Dermatoses Resulting from:

Physical factors

By:Dr. Kazhan a. Kadir

December 2011

The skin can react to a large number of mechanical, physical, biological and chemical agents, acting alone or in combination .

Human skin, except for palms and soles, is quite thin and of variable thickness .

It has two layers: the epidermis (outer) and dermis (inner). Collagen and elastic components in the dermis allow it to function as a flexible barrier .

Cutaneous Defence

The skin provides a unique shield which protects within limits against different physical agents .

The skin limits water loss from the body and guards against the effects of natural and artificial light, heat and cold. Intact skin and its secretions provide a fairly effective defence zone against these factors providing that the degree or the severity of the injury does not impair this defence.

 

Cutaneous defence systems are effective only within limits. Anything which breaches one or more of the links endangers the entire defence chain .

 A remarkable feature of cutaneous defence is the ability of the skin to continually replace the basal cells which provide the epidermis with its own built-in, replication and repair system .

The skin’s ability to act as a heat exchanger is essential to life. Sweat gland function, vascular dilation and constriction under nervous control are vital to regulating body heat, as is evaporation of surface water on skin .

Constriction of the blood vessels protects against cold exposures by preserving central body heat. Multiple nerve endings within the skin act as sensors for heat, cold and other stimuliants .

A major skin component against injury from ultraviolet radiation, a potentially harmful part of sunlight and some forms of artificial light is the pigment (melanin) manufactured by the melanocytes located in the basal cell layer of the epidermis .

Melanin granules are picked up by the epidermal cells and serve to add protection against the rays of natural or artificial light which penetrate the skin.

 

Sweat-induced reactions Many types of work or life style involve exposure to heat and where there is too much heat and sweating, followed by too little evaporation of the sweat from the skin, prickly heat (Miliaria) can develop .

When there is skin rubbing against skin, a secondary bacterial or fungal infection may frequently occur. This happens particularly in the axillae, under the breast, in the groin and gluteal folds .

Pigment change Exposure to ultraviolet light may cause hyperpigmentation which generally results from melanin stimulation and overproduction .

Hypopigmentation or depigmentation at selected sites can be caused by a previous burn, contact dermatitis, contact with certain hydroquinone compounds or other antioxidant agents.

Neoplastic growths Neoplastic lesions may be malignant or benign (cancerous or non-cancerous) .

Melanoma and non-melanocytic skin cancer are probable. Traumatic cysts, fibromata and keratoacanthoma, are typical benign new growths. Keratoacanthomas can be associated with excessive exposure to sunlight and it is a premalignant condition .

 

sunlight and ionizing radiation, among other agents, can damage the skin cells so that abnormal cell growth results in cancerous change of the exposed skin .

 Unlike primary irritation, allergic sensitization is the result of a specifically acquired alteration in the capacity to react, brought about by T-cell activation.

Physical agents Heat, cold, electricity, sunlight, artificial ultraviolet, laser radiation and high energy sources such as x rays, radium and other radioactive substances are potentially injurious to skin and to the entire body .

High temperature and humidity at work or in a tropical environment can impair the sweat mechanism and cause systemic effects known as sweat retention syndrome. Milder exposure to heat may induce prickly heat, intertrigo (chafing), skin maceration and supervening bacterial or fungal infection, particularly in overweight and diabetic individuals .

 

Thermal burns are frequently experienced in certain occupations. Prolonged exposure to cold water or lowered temperatures causes mild to severe injury ranging from erythema to blistering, ulceration and gangrene. Frostbite affecting the nose, ears, fingers and toes of construction workers, firemen, postal workers, military personnel and other outdoor workers is a common form of cold injury .

 Electricity exposure resulting from contact with short circuits, bare wires or defective electrical apparatus cause burns of the skin and destruction of deeper tissue .

High-intensity electromagnetic energy associated with laser beams is well able to injure human tissue, notably the eye. Skin damage is less of a risk but can occur .

 

Heat Injuries

-Thermal Burns

-Electrical Burns

-Miliaria

Thermal Burns

First-degree burn: active congestion of superficial blood vessels

This causes erythema, sometimes followed by epidermal desquamation

Constitutional reactions occur if large area involved

Pain and increased surface heat may be severe

Second-degree burns

Deep

Pale and anesthetic

Injury to reticular dermis compromises blood flow and destroys appendages

Healing takes > 1 month

Scarring occurs

Superficial

Transudation of serum causing edema of superficial tissues

Vesicles and blebs

Complete recovery without scar or blemish is usual

Second-degree burn

Thermal burn: This superficial second degree burn is characterized by bullae that contain serous fluid.

