Hyper Hydro Sis Final

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Hyperhidrosis

Introduction

One of the oldest described dermatologic conditions, primaryhyperhidrosis is an embarrassing disorder that, even today, is

misconceived as rare and untreatable.

Hyperhidrosis is a disorder characterized as perspiration in excess

of the bodys physiologic need and can significantly impact ones

occupational, physical, emotional, and social life.

Hyperhidrosis is delineated into two classifications of either

primary or secondary hyperhidrosis.

Primary hyperhidrosis is distinguished as a chronic, idiopathic

disorder of excessive perspiration in a bilateral, symmetrical

manner.

Primary hyperhidrosis has been associated with hyperactivity of

the sympathetic nervous system and can affect the palms, soles,

axillae, face, and scalp as well as other areas.

Secondary hyperhidrosis is due to an underlying condition, such

as an infection, endocrine disorders, metabolic disorders,

neoplastic diseases, neurologic conditions, spinal cord injuries,

cardio-vascular disorders, respiratory disorders, anxiety, and

stress.

Epidemiology

Primary focal hyperhidrosis has an average age of onset of 25

years.


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It would appear that hyperhidrosis is a disease of childhood which

may peak in early adulthood.

A large epidemiologic survey revealed that approximately 70% of

people didnot consult a physician for this presentation.

Primary hyperhidrosis is a relatively common disorder, affecting

nearly 3% of the population, with the highest prevalence rates

among those aged 18 to 54 years.

A genetic component has been suggested to contribute toprimary hyperhidrosis as family history has been positive in 30%

to 65% of patients.

PathophysiologyHyperhidrosis is a disease of the eccrine sweat glands.

The human body has up to 4 million sweat glands, of which

approximately 3 million are eccrine sweat glands. The remainder

are apocrine glands which are not involved in hyperhidrosis.

Hyperhidrosis appears to be due to excessive sympathetic activity

as there are no histopathologic changes of the eccrine glands.

Thermoregulatory sweating is the major mechanism of heat

dissipation by whole-body eccrine glands, is controlled by the

preoptic area of the hypothalamus, and is diurnal or nocturnal.


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Emotional sweating, always diurnal, is controlled by the anterior

cingulate cortex, and its distribution is limited usually to the face,

axillas, palms, and soles.

Both higher centers descend to synapse on the intermediolateralcell column neurons of the spinal cord.

From there, myelinated preganglionic sympathetic nerves exit the

cord via the ventral roots and enter the segmental paravertebral

sympathetic ganglia or course up and down the sympathetic

chain and enter paraverterbral ganglia at other levels.

Unmyelinated postganglionic sympathetic fibers exit the ganglion

and rejoin the segmental spinal nerve or plexus, eventually

innervating hair follicles, sweat glands, and vascular effectors of

the skeletal muscle and skin of the trunk and limbs.

The nerves release acetylcholine onto the muscarinic cholinergic

receptors of the sweat glands.

Primary Focal (Essential) Hyperhidrosis

Primary Focal (Essential) Hyperhidrosis is one of the most

common disorders of eccrine sweating.

Primary focal hyperhidrosis is characterized by excessive

sweating of small regions of the skin, such as the axilla, palms,

soles, or face. The onset is usually in adolescence (usually under

25 years of age), although it can begin early in childhood,

especially the palmar-plantar variants. The disease manifests as

bilateral and relatively symmetric sweating, often with cessationduring sleep.

Sweating may be phasic or continuous; when continuous;

sweating is most troublesome in summer.


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Phasic outbursts with minor emotional activity are similar year

round.

Palmo Plantar hyperhidrosis

The sweating of the palms and soles may be either continuous or

phasic. When continuous it is worse in the summer, and not so

clearly precipitated by mental factors.

When phasic, it is usually precipitated by minor emotional or

mental activity, and is not markedly different in summer and

winter.

The hands may be cold, and show a tendency to acrocyanosis.

Hyperhidrosis may be associated with Raynauds phenomenon

and reflex sympathetic dystrophy , or may follow cold injury.

Apart from the embarrassing nature of the disorder, complications

include pompholyx and contact dermatitis. Control of plantar

hyperhidrosis may reduce the exacerbations of contact dermatitis

to footwear constituents.

The condition of pitted keratolysis of the feet, due to infection

with Micrococcus sedentarius , is associated with hyperhidrosis.

Axillary sweating may be continuous, or more commonly

phasic, and may or may not be aggravated by heat or mental

activity. It is uncommon before puberty. Axillary sweating on

undressing is very common.

Axillary hyperhidrosis is due to overactivity of eccrine glands,

unlike axillary odour which is mainly apocrine in origin.

Craniofacial hyperhidrosis is often phasic, occurs in middle age

and may be exacerbated by heat, exercise and eating, but, unlike

true gustatory hyperhidrosis, not exclusively so. It may be more

persistent and presents at a later age than palmoplantar


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hyperhidrosis. Sweating sufficient to soak the hair is an additional

embarrassment.

Cold-induced sweating syndrome.

