Flat Lesions

Introduction

Flat lesions represent the foundation of dermatologic diagnosis. Unlike palpable lesions that demand tactile confirmation, flat lesions are appreciated purely through visual inspection—they are changes in skin color or transparency without elevation or depression of the skin surface. The term macule (from Latin macula, meaning "spot" or "stain") describes these non-palpable, localized color changes.

Understanding flat lesions requires mastery of cutaneous chromatics: the physiological and pathological mechanisms that produce skin coloration. The color of a macule provides immediate diagnostic information, narrowing the differential before a single question is asked. White, brown, red, blue, purple, yellow—each hue tells a story of melanin, hemoglobin, exogenous pigments, or pathological deposits.

This chapter systematically examines flat lesions according to their color and underlying mechanisms, integrating clinical terminology with dermoscopic and histopathological correlates.

Macule

Definition

A macule is a circumscribed, non-palpable alteration in skin color. Traditionally, macules are defined as lesions measuring less than 2 cm, with larger flat lesions termed patches. However, this size distinction has limited clinical utility; the term macule is appropriately used for any flat, color-altered lesion regardless of size.

The key defining feature is non-palpability: when the examiner runs a fingertip across the lesion, there is no perceptible elevation, depression, or textural change.

Anatomical Origin

Macules can arise from pathology at different levels:

Anatomical Level	Mechanism	Examples
Epidermis alone	Melanocyte abnormality	Vitiligo, lentigo
Dermis alone	Vascular or inflammatory	Petechiae, erythema
Epidermis and dermis	Combined pigmentary	Postinflammatory hyperpigmentation
Subcutis visible	Transparency	Dermal atrophy

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Classification by Color

The color of a macule is the single most important diagnostic feature. Macules are classified according to their predominant hue:

White Macules (Leukoderma)

Leukoderma refers to white or hypopigmented macules. The mechanisms include:

Mechanism	Pathophysiology	Examples
Melanocytopenic	Decreased/absent melanocytes	Vitiligo, piebaldism
Melanopenic	Normal melanocytes, decreased melanin	Pityriasis alba, tinea versicolor
Vasoconstriction	Reduced blood flow	Nevus anemicus
Sclerosis/Hyalinization	Collagen changes	Lichen sclerosus, morphea
Deposits	White substance in skin	Calcinosis cutis

Vitiligo is the prototype of melanocytopenic leukoderma, characterized by the autoimmune destruction of melanocytes. Dermoscopically, vitiligo shows:

Complete absence of pigment network
"Perifollicular pigmentation" in repigmenting lesions
Starburst pattern at margins in active disease

[!TIP] Wood's Lamp Examination: Under 365 nm UV light (Wood's lamp), vitiligo appears "milk-white" or enhanced bright white due to complete absence of melanin. This distinguishes true depigmentation from hypopigmentation.

Pigmented Macules (Melanoderma)

Brown and black macules result from increased melanin—either through increased melanocyte number (hypermelanocytosis) or increased melanin production (hypermelanosis).

Subtype	Definition	Examples
Epidermal hypermelanocytosis	Increased melanocyte number	Lentigo simplex, melanocytic nevus
Epidermal hypermelanosis	Increased melanin, normal melanocytes	Ephelides (freckles), café-au-lait
Dermal melanosis	Melanin in dermis	Postinflammatory hyperpigmentation
Dermal melanocytosis	Melanocytes in dermis	Mongolian spot, nevus of Ota

The Tyndall effect explains why dermal pigment appears blue-gray: shorter wavelength light (blue) is scattered more by dermal collagen, while longer wavelengths penetrate and are absorbed by deep melanin, allowing only blue light to return to the observer.

Blue-Gray Macules (Ceruloderma)

Blue-gray coloration indicates dermal pigmentation through the Tyndall effect:

Condition	Type	Clinical Features
Mongolian spot	Dermal melanocytosis	Lumbosacral, infants, Asian/African
Nevus of Ota	Dermal melanocytosis	V1/V2 distribution, unilateral
Nevus of Ito	Dermal melanocytosis	Shoulder, acromioclavicular
Drug-induced	Dermal deposits	Minocycline, amiodarone, chloroquine
Heavy metal	Dermal deposits	Argyria (silver), chrysiasis (gold)

Yellow Macules (Xanthoderma)

Yellow coloration results from:

Mechanism	Examples
Lipid deposits	Xanthoma, xanthelasma
Carotenoid accumulation	Hypercarotenemia
Connective tissue changes	Pseudoxanthoma elasticum
Bilirubin	Jaundice
Hemosiderin	Post-purpuric staining