Third-degree burnsFull-thickness tissue loss

Skin appendages are destroyed ◦There is no epithelium for regeneration

Healing leaves a scar

Fourth-degree burns

Destruction of entire skin and subcutaneous fat with any underlying tendons

Electrical Burns

Contact- small but deep, causing some necrosis of underlying tissues

Flash-burns usually cover a large area and are similar to a surface burn and should be treated as such

Lightning is the most lethal type of strike, cardiac arrest or other internal injuries may occur

Miliaria-Retention of sweat as a result of occlusion

-Common in hot, humid climates

-Occlusion of eccrine sweat gland obstructs delivery of sweat to the skin surface

-Eventually backed-up pressure causes rupture of sweat gland or duct at different levels

-Escape of sweat into adjacent tissue produces miliaria

-Different forms of miliaria occur depending on the level of injury to the sweat gland

Erythema (pigmentatio) Ab Igne

Aka “toasted skin” syndrome

Persistent erythema or coarsely reticulated residual pigmentation resulting from it

Produced by long-continued exposure to excessive heat without production of a burn

It begins as a mottling caused by local hemostasis and becomes a reticulated erythema, leaving pigmentation

Photoaging (Dermatohelioisis)

Characteristic changes induced by chronic sun exposure.

Poikiloderma of Civatte :refers to reticulate hyperpigmentation with telangiectasia, and slight atrophy of sides of the neck, lower anterior neck and V of chest

Submental area is spared

Frequently presents in fair-skinned men and women in their middle to late thirties or early forties

Cold Injuries

-Chilblains

-Frostbite

-Immersion injury

Chilblains

Acute chilblains is the mildest form of cold injury

Patients are usually unaware of injury until they develop burning, itching, swelling and redness

FrostbiteWhen soft tissue is frozen and locally deprived of blood supply

Frozen part is painless and becomes pale and waxy

Four stages :I- Frost-nip erythema, edema, cutaneous anesthesia & transient painII- second degree: hyperemia, edema & blistering, with clear fluid in bullaeIII- third-degree: full-thickness dermal loss with hemorrhagic bullae formation or waxy, dry, mummified skinIV- full-thickness loss of entire part

Treatment

Nifedipine 20mg TID

Vasodilators (nicotinamide 100 mg TID or dipyridamole 25 mg TID)

Systemic corticoid therapy is helpful in chilblain lupus erythematosus

Pentoxifylline may be useful

Smoking strongly discouraged

Immersion Foot SyndromesTrench Foot

Warm Water Immersion Foot

Trench Foot

Term derived from trench warfare in World War I, when soldiers stood, sometimes for hours, in trenches with a few inches of cold water in them

Results from prolonged exposure to cold, wet conditions without immersion or actual freezing

Treatment:-removal from environment

Tropical Immersion FootAKA “paddy foot” in Vietnam

Seen after continuous immersion of the feet in water or mud of temperatures above 71.6 degrees F (22 degrees Cº) for 2-10 days

Erythema, edema, and pain of the dorsal feet

Also fever and lymphadenopathy

Resolution occurs 3 to 7 days after the feet have been dried

Sunburn and Solar ErythemaParts of solar spectrum important to photomedicine:

Visible light 400 to 760 nm

Infrared radiation beyond 760 nm

Visible light has little biologic activity, except for stimulating the retina

Infrared radiation is experienced as radiant heat

Below 400 nm is the ultraviolet spectrum, divided into three bands:UVA, 320 to 400 nmUVB, 290 to 320 nmUVC, 200 to 290 nm

Virtually no UVC reaches the earth’s surface, because it is absorbed by the ozone layerException: Australia, welders

UVB is 1000 times more erythemogenic than UVA

UVA is 100 times greater than UVB radiation during the midday hours

Most solar erythema is cause by UVB

UVA is more melanogenic and reflected from sand, snow, or ice to a greater degree than UVB

Amount of ultraviolet exposure increases at higher altitudes, is greater in tropical regions, and temperate climates in summer

Sunburn and Solar Erythema

Clinical signs and symptomsSunburn is normal cutaneous reaction to sunlight in excess of MED (minimum erythema dose=the amount that will induce reddening)

UVB erythema peaks at 12 to 24 hrs after exposure

Desquamation is common about a week after sunburn even in non-blistering areas

Sunburn treatment

Cool compresses

Topical steroids

Topical remedy:

Indomethacin 100 mg

Cooling agents:*Absolute ethanol

*Propylene glycolspread widely over burned area with palms and let dry

Prophylaxis

Avoid sun exposure between 10 am and 2 pm

Barrier protection with hats and clothing

Sunscreen agents include UV-absorbing chemicals, and UV-scattering or blocking agents (physical sunscreens)

Phototoxicity vs photoallergyIn the case of external contactants (photosensitizers) –phototoxicity occurs on initial exposure, has onset < 48 hrs, occurs in most people exposed to the phototoxic substance and sunlight

Photoallergy, in contrast, occurs only in sensitized persons, may have delayed onset, up to 14 days (a period of sensitization), and shows histologic features of contact dermatitis

Skin Types:- “Fitzpatrick classification”

Thank you