshide allpresence of risk factors (common)

Key risk factors for primary hyperhidrosis include family history, high emotional states, hot or humid

climates.

Key risk factors for secondary hyperhidrosis include drugs and substance abuse, endocrine

disorders, cardiovascular diseases, hypoglycaemia, menopause, infectious diseases, sepsis,

neoplastic diseases, carcinoid tumours, and neurological injuries.excessive palmar sweating (common)


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Mild disease is a moist palmar surface without visible droplets of perspiration. If palmar sweating

extends towards the fingertips, the condition can be considered moderate. If sweat drips off the

palm and reaches all the fingertips it is severe.View imageexcessive plantar sweating (common)

Moist socks and shoes as well as increased foot odour.

In some patients, soles of feet sweat to a level approximating excessive palmar sweating.

onset in early childhood or puberty (common)

Typically, palmoplantar hyperhidrosis has a bimodal onset starting in early childhood or at

puberty.[1] [4] [5]exacerbation of palmar sweating with use of hand lotion(common)

Usually, patients with a history for palmoplantar (or palmar) hyperhidrosis present with completely

dry hands. However, on application of ordinary hand lotion, their palms sweat profusely within

minutes. View imagesevere facial sweating (common)

Occurs in patients with primary facial hyperhidrosis.

severe axillary sweating (common)

Occurs in patients with primary axillary hyperhidrosis.

generalised sweating (common)

Secondary hyperhidrosis tends to occur as a more generalised all-over body sweating.

Risk factorshide all

Strong

family history

At least 50% of patients with palmar hyperhidrosis report a positive family history.[7] [8]

high emotional states

Intense emotional reactions such as fear, anger, or stress may provoke the symptoms of primary

hyperhidrosis, either focal or generalised.hot or humid climates

Can provoke the symptoms of primary hyperhidrosis, either focal or generalised.

medications

Several types of medications can cause secondary hyperhidrosis as a side effect. These include

insulin, meperidine, emetics, cholinesterase inhibitors, selective serotonin reuptake inhibitors,

opioids, propranolol, pilocarpine, and physostigmine.

substance abuse

Substance or alcohol abuse, or withdrawal from these, is associated with secondary hyperhidrosis.

endocrine disorders

Generalised secondary hyperhidrosis may be caused by disorders of the thyroid, pituitary,

pancreas, or adrenal glands (e.g., thyrotoxicosis, pituitary tumours, diabetes, or

phaeochromocytoma).cardiovascular diseases
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Cardiovascular disorders, including congestive heart failure, acute coronary syndrome, and rhythm

disorders, may cause generalised secondary hyperhidrosis.hypoglycaemia

May cause generalised secondary hyperhidrosis.

menopause

May cause secondary hyperhidrosis or 'hot flushes'.infectious diseases

Infectious agents such as tuberculosis and malaria may cause generalised secondary

hyperhidrosis.sepsis

Septic states can cause secondary hyperhidrosis.

neoplastic diseases

May cause generalised secondary hyperhidrosis. For example, a patient with a neoplasia such as a

lymphoma may have extensive night sweats of the entire body, lymphadenopathy, and shaking

chills.carcinoid tumours

May cause generalised secondary hyperhidrosis.

neurological injuries

May cause focal secondary hyperhidrosis. Injuries such as acute spinal cord injury, cerebral or

medullary infarcts, or other nerve injuries (e.g., post-traumatic vasomotor dystrophy) may cause

focal sweating. In addition, Frey's syndrome (sweating on one side of the forehead, face, scalp, and

neck occurring soon after ingesting food as a result of damage to the nerve that innervates the

parotid gland) may cause facial gustatory sweating.

Weak

spicy foods

May provoke the symptoms of primary hyperhidrosis, particularly the focal craniofacial variety.

obesity

Although obesity is not a direct cause of hyperhidrosis, it may lead to a condition of generalised

secondary hyperhidrosis.

Diagnostic testsTests to considerhide all

Test

starch-iodine test

Reaction with sweat produces a purple sediment.

This is a qualitative test that indicates the extent of sweat activity. May be useful to map areas for local p

axillary sweat gland excision or botulinum type A toxin injection.


