Assessment of skin moisture
Moisture is assessed by the presence of pathological sweating or pronounced dryness.
Increased moisture (hyperhidrosis) occurs for various reasons. Physiologically, these can be constitutional features or menopausal syndrome ("hot flashes"). In pathology, profuse sweating is characteristic of the period of body temperature decrease (lysis or crisis) in sepsis, lobar pneumonia, and malaria. Prolonged night sweats accompany tuberculosis, infective endocarditis, and HIV infection. Endocrine causes include hyperthyroidism and hypoglycemia. Hyperhidrosis also accompanies pain, fear (increased sympathetic nervous system tone), and pronounced hypercapnia in severe dyspnea.
The characteristics of sweat are of clinical importance: hot sweat with hyperemia indicates a fever, while cold, sticky sweat with skin pallor indicates vascular collapse (arterial hypotension). Sometimes, due to blockage of the excretory ducts of the sweat glands, miliaria occurs—a fine vesicular rash the size of a poppy seed, resembling dew drops.
Skin dryness (xerosis) is normally observed during aging and menopause (due to decreased estrogens). Pathological dryness accompanies:
- Dehydration: with fluid loss through the gastrointestinal tract (vomiting, diarrhea), extensive burns, insufficient fluid intake, or iatrogenic factors (use of diuretics, laxatives).
- Endocrine disorders: hypothyroidism, as well as diabetic comas (due to osmotic diuresis).
- Fever: dryness is typical for the temperature rise period (stadium incrementi).
- Intoxications: for example, in belladonna (atropine) poisoning.
Exceptions: in certain infections, such as scarlet fever and typhoid fever, sweating is uncharacteristic, and the skin remains dry.
Examination of turgor (elasticity)
Skin turgor depends on the interstitial fluid content and the properties of connective tissue colloids (primarily proteins).
Examination technique: the physician forms a skin fold with their fingers and observes the speed of its flattening after release. Normally, in a young person, the fold should flatten instantly.
In older age, elasticity naturally decreases, the skin becomes stretchable, and the fold flattens with a delay. Among pathological causes, a sharp decrease in turgor is caused by dehydration (exicosis). A classic example of severe dehydration is cholera, in which massive fluid loss occurs due to profuse diarrhea, the skin wrinkles, and the specific "washerwoman's hands" sign appears. Also, anomalous, excessive skin stretchability is observed in a genetic disorder — Ehlers-Danlos syndrome.
Local temperature and sweat composition
Skin temperature is examined by palpation to detect local changes.
- Local temperature increase (Hyperthermia localis) is associated with arterial hyperemia, i.e., increased blood inflow in the inflammation focus. This is vividly manifested in erysipelas or acute deep vein thrombosis of the lower extremities.
- Local temperature decrease (Hypothermia localis) manifests as the "cold extremities" symptom. The mechanism lies in impaired arterial blood flow (ischemia), for example, against the background of severe atherosclerosis of major vessels.
Sweat composition has additional diagnostic value. Normally, it is hypotonic (fewer electrolytes than in plasma). However, in cystic fibrosis (mucoviscidosis), the concentration of chloride ions in sweat sharply increases, which is the main laboratory marker of the disease. In diabetes mellitus, glucose appears in sweat, which becomes an excellent nutrient medium for bacteria, predisposing patients to pustular lesions.
Briefly: answers to topical questions
How are degrees of dehydration classified based on the skin fold flattening time?
Degrees of dehydration are classified based on the assessment of turgor and the speed of skin fold flattening.
- Mild degree (grade I) — skin turgor is normal (normally the fold flattens instantly).
- Moderate degree (grade II) — there is a clinical decrease in skin elasticity.
- Severe degree (grade III) — skin turgor is critically reduced, the skin fold takes longer than 2 seconds to flatten or remains unflattened.
Temperature "swings" of sweat: at the fever rise, the skin is dry (like an oven); at the decline, it sweats profusely (cools down).
Class and exam questions
How to differentiate hypoglycemic coma from diabetic coma based on skin condition?
In hypoglycemic coma, the skin is moist (profuse sweating), whereas in diabetic comas (ketoacidotic, hyperosmolar), the skin is dry due to pronounced osmotic diuresis and dehydration.
In which infectious diseases with fever does sweating not occur?
Dry skin without profuse sweating, despite fever, is characteristic of typhoid fever and scarlet fever.
How to properly check skin turgor?
It is necessary to pinch a skin area with two fingers, form a fold, and then release it. The speed of the skin returning to its initial state is assessed (normally — instantly).
What else to study on this topic
- Stages of fever and skin changes
- Differential diagnosis of diabetic and hypoglycemic coma
- Pathogenesis of the "washerwoman's hands" sign in cholera
- Mechanism of miliaria development (vesicular rash)
- Laboratory diagnosis of cystic fibrosis by sweat composition
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