This is a rare, familial condition in which profuse sweating of thetrunk occurs when the skin is cooled to between 7 and 10C [7].

There are associated physical anomalies including a high arched

palate, inability to fully extend the elbows and scoliosis.

Chromosomal anomalies have recently been identified.

Gustatory hyperhidrosis

Sweating on the lips, forehead and nose after eating certain foods

occurs physiologically in many people. Hot spicy foods are the

most likely cause. The central connections of this reflex are not

fully known.

Gustatory hyperhidrosis also occurs in pathological conditions

involving the autonomic nervous system. Localized areas of

intense hyperhidrosis may occur on the face, and even on the

knees. These disorders are very rare, usually start in childhood

and are not progressive.

The commonest cause is damage to the sympathetic nerves

around the head and neck.

The commonest site is within the distribution of the

auriculotemporal nerve, following injury, abscess or operation in

the parotid region (auriculotemporal or von Freys syndrome).

Submental gustatory sweating follows injuries involving the

chorda tympani, and sweating in the distribution of the greater

auricular nerve commonly follows radical neck surgery.


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Gustatory sweating may

occur in diabetes as part of

a wide-spread autonomic

neuropathy. It has also

followed herpes zoster.

Classification Of

Hyperhidrosis

Primary Hyperhidrosis


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Secondary

Hyperhidrosis


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Measuring hyperhidrosis

The Minor starch iodine test is a simple way to detect the

presence of sweat. After the area to be studied is dried

thoroughly, iodine solution is painted over the affected area, and

a starch powder such as corn starch is applied. With the

interaction of sweat, the area turns a purple black color.For iodine-sensitive patients, Alizarin or Ponceau red dye and

starch can be used. The pink powder turns to a bright red color

when wet. The Ninhydrin sweat test is another variant that can be

used.

Gravimetric assessment identifies the amount of sweat produced

during a given time. The technique involves applying pre-weighed

filter paper to the affected area (typically 5 min) and then

measuring the production of sweat by reweighing the filter paper.

Evaporation must be prevented from occurring.

Hund suggests a minimum of 100 mg/5 min for men and 50 mg/5

min for women to identify axillary hyperhidrosis.

A third method used to measure disease severity is the use of

quality of life scales and questionnaires.

Several tools are available, but two of the more commonly usedscales are the DLQI and the HyperHidrosis Impact Questionnaire

(HHIQ), which help to quantify the impact, burden and disease

severity.


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A newer tool, the hyperhidrosis disease severity scale (HDSS) is

based on one question that the patient can answer in the office.

Treatment

Many treatments are available for hyperhidrosis, but none are

effective in everyone.

Therapy should be tailored to the needs of the individual based on

factors such as age and health status of the patient, location of

disease, occupation and lifestyle.

Treatment of hyperhidrosis can be divided into topical, oral,surgical, and nonsurgical treatments (botulinum toxin).

These therapeutic options differ with respect to their efficacy,

duration of action, side effects, and cost of treatment.

Topical treatments.

Topical treatments are limited to antiperspirants containing

aluminum chloride in concentrations ranging from 20% to 25%.

The mechanism of action involves mechanical obstruction of the

eccrine gland duct. The major limitation of aluminum chloride is

localized burn-ing, stinging, and irritation. The main indication for

these products is as a first-line treatment for mild axillary

hyperhidrosis.


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Atropine-like drugs may be absorbed sufficiently to produce a

beneficial local effect without associated systemic side effects,

but none of those at present available can be relied upon to do

so.

Poldine methosulphate, 14% in alcohol, suppresses

experimentally induced sweating, but unfortunately is less

valuable on the palms, soles and axillae. Topical 0.5%

glycopyrronium bromide cream has been successfully used in

gustatory hyperhidrosis in diabetics and 2% aqueous solution has

been used in scalp hyperhidrosis.

Eccrine duct blocking agents.

These drugs act by impeding the delivery of sweat to the skin

surface.

Formalin 1% soaks have long been used for treatment of

hyperhidrosis of the feet, but are unsuit-able for the hands and

axillae.

Glutaraldehyde 10% in a buffered solution, pH 7.5, swabbed

onto the feet three times weekly, has helped some patients.

Systemic treatments

Oral anti-cholinergic agents such as glycopyrrolate or

amitriptyline represent the main systemic medications for

hyperhidrosis.

They inhibit synaptic acetylcholine and therefore interfere with

neuroglandular signaling.

Atropine-like drugs have been used to block the effect of acetyl-

choline on the sweat glands, but their side effects are often more

troublesome than the hyperhidrosis itself. These include dryness

of the mouth, constipation, urinary retention and disturbances of

vision, due to paralysis of accommodation, but more serious side


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effects, for example glaucoma, hyperthermia and convulsions,

can occur.

The oral antimuscarinic agent oxybutinin, usually used to treat

bladder instability, has been reported to be effective forgeneralized hyperhidrosis in a small series of case.

Calcium-channel blockers, such as diltiazem, have helped some

cases. In cases with a pronounced emotional factor, sedative or

tranquillizing drugs are often useful, but psychiatric treatment

may be necessary.