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During the test, a 1% to 5% solution of iodine in alcohol is applied to the area in question and allowed to

then applied to the area.

gravimetry

A quantitative test that involves the measurement of sweat accumulation by filter paper.[4] [12]

Filter paper is weighed before and after contact with a sweaty body region and so provides a measure o

production in milligrams per minute.

thyroid function test

Performed if thyrotoxicosis is suspected as the cause of secondary hyperhidrosis.

metabolic panel

Performed if endocrine disorders, diabetes, or glucagonoma are suspected as the cause of secondary h

24-hour urine collection for catecholamines, metanephrines, normetanephrines

Performed if phaeochromocytoma is suspected as the cause of secondary hyperhidrosis.

serum free metanephrines, normetanephrines

Performed if phaeochromocytoma is suspected as the cause of secondary hyperhidrosis.

urine 5-hydroxyindoleacetic acid

To exclude or confirm carcinoid tumours that secrete serotonin if these are suspected as the cause of se

hyperhidrosis.

urine drug screen

To rule out recreational drug use as the cause of secondary hyperhidrosis.

chest x-ray

May be used to rule out tuberculosis or a neoplastic cause if these are suspected as the cause of secon

CT scans

Performed if neoplastic disorders, pituitary tumours, or neurological injury is suspected as the cause of s

hyperhidrosis.
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Step-by-step diagnostic approachFor primary hyperhidrosis, history confirmed by physical examination isusually all that is required for correct diagnosis. The skillful use of strategicquestions will usually predict the physical findings. For secondary

hyperhidrosis, the diagnosis is more complex because a thorough physicalexamination and detailed laboratory evaluations are required to identify theorganic pathology that is the cause of the hyperhidrosis.[4]

HistoryThe patient's symptoms and medical history should be ascertained. Inprimary hyperhidrosis the condition may be localised and patients may reportexcessive hand (palmar), foot (plantar), underarm (axillary), or head/facial(craniofacial) sweating. In secondary hyperhidrosis, patients may report more

generalised all-over body sweating. Patients may also report changes in theamount or pattern of sweating, changes in the odour associated withsweating, and/or stained clothing. Some patients may report a family historyof the condition. At least 50% of patients with palmoplantar hyperhidrosisreport a positive family history.[7] [8]

Physical examPalmar hyperhidrosis

Mild disease occurs as a moist palmar surface without visible droplets of perspiration. If palmar sweating

extends towards the fingertips, the condition can be considered moderate. If sweat drips off the palm and

reaches all the fingertips, it is severe.

Plantar hyperhidrosis

Usually occurs in conjunction with palmar sweating. Patients with this variety have excessive sweating of

the feet that leads to moist socks and shoes as well as increased foot odour.

Palmoplantar hyperhidrosis

This is severe palmar and plantar sweating, which usually has four hallmark characteristics:[5] [10] [11]

o Severe palmar (hands) sweating to the point of dripping or near dripping

o Severe plantar (feet) sweating similar to the palms

o Bimodal onset, either in early childhood or at puberty (or worsened at puberty)
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o Exacerbation with application of hand lotion.View image

Craniofacial hyperhidrosis

History and physical examination usually point to a debilitating level of craniofacial sweating often

exacerbated by emotional stress or spicy foods. The point at which normal stress-induced facial sweating

becomes pathological depends on the objective quantity of sweating (e.g., dripping) and the subjective impactlevel of the disorder on the patient's daily activities.

It is important to consider whether normal, physiological sweating has been misinterpreted as

pathological and abnormal by the patient. Therefore, the overall psychological stability of the patient should also

be considered.

Axillary hyperhidrosis

The point at which normal stress-induced axillary sweating becomes pathological depends on the

objective quantity of sweating (e.g., dripping down the torso) and the subjective impact level of the disorder on

the patient's daily activities.

As with craniofacial sweating, it is important to consider whether normal, physiological sweating has

been misinterpreted as pathological and abnormal by the patient. Therefore, the overall psychological stability of

the patient should also be considered.

