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Propedeutics · Examination of the skin, lymph nodes, and individual body parts

Skin discoloration

Skin color changes are a crucial diagnostic marker reflecting hemodynamics, blood composition, or systemic diseases. The appearance of pallor, cyanosis, jaundice, or atypical pigmentation allows a physician to suspect hidden internal organ pathology even during the visual examination stage.

Occult hypoxiaIn patients with anemia, cyanosis is often absent even during severe oxygen deprivation.
Liver markerErythema in the thenar and hypothenar eminences often indicates chronic liver disease.
Danger of coolingIn «pale fever», physical body cooling methods are strictly contraindicated.
Drug effectAmiodarone intake can impart a specific blue-gray hue to the skin.
5 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Pallor and Redness (Hyperemia)

Skin color is sensitive to temperature and vascular tone changes. Normally, during fever, arterioles dilate to release excess heat, and the skin turns pink. However, in pathological «pale fever», total vascular spasm occurs. It is important to remember that physical cooling methods must not be used in this condition.

Fluctuations in small artery tone due to autonomic nervous system lability can cause alternating pallor and redness. A specific vascular disorder is Raynaud's syndrome: in response to cold or stress, fingertips abruptly turn white and become numb («dead fingers» sign).

Skin color is directly affected by blood composition:

  • Anemia: acute blood loss or hematological diseases lead to a decrease in hemoglobin, causing persistent, progressive pallor.
  • Erythrocytosis: an excess of red blood cells and a high concentration of deoxygenated hemoglobin give the skin a dark cherry color.

Local changes also have high diagnostic value. For example, palmar erythema (bright redness of the thumb and little finger eminences) indicates liver problems or vasculitis. Local inflammatory hyperemia (as in erysipelas) is always accompanied by pain, edema, and local heat.

When vascular pathology is suspected, it is important to evaluate the nature of the changes: if an artery is occluded by an embolus, the limb becomes abruptly pale and cold, whereas venous congestion usually causes cyanosis.

Cyanosis: mechanisms of skin blueness

A bluish hue (kyanos — dark blue) is most noticeable on the lips, nail beds, gums, and earlobes. The main cause is a high concentration of deoxygenated (oxygen-depleted) hemoglobin in the capillaries. The paradox of cyanosis is that its severity depends on the total hemoglobin level: in polycythemia, a person turns blue quickly even without respiratory failure, while in severe anemia, cyanosis may not appear at all due to a lack of the pigment itself.

There are two fundamentally different types of cyanosis:

  1. Central cyanosis

Caused by a global impairment of blood oxygen saturation. Not only the skin but also the mucous membranes become discolored, and the blueness increases with physical exertion. Causes: pulmonary pathologies, high-altitude exposure, anatomical shunts with venous blood discharge into arteries (e.g., in Tetralogy of Fallot), or pathological hemoglobin variants (methemoglobin).

  1. Peripheral cyanosis

Associated with local slowing of blood flow (stasis). Tissues manage to extract more oxygen from the slowly flowing blood, increasing the proportion of deoxygenated hemoglobin. Meanwhile, arterial blood saturation (SaO_2) remains normal. Causes: heart failure with centralization of circulation (causes blue extremities — acrocyanosis), venous hypertension due to thrombi (accompanied by marked edema), or simple hypothermia.

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Specific hues and jaundice

Many systemic diseases have their own characteristic color «signature». In infective endocarditis, the face acquires a characteristic «café-au-lait» pallor. Uremia associated with renal failure produces a pale greenish color (the result of combined anemia and urochrome accumulation in tissues). Hyperpigmentation resembling a persistent sun tan may indicate adrenal insufficiency or hemochromatosis (iron deposition), but a recent visit to a tanning salon must be ruled out before making a diagnosis.

Special attention should be paid to jaundice (icterus), which occurs with excess bilirubin. Discoloration develops sequentially:

  1. Sclera.
  2. Sublingual mucosa.
  3. Face and palms.
  4. Torso and limbs.

The color ranges from lemon and saffron to greenish or earthy-gray (in prolonged hyperbilirubinemia). Jaundice can be prehepatic (red blood cell breakdown), hepatic, or posthepatic (bile duct obstruction). During anamnesis taking, it is important to differentiate it from pseudojaundice (carotenoderma) caused by an excess of carrots or tomatoes in the diet — in this case, mainly the palms and soles turn yellow.

Briefly: answers to topical questions

What types of pathological jaundice exist according to their mechanism of development, and what causes them?

According to the mechanism of development, there are three main types of pathological jaundice associated with impaired bilirubin metabolism.

  • Prehepatic jaundice (Icterus) — caused by the overproduction of unconjugated bilirubin due to massive erythrocyte destruction when hepatocytes cannot conjugate it quickly enough.
  • Hepatic jaundice (Icterus) — occurs due to direct hepatocyte damage and impaired function, leading to intracellular cholestasis and regurgitation of conjugated bilirubin into the blood.
  • Posthepatic jaundice (Icterus) — caused by mechanical obstruction of the biliary tract, preventing bile from entering the intestine and leading to its regurgitation into the bloodstream.

What endocrine and metabolic disorders lead to diffuse skin hyperpigmentation?

Diffuse skin hyperpigmentation is caused by primary adrenal insufficiency and hereditary iron metabolism disorders.

  • Addison's disease — an endocrine disorder in which the destruction of the adrenal cortex leads to decreased cortisol; via feedback, this stimulates pituitary ACTH synthesis, which activates tyrosinase and enhances melanin synthesis in the skin and mucous membranes.
  • Idiopathic hemochromatosis — a hereditary metabolic disorder characterized by high intestinal iron absorption and its primary deposition in hepatocytes, as well as in extrahepatic tissues, including endocrine glands, the heart, mucous membranes, and skin.

Which medications can cause specific skin discoloration?

Drug-induced specific skin color changes must be differentiated from true diseases during differential diagnosis and anamnesis taking.

  • Amiodarone — intake of this drug can cause a gray-blue skin color.

Aside from medication causes, pseudojaundice may be associated with consuming carotene-rich foods, such as carrots or tomatoes; this discoloration is mainly localized on the palms and soles.

How to memorize

To memorize the classic tetrad of inflammatory hyperemia, look for four signs: redness, edema, pain, and increased temperature (typical for erysipelas).

Class and exam questions

How to quickly distinguish central cyanosis from peripheral?

Pay attention to the mucous membranes and their response to exertion. Central cyanosis colors the mucous membranes and worsens with movement. Peripheral cyanosis (e.g., acrocyanosis) primarily affects the distal parts of the body, while arterial blood oxygen saturation remains normal.

What do «liver palms» indicate?

The bright red color of the thumb (thenar) and little finger (hypothenar) eminences is a classic diagnostic marker of chronic liver disease or systemic vasculitis.

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What else to study on this topic

  • Pathogenesis and differential diagnosis of the three types of jaundice (prehepatic, hepatic, obstructive).
  • Right-to-left hemodynamic shunts and their role in arterial hypoxemia.
  • Iron metabolism disorders in hemochromatosis and tissue pigmentation mechanisms.
  • Pathological hemoglobin variants: methemoglobinemia and sulfhemoglobinemia.
  • Mechanisms of compensatory centralization of circulation in acute heart failure.

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