Iontophoresis.

Iontophoresis involves the passage of ions by means of anelectrical current into the skin. This electrical charge appears to

occlude the eccrine duct and interferes with eccrine gland

secretion.

One of the more satisfactory methods of control-ling

hyperhidrosis of the hands and feet is by iontophoresis, either

using tap water or anticholinergic drugs such as glycopyrronium

bromide.

The main indication for iontophoresis is in palmar or plantar

hyperhidrosis, where the efficacy ranges from 80% to 90%.

Direct current is usually used, with each palm or sole being

treated for 30 min with 20 mA, initially three times a week. Once

euhidrosis is established, monthly maintenance treatment may be

sufficient. Alternating current is less effective, but may usefully be

combined with direct current (alternating current offset) to

produce a safer, more comfortable treatment.

The main limitation of this therapeutic modality is that it is time

consuming (requires 30 to 40 minutes per treatment site daily for

at least 4 days of the week) and may cause skin irritation,

dryness, or peeling.


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Sweating is well controlled after 6 to 10 treatments; however,

long-term maintenance therapy is generally required at 1 to 4

week intervals.

Iontophoresis is considered a second-line treatment for palmar orplantar hyperhidrosis, following aluminum chloride

antiperspirants.

Surgical treatments.

Surgical treatment primarily involves thoracoscopic

sympathectomy with success rates in the range of 80% to 90%

for primary focal hyperhidrosis of the axilla, palms, soles, and

face.

A major limitation of this surgical procedure is compensatory

hyperhidrosis with an incidence of 80%. Other surgical

complications include pneumothorax and hemothorax.

Although this procedure has a high efficacy rate, the associated

risk of complications necessitates proper patient selection

(generally those with severe hyperhidrosis who are unresponsive

to other treatments) and detailed informed consent to avoid

unnecessary frustration following treatment.

Other surgical procedures with reported efficacy in axillary

hyperhidrosis include liposuction and subcutaneous curettage.

Botulinum toxin A (Botox).

Botulinum toxin is produced by Clostridium botulinum and acts by

inhibiting acetylcholine release at the neuromuscular junction.


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Previously used as an off-label treatment for hyperhidrosis, the US

Food and Drug Administration approved the use of botulinum

toxin type A (BT-A) for axillary hyperhidrosis in July 2004.

Odorless, tasteless, and colorless, botulinum is the mostpoisonous substance known. Botulinum toxin type A is 1 of 7

types (A-G) of botulinic toxins from thegram-positive bacillus

Clostridium botulinum.

Botulinum toxin has a reported efficacy of greater than 90% for

primary focal hyperhidrosis of the axilla, palms, and soles. This

treatment method is extremely safe. Transient intrinsic muscle

weakness is reported in less than 1% of patients treated for

palmar hyperhidrosis.

The major contraindications include neuromuscular disorders such

as myasthenia gravis, pregnancy and lactation, organic causes of

hyperhidrosis, and medications that may interfere with

neuromuscular transmission.

The cost of the drug and need for repeated treatments appear to

be a notable limitation to this modality.

Botulinum toxin for axillary hyperhidrosis is a safe, well tolerated,

and highly efficacious treatment modality. Dosages range from 50

to 100 units per axilla. The usual starting dose is 50 units per

axilla. A starch iodine test is often used and results in purple to

black discoloration which delineates the affected area of

excessive sweating. Pain associated with these intradermal

injections is minimal; however, a topical anesthetic can be used to

further minimize the discomfort.

The mean duration of effect is 6 to 7 months.

Botulinum toxin for palmar or plantar hyperhidrosis is also

reported to be safe and effective; however, the main limitation of

this indication is the fact that most patients find the injections in


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the palms and soles quite painful. Therefore, a regional nerve

block is required prior to the botulinum toxin injections.

The duration of efficacy for palmar and plantar hyperhidrosis

treated with botulinum toxin is in the range of 4 to 6 months.

International Hyperhidrosis Society

http://www.sweathelp.org
http://www.sweathelp.org/http://www.sweathelp.org/


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REFERENCES

BOOKS

1. Fitzpatrick's Dermatology in General Medicine, 7e CHAPTER 82 (pg720 pg726)

2. Rook's Textbook of Dermatology, 8e CHAPTER 44

3. Clinical Uses of Botulinum Toxins, CHAPTER 9

ARTICLES

4. An Epidemiological Study of Hyperhidrosis

2007 American Society for

Dermatologic Surgery

5. A Comprehensive Approach to the Recognition,

Diagnosis, and Severity-Based Treatment of Focal

Hyperhidrosis: Recommendations of the Canadian

Hyperhidrosis Advisory Committee

2007 American Society for

Dermatologic Surgery

6. Hyperhidrosis: An Approach to Diagnosis And

Management

Dermatology Nursing Dec 2004

7. Hyperhidrosis: Evolving Therapies for a Well-

Established Phenomenon

Mayo Clin Proc. 2005;80(5):657-666

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Hyper Hydro Sis Final