Secondary hyperhidrosis

Diagnosis depends on recognising the underlying organic pathology that is causing the excess

sweating.[1] [4] For example, focal sweating may result from acute spinal cord injury, cerebral or medullary

infarcts, or other nerve injuries (e.g., post-traumatic vasomotor dystrophy), and facial gustatory sweating may be

caused by Frey's syndrome (sweating on one side of the forehead, face, scalp, and neck occurring soon after

ingesting food as a result of damage to the nerve that innervates the parotid gland). More generalised sweating

may be due to endocrine, neoplastic, infectious, drug, and toxicological-related problems and, depending on the

history and physical examination, may require additional testing. These disorders may include thyroid, pituitary,

diabetic, infectious, and neoplastic diseases, as well as phaeochromocytoma and carcinoid tumours. Acute

coronary syndromes, heart failure, and rhythm disturbances may also cause sweating, as can substance abuse.

Objective diagnostic testingIn most cases of primary hyperhidrosis, history confirmed by physicalexamination is diagnostic; therefore, objective testing is usually not required.However, it may be used for difficult or questionable cases.[4] There are twomain tests: starch iodine test and gravimetry.

Starch-iodine test
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This is a qualitative test that indicates the extent of sweat activity, and may be useful to map areas for

local procedures, such as axillary sweat gland excision or botulinum type A toxin injection. During the test, a 1%

to 5% solution of iodine in alcohol is applied to the area in question and allowed to dry. Cornstarch is then

applied and the reaction with sweat produces a purple sediment.

Gravimetry This is a quantitative test that involves the measurement of sweat accumulation by filter

paper.[4] [12] Filter paper is weighed before and after contact with a sweaty body region and so provides a

measure of the rate of sweat production in milligrams per minute. Axillary hyperhidrosis is diagnosed if sweat

production is >100 mg/5 minutes in men and >50 mg/5 minutes in women. Palmar hyperhidrosis is diagnosed if

sweat production is >30-40 mg/minute.

Laboratory tests

Unnecessary for the diagnosis of primary hyperhidrosis, they are useful whensecondary hyperhidrosis is suspected. Thyroid function tests, metabolic andelectrolyte panel, urine evaluation for metanephrines, catecholamines, and 5-hydroxyindoleacetic acid, plain x-ray, and CT scanning can help distinguishbetween thyroid, pituitary, diabetic, infectious, and neoplastic disorders, aswell as phaeochromocytoma and carcinoid tumours. An ECG andechocardiogram may be helpful to rule out acute coronary syndromes, heartfailure, and rhythm disturbances. In addition, where suspected, urine analysisfor substance abuse may be required.

Click to view diagnostic guideline references.

Diagnostic criteriaHyperhidrosis Disease Severity Scale by the International

Hyperhidrosis Society[4]The severity of the hyperhidrosis, as judged by the level of impairment of theactivities of daily living, can be assessed with the 4-point HyperhidrosisDisease Severity Scale:

Level 1 is non-significant sweating that does not interfere with the activities of daily living

Level 2 is tolerable sweating that sometimes interferes with the activities of daily living

Level 3 is barely tolerable and frequently interferes with the activities of daily living

Level 4 is intolerable and always interferes with the activities of daily living.
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Case history #1A 15-year-old boy presents with profound palmar sweating, with sweatdripping down from his hands. He says that he has had it for as long as hecan remember. His feet sweat nearly as much as his hands, but this bothers

him less. His sweating can occur randomly or be provoked by meeting newpeople, any stressful situation, or by application of hand lotion. One of his twobrothers has the same problem. He avoids parties and social contact.

Case history #2A 25-year-old actress presents with severe axillary sweating that is quiteproblematic for her career. Despite her use of over-the-counter clinicalstrength topical antiperspirants, underarm sweat is still quite obvious throughher blouse.

Treatment Options

Patient group

Treatment

line Treatmenthide all

primary: axillary

hyperhidrosis

1st topical aluminium chloride

Topical aluminium chloride for up to 1 week is the first-line

treatment for axillary hyperhidrosis.[4] [9] [13]

Commonly used preparations include 20% aluminium

chloride in ethanol and 6.25% aluminium tetrachloride.

Local stinging and burning may occur due to formation of

hydrochloric acid when sweat combines with the aluminium

chloride. Topical baking soda or hydrocortisone cream may

help if this occurs.[9]

Primary Options

aluminium chloride topical : apply to the affected area(s)

once daily at bedtime until desired effect is achieved, then

taper to once weekly

adjunct

[?]


For those patients with symptoms exacerbated in known

anxiety-provoking situations, a short-term oral


14/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options




anticholinergic taken as required can be considered

together with any of the other therapies, although its side

effects may limit its usefulness.