Red Macules

Red macules result from vascular phenomena and require characterization by diascopy—applying firm pressure with a glass slide or dermatoscope to distinguish:

Diascopy Result	Mechanism	Examples
Blanches completely	Vasodilation (active)	Erythema, exanthema
Blanches completely	Vascular malformation	Capillary malformation (port-wine stain)
Does not blanch	Extravascular blood	Purpura, petechiae
Partial blanching	Mixed vascular/hemorrhage	Early vasculitis

Erythema

Erythema is redness of the skin that blanches on diascopy, indicating intravascular blood. It may be localized or diffuse, transient or persistent.

Types of Erythema

Type	Description	Mechanism
Active erythema	Bright red, warm	Arteriolar dilation
Passive erythema	Dusky, bluish-red	Venous congestion
Reticulated erythema	Netlike pattern	Livedo
Figurate erythema	Annular, polycyclic	Inflammatory

Exanthemas

An exanthem (or exanthema) refers to the sudden, widespread eruption of confluent erythematous lesions. Classification includes:

Subtype	Clinical Features	Examples
Morbilliform	Red macules/papules, coalescent, islands of sparing	Measles, drug eruption
Scarlatiniform	Confluent erythema, sandpaper texture, no sparing	Scarlet fever, TSS
Roseola	Discrete pink macules, <2 cm	Secondary syphilis, roseola infantum
Rubelliform	Fine pink macules	Rubella

Erythroderma

Erythroderma is defined as erythema affecting ≥90% of the body surface area, typically with scaling and systemic symptoms. This represents a dermatologic emergency.

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Cyanosis

Cyanosis is a bluish-purple discoloration reflecting deoxygenated hemoglobin. It becomes clinically apparent when deoxygenated hemoglobin exceeds 5 g/dL.

Type	Mechanism	Location	Mucous Membranes
Central	Arterial desaturation	Lips, tongue, extremities	Affected
Peripheral	Increased O₂ extraction	Extremities, nose	Spared

Telangiectases

Telangiectases are permanently dilated superficial blood vessels, visible as fine red or purple lines.

Type	Size	Depth	Color
Capillary telangiectasia	<0.5 mm	Superficial	Red
Venular telangiectasia	0.5-2 mm	Mid-dermal	Blue-purple
Phlebectasia	>1 mm	Deep	Blue

Spider Angioma (Nevus Araneus)

A spider angioma consists of a central arteriole with radiating telangiectatic vessels. Pressure on the central point empties the radiating vessels. Associated with:

Hyperestrogenic states (pregnancy, cirrhosis)
Normal finding in children

Dermoscopic Features

Dermoscopy of telangiectases reveals:

Linear telangiectases: Parallel or branching vessels
Arborizing telangiectases: Tree-like branching (BCC)
Comma vessels: Curved, comma-shaped (dermal nevus)
Crown vessels: Radial at periphery of lesion (sebaceous hyperplasia)

Purpura

Purpura refers to visible hemorrhage into the skin—blood that has extravasated from vessels. Unlike erythema, purpura does not blanch on diascopy.

Classification by Size

Term	Size	Description
Petechiae	<3 mm	Pinpoint hemorrhages
Purpura	3 mm - 1 cm	Small hemorrhagic patches
Ecchymosis	>1 cm	Large hemorrhagic patches
Vibices	Linear	Streak-like hemorrhages

Classification by Palpability

Type	Palpability	Mechanism	Significance
Non-palpable	Flat	Platelet/coagulation disorder	Medical emergency workup
Palpable	Raised	Vasculitis	Inflammatory cause
Retiform	Stellate, branching	Vessel occlusion	Thrombotic/embolic

[!IMPORTANT] Palpable purpura = Vasculitis until proven otherwise. The elevation indicates inflammatory vessel wall involvement with leukocytoclastic vasculitis (LCV) as the most common cause.

Retiform Purpura

Retiform (net-like, stellate) purpura with angulated borders suggests vessel occlusion rather than inflammation:

Cause	Mechanism	Clinical Context
DIC	Consumptive coagulopathy	Sepsis, malignancy
Warfarin necrosis	Protein C/S depletion	Days 3-5 of warfarin
Calciphylaxis	Arteriolar calcification	ESRD, secondary HPT
Cholesterol emboli	Atheroemboli	Post-catheterization
Cryoglobulinemia	Cold-precipitating proteins	Hepatitis C, lymphoma

Color Evolution of Purpura

Purpuric lesions undergo characteristic color evolution as hemoglobin degrades:

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Livedo

Livedo is a reticulated (netlike) pattern of erythema/cyanosis caused by reduced blood flow in the cutaneous vasculature.

