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