Primary Options

glycopyrronium bromide: 1-2 mg orally twice or three times

daily when required

OR

propantheline : 15 mg orally twice or three times daily when

required

2nd botulinum toxin type A

If symptoms do not resolve with aluminium chloride,

botulinum toxin type A injections may be considered.

Approved in many countries for axillary use and can be

effective for months at a time.[9] [14] [B Evidence]

The injection process may be painful. However, local topical

anaesthetic may help.[9]

Primary Options

botulinum A toxin : 50 units intradermally given in 0.1 to 0.2
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Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options




mL aliquots to multiple sites (10-15) 1-2cm apart in each

axilla

adjunct

[?]







Primary Options


daily when required

OR


required

3rd local sweat gland excision

If the patient does not respond to botulinum toxin type A or

does not want repeated painful injections with temporary

results, local sweat gland excision by curettage or
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16/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options




liposuction should be considered next.

Local axillary gland surgeries (including subcutaneous

gland resection with or without resection of the overlying

skin, curettage-liposuction, or electrosurgical or laser

glandular destruction) have been shown to be

effective.[15] [16] [17][18] [19] Local procedures seem to

be more effective, with better patient satisfaction than

thoracoscopic sympathetic surgeries, and have less

compensatory and gustatory sweating.[20]

The procedure may be complicated by poor wound healing

or scarring. Unlike surgical sympathectomy, local surgical

procedures generally have no systemic manifestations

(e.g., compensatory hyperhidrosis).

adjunct

[?]







Primary Options
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Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options





daily when required

OR


required

4th endoscopic thoracoscopic sympathectomy (ETS)

If symptoms persist, ETS may be considered. The

procedure is generally done on both sides at one sitting,

under general anaesthesia, and is a short-stay procedure in

the majority of instances.

The specific hyperhidrosis disorder determines the level of

the sympathetic procedure.

For example, surgery at the third (T3), fourth (T4), or fifth

(T5) thoracic ganglia is for axillary hyperhidrosis. View

image

Some controversy exists whether compensatory sweating is

more problematic at higher sympathectomy levels, but

patient selection is likely to be far more important.[21]

Sympathetic surgery at T3 or T4 can be expected to benefit

80% to 90% of patients with axillary hyperhidrosis.
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18/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options




However, several studies have shown that sympathetic

surgery in patients with axillary hyperhidrosis is less

successful and that the level of patient satisfaction is lower

than it is for patients with palmar

hyperhidrosis.[10] [22] [23] [24] [25] [26] [27]

adjunct

[?]







Primary Options


daily when required

OR


required
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19/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options




primary: palmar

hyperhidrosis


Topical aluminium chloride is often the first-choice

treatment for palmar hyperhidrosis but tends not to be as

effective as it is for treating axillary

hyperhidrosis.[4] [9] [13] [28] Commonly used preparations include 20% aluminium






Primary Options




adjunct

[?]




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20/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options






Primary Options


daily when required

OR


required

2nd iontophoresis

For patients who do not respond or cannot tolerate topical

aluminium chloride on their hands, iontophoresis with tap

water may be used.

Using an iontophoresis device, ions are introduced into

cutaneous tissues via an electrical current.

The mechanism most probably involves the ionic current

temporarily blocking the sweat duct at the level of the

stratum corneum.

The addition of anticholinergics or botulinum toxin A to the

iontophoresis tap water may improve its efficacy.[9] [29]
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21/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options




Skin irritation from galvanic currents may occur.

Iontophoresis is contraindicated in patients with

pacemakers or metal implants, or who are pregnant.[9]

adjunct

[?]


For those patients with symptoms exacerbated in knownanxiety-provoking situations, a short-term oral




Primary Options


daily when required

OR


required

3rd endoscopic thoracoscopic sympathectomy (ETS)

ETS is appropriate for severe, debilitating palmar sweating

when other treatments have failed.

In these cases, the expected benefits generally outweigh
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Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options




the known side effects, which may include compensatory

sweating.[5] [10]

The specific hyperhidrosis disorder determines the level of

the sympathetic procedure. For example, surgery at the

second (T2) or third (T3) thoracic ganglia is recommended

for palmar hyperhidrosis.View imageView image

ETS is also appropriate for patients with severe palmar and

severe plantar hyperhidrosis (palmoplantar hyperhidrosis)

when other treatments have failed. It is emphasised that the

ETS procedure is meant to cure the palmar hyperhidrosis,

and any benefit for the feet is never the primary intent of the

surgery.

