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ULY CLINIC

ULY CLINIC

18 Mei 2025, 19:26:15

Anhidrosis

Anhidrosis
Anhidrosis
Anhidrosis

Anhidrosis refers to the complete or partial absence of sweating, which may impair the body's ability to regulate temperature. It is categorized as:

  • Generalized Anhidrosis: Involves the majority of the body’s surface. It poses a significant risk for hyperthermia and may be life-threatening.

  • Localized Anhidrosis: Affects only a specific region of the body. Thermoregulation is typically preserved due to the limited area of sweat gland involvement.


Pathophysiology

Sweating is controlled by the autonomic nervous system via cholinergic sympathetic fibers that stimulate eccrine glands. Anhidrosis may result from:

  1. Neurologic dysfunction:

    • Disruption in the sympathetic pathways (central or peripheral).

    • Disorders affecting the hypothalamus, spinal cord, or peripheral nerves.

  2. Glandular dysfunction:

    • Congenital absence or acquired atrophy of eccrine glands.

    • Obstruction or destruction of sweat ducts (e.g., burns, skin diseases).

  3. Pharmacologic interference:

    • Anticholinergic agents block muscarinic receptors, inhibiting sweat production.

Despite intact neurological signaling, absence or malfunction of sweat glands leads to failure of sweat production at the skin surface.


Clinical Presentation

Generalized Anhidrosis
  • Patients may not be aware until exposed to heat or exertion.

  • Presents with:

    • Hot, dry, flushed skin

    • Fatigue, dizziness, palpitations

    • Inability to tolerate heat

    • Risk of heat exhaustion or heatstroke


Localized Anhidrosis

Often identified incidentally or via:

  • Compensatory hyperhidrosis in unaffected regions

  • Localized skin dryness or scaling

  • Chief complaint may be excess sweating in compensatory areas


Emergency Evaluation: Suspected Heatstroke

Key signs of life-threatening anhidrotic asthenia (heatstroke):

  • Skin: Hot, dry, flushed

  • Core temperature: > 102.2°F (39°C)

  • CNS: Confusion, seizures, altered LOC

  • CVS: Tachycardia, hypotension

  • Other: Nausea, vomiting, muscle cramps, substernal tightness


Immediate Interventions

  1. Measure rectal temperature (gold standard for core temp).

  2. Check vital signs and LOC frequently.

  3. Rapid cooling measures:

    • Ice water immersion

    • Evaporative cooling (cool mist + fan)

    • Cold IV fluids

  4. Supportive care:

    • Oxygen supplementation if needed

    • Monitor urine output and electrolytes

    • Avoid antipyretics (ineffective in heatstroke)


History and Physical Examination

History
  • Sweating pattern: Normal vs. diminished, profuse vs. absent

  • Onset: Sudden or gradual

  • Environmental exposure: Heat, physical activity

  • Associated symptoms: Fever, weakness, heat intolerance

  • Medical history:

    • Neurological diseases (e.g., diabetes, Parkinsonism)

    • Dermatologic disorders (e.g., psoriasis, ichthyosis)

    • Autoimmune conditions (e.g., scleroderma)

  • Medication review: Especially anticholinergics, antidepressants, antipsychotics


Physical Examination
  • Skin: Inspect for texture, dryness, scaling, or lesions

  • Lesions: Document morphology, size, pattern, distribution

  • Neurologic exam:

    • Sensory and motor deficits

    • Autonomic signs: orthostatic hypotension, urinary retention


Medical causes of anhidrosis

Condition

Description

Key Features / Associated Signs

Anhidrotic Asthenia (Heatstroke)

Life-threatening acute generalized anhidrosis.

Early: Sweating may persist; Temp >102.2°F (39°C); headache, muscle cramps, fatigue, N/V, dizziness, palpitations, substernal tightness → Later: Anhidrosis, flushed skin, tachycardia, tachypnea, hypotension, confusion, seizures, unconsciousness.

Burns

Permanent damage to sweat glands depending on severity.

Local anhidrosis, blistering, edema, pain or loss of sensation in affected areas.

Miliaria Crystallina

Mild, innocuous sweat gland obstruction.

Localized anhidrosis; clear, fragile blisters (typically under arms and breasts).

Miliaria Profunda

Deep sweat gland blockage; can become severe.

Localized anhidrosis with compensatory facial hyperhidrosis, whitish papules (mainly trunk, extremities), lymphadenopathy, weakness, SOB, palpitations, fever.