Types of Livedo

Type	Characteristics	Significance
Livedo reticularis (physiologic)	Fine, regular, closed meshes; reversible with warming	Normal vasomotor response
Livedo racemosa (pathologic)	Irregular, open, broken meshes; persistent	Underlying vascular pathology

Causes of Pathologic Livedo

Category	Examples
Thrombotic	Antiphospholipid syndrome, Sneddon syndrome
Embolic	Cholesterol emboli, atrial myxoma
Inflammatory	Polyarteritis nodosa, lupus vasculitis
Hyperviscosity	Cryoglobulinemia, polycythemia
Vasospastic	Cold agglutinins

[!WARNING] Sneddon Syndrome: The triad of livedo racemosa + cerebrovascular disease (strokes/TIAs) + associated antiphospholipid antibodies. Young patients with unexplained livedo warrant neurologic and coagulation workup.

Poikiloderma

Poikiloderma is a composite finding consisting of three elements:

Atrophy (thin, wrinkled skin)
Dyspigmentation (hyper- and hypopigmented areas)
Telangiectases

While classically listed as a "primary lesion," poikiloderma is actually a syndrome or combination of primary lesions.

Condition	Distribution	Association
Mycosis fungoides (CTCL)	Bathing suit distribution	Lymphoma
Dermatomyositis	V-sign, shawl sign	Myopathy, malignancy
Radiodermatitis	Prior radiation field	Post-radiation
Rothmund-Thomson syndrome	Face, extremities	Genodermatosis
Poikiloderma of Civatte	Lateral neck, sparing submental	Chronic sun + perfume

Atrophic Macule

An atrophic macule is a flat lesion visible due to increased transparency of thinned skin, allowing underlying structures (vessels) to become visible. The skin appears:

Smooth, shiny
Finely wrinkled ("cigarette paper")
Translucent with visible vessels

Condition	Features
Lichen sclerosus	White, porcelain-like, genital predilection
Morphea (late)	Ivory-colored, lilac ring in active phase
Corticosteroid atrophy	Thin, telangiectatic, striae
Necrobiosis lipoidica	Yellow-brown, waxy, pretibial

Clinicopathological Correlations

Mechanisms of Erythema and Angioma

Erythema indicates dermal vascular abnormality:

Inflammatory erythema: Perivascular lymphocytic infiltrate causes vasodilation; readily blanches on diascopy
Non-inflammatory erythema: Structural vascular dilation (angioma); blanches completely but color is "wine-red" or burgundy

Mechanisms of Purpura

Pattern	Histopathology	Clinical Correlation
Petechial (non-palpable)	RBC extravasation, no inflammation	Thrombocytopenia, trauma
Palpable (papular)	Leukocytoclastic vasculitis	LCV, HSP, infection
Retiform/stellate	Vessel occlusion (thrombi)	DIC, calciphylaxis, cryos

Mechanisms of Pigmentation

Color	Mechanism	Location	Examples
Brown/Black	↑ Melanin	Epidermis	Lentigo, PIH
Blue/Gray	Melanin + Tyndall	Dermis	Mongolian spot, drug
Yellow	Lipid/carotene/bilirubin	Variable	Xanthoma, jaundice
White	↓ Melanin or sclerosis	Epidermis/dermis	Vitiligo, morphea

Summary: Diagnostic Algorithm for Flat Lesions

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Clinical Pearls

Topic	Pearl
Diascopy	Red + blanches = vascular; Red + persists = purpura
Palpable purpura	Always consider vasculitis; biopsy indicated
Retiform purpura	Think vessel occlusion, not inflammation
Wood's lamp	Enhances depigmentation (vitiligo) and fluorescence (tinea, erythrasma)
Tyndall effect	Deep melanin appears blue-gray (Mongolian spot, drugs)
Livedo racemosa	Irregular, open pattern = pathologic; workup for thrombophilia
Poikiloderma distribution	"Bathing suit" = consider mycosis fungoides
Color evolution	Resolving purpura → red → purple → green → yellow/brown

Cross-References

Volume 04, Chapter 4: Palpable and Solid Lesions
Volume 04, Chapter 5: Fluid-Filled Lesions
Volume 07: Dermoscopy
Volume 21: Pigmentary Disorders
Volume 27: Vascular Diseases