Surgery can be performed at the T2 or T3 level. The best

level to select is unclear and controversial. Surgery at the

T2 level may be more consistently curative with less

dramatic failures than at T3,[37] [36] but is associated with

an increased incidence of compensatory hyperhidrosis

postoperatively.[37][38] [35] [36]

Successful outcomes for palmar sweating are achieved in

>95% of cases. Plantar sweating is improved in the short

term in approximately 80% of cases, although not as
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23/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options




dramatically as the palmar sweating.

Because of the higher incidence of moderate or severe

compensatory hyperhidrosis, some recommend avoiding T2

procedures altogether. Some even recommend levels of

sympathetic intervention for palmoplantar hyperhidrosis at

levels lower than T3 (i.e., over the 4th or 5th rib levels),

although it is acknowledged by the authors that this may

result in moister hands.[35] Some surgeons perform

ramicotomy rather than sympathetic nerve/ganglion

intervention to limit the severity of compensatory sweating.

However, the incidence of recurrent sweating does seem to

be higher with ramicotomy.[39] Thoracoscopic sympathetic

intervention can be safe and effective in younger patients,

even in early teenage years, and has been shown to result

in markedly improved long-term quality of life compared to

non-operative cohorts.[40]

adjunct

[?]




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24/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options






Primary Options


daily when required

OR


required

primary: plantar

hyperhidrosis

1st supportive care

Initial management should include keeping the feet as dry

as possible by use of absorbent foot powders and shoeinserts, and frequent changing of socks and shoes.

adjunct

[?]





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25/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options





Primary Options


daily when required

OR


required

2nd topical aluminium chloride with supportive care

Management of localised plantar sweating is primarily

medical.

Topical aluminium chloride tends not to be as effective for

plantar hyperhidrosis as it is for axillary hyperhidrosis.[28]







Patients should keep their feet as dry as possible using
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26/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options




absorbent foot powders and/or shoe inserts, with frequent

changing of socks and shoes.

Primary Options

aluminium chloride topical : apply to the affected area(s)once daily at bedtime until desired effect is achieved, then


adjunct

[?]







Primary Options


daily when required

OR


required
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27/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options




3rd iontophoresis with supportive care

For patients who do not respond or cannot tolerate topical

aluminium chloride, iontophoresis with tap water may be

used.

The mechanism most probably involves the ionic current

temporarily blocking the sweat duct at the level of the

stratum corneum.

Oral anticholinergics or botulinum toxin A added to the

iontophoresis tap water may improve its efficacy.[9] [29]

Skin irritation from galvanic currents may occur.

Iontophoresis is contraindicated in patients with

pacemakers or metal implants, or who are pregnant.[9]

Patients should keep their feet as dry as possible using

absorbent foot powders and/or shoe inserts, with frequent

changing of socks and shoes.

adjunct

[?]





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28/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options





Primary Options


daily when required

OR


required

primary: craniofacial

hyperhidrosis


Topical aluminium chloride can be used for facial sweating.


chloride in ethanol and 6.25% aluminium tetrachloride. Local stinging and burning may occur due to formation of




Primary Options
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29/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options







adjunct

[?]






effects may limit its usefulness. Topical glycopyrrolate

(glycopyrronium bromide) has been successfully used for

craniofacial hyperhidrosis but it is not approved in some

countries.[41]

Primary Options


daily when required

OR


required
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30/39

Patient group

Treatment


primary: axillary

hyperhidrosis










Primary Options




2nd endoscopic thoracoscopic sympathectomy (ETS)

ETS is used for craniofacial sweating, although there is a

higher incidence of patient dissatisfaction and complaints of

compensatory sweating compared with palmar

hyperhidrosis.[10] [22] [23] [24] [26] [25] [27] Treatment of

craniofacial hyperhidrosis surgically should be considered

very carefully as the side effects can be severe.

However, most patients with craniofacial hyperhidrosis will

have significant benefit from sympathetic surgery at the T2

level.View image

adjunct

[?]






effects may limit its usefulness. Topical glycopyrrolate

(glycopyrronium bromide) has been successfully

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