Miliaria Rubra (Prickly Heat)

Inflammatory form of miliaria; rarely severe.

Localized anhidrosis, small red papules with blisters (mainly trunk, neck), paroxysmal itching, paresthesia, possible pustules in chronic cases. Rarely → heatstroke.

Peripheral Neuropathy

Nerve damage leading to disrupted sweating.

Anhidrosis (usually legs) + compensatory hyperhidrosis (head/neck), glossy red skin, sensory loss, footdrop, burning pain, absent reflexes, muscle wasting.

Shy-Drager Syndrome

Degenerative neurologic disorder (MSA type).

Ascending anhidrosis (starts in legs), orthostatic hypotension, impotence, constipation, urinary issues, dry mouth/eyes, dilated pupils, leg tremors, ataxia, muscle wasting.

Spinal Cord Lesions

Interrupt central autonomic pathways.

Symmetrical anhidrosis below lesion, compensatory hyperhidrosis nearby, motor/sensory loss, cardiovascular or respiratory dysfunction.

Other Causes

Cause

Description

Key Features

Drugs

Especially anticholinergics (e.g., atropine, scopolamine).

Generalized anhidrosis due to inhibition of sweat gland stimulation.


Diagnostic Investigations

When diagnosis is unclear, consider specialized testing:

  1. Thermoregulatory Sweat Testing (TST):

    • Uses a color-changing powder or indicator (iodine-starch test)

    • Detects sweat distribution under controlled heat exposure

  2. Quantitative Sudomotor Axon Reflex Test (QSART):

    • Assesses postganglionic sympathetic function by stimulating sweat via acetylcholine

  3. Acetylcholine Sweat Stimulation Test:

    • Systemic cholinergic agents (e.g., pilocarpine) to induce sweating

  4. Skin biopsy:

    • Evaluates sweat gland structure in cases of suspected congenital or acquired gland absence


Management


General Approach
  • Treat underlying cause (neuropathy, dermatologic condition, medication withdrawal)

  • Prevent heat-related complications


Patient Counseling
  • Maintain cool environment

  • Avoid strenuous activity and hot weather

  • Use air conditioning, fans, light clothing

  • Hydrate well, especially during warm weather

  • Avoid spicy foods and alcohol


Medication Review
  • Discontinue or replace offending drugs when possible

  • Monitor for resolution or improvement in sweating


Special Populations


Pediatric considerations
  • Common causes:

    • Congenital ectodermal dysplasia

    • Ichthyosis

    • Miliaria rubra (prickly heat)

  • Premature infants: Delayed maturation of sweat glands can lead to transient anhidrosis

  • Parental guidance: Avoid overdressing, monitor for signs of overheating


Summary

Anhidrosis, whether localized or generalized, demands a detailed clinical assessment due to its potential to impair thermoregulation and signal underlying systemic or neurologic disease. Generalized forms require urgent intervention, particularly in heatstroke scenarios. Diagnosis relies on history, physical exam, and targeted autonomic testing. Management includes treatment of underlying causes, supportive care, and patient education to prevent heat-related morbidity and mortality.


References
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  2. Jindal G, Parmar VR, Gupta VK. Isolated ptosis as acute ophthalmoplegia without ataxia, positive for anti-GQ1b immunoglobulin G. Pediatr Neurol. 2009;41(6):451–2.

  3. Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, editors. Fitzpatrick's Dermatology in General Medicine. 6th ed. New York: McGraw-Hill; 2003.

  4. Low PA, Tomalia VA, Park KJ. Autonomic function tests: Some clinical applications. J Clin Neurol. 2013;9(1):1–8.

  5. Sato K, Kang WH, Saga K, Sato KT. Biology of sweat glands and their disorders. I. Normal sweat gland function. J Am Acad Dermatol. 1989;20(4):537–63.

  6. Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 6th ed. Philadelphia: Elsevier; 2016.

  7. Robertson D, Biaggioni I, Burnstock G, Low PA, Paton JFR, editors. Primer on the Autonomic Nervous System. 3rd ed. San Diego: Academic Press; 2012.

  8. Smith AG, Singleton JR. Impaired glucose tolerance and neuropathy. Neurologist. 2008;14(1):23–9.

  9. Clayman CB. The American Medical Association Family Medical Guide. 4th ed. New York: Wiley; 2004.

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