1. By:
Dr. Kazhan a. Kadir
December 2011

2. 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.

3. 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.

4. 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.

5. 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.

6. 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.


7. 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.

8. 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.

9. 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.

10. 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.

11. 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.

12. 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.

13. -Thermal Burns
-Electrical Burns
-Miliaria

14. 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

15. Deep
Superficial
Pale and anesthetic
Transudation of serum
causing edema of Injury to reticular dermis
superficial tissues compromises blood flow
and destroys
Vesicles and blebs appendages
Healing takes > 1 month
Complete recovery without
scar or blemish is usual
Scarring occurs

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

17. Full-thickness 
tissue loss
Skin appendages 
are destroyed
There is no ◦
epithelium for
regeneration
Healing leaves a 
scar

18. Destruction of entire 
skin and subcutaneous
fat with any underlying
tendons

19. 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

20. -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

21. 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

22. 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

23. -Chilblains
-Frostbite
-Immersion injury

24. Acute chilblains is the 
mildest form of cold
injury
Patients are usually 
unaware of injury until
they develop burning,
itching, swelling and
redness

25. When 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
pain
II- second degree: hyperemia,
edema & blistering, with clear
fluid in bullae
III- third-degree: full-thickness
dermal loss with hemorrhagic
bullae formation or waxy, dry,
mummified skin
IV- full-thickness loss of entire part

26. 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

27. Trench Foot
Warm Water Immersion Foot

28. 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

29. AKA “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

30. Parts of solar spectrum Below 400 nm is the
important to ultraviolet
photomedicine: spectrum, divided into
three bands:
Visible light 400 to 760 nm UVA, 320 to 400 nm
UVB, 290 to 320 nm
Infrared radiation beyond UVC, 200 to 290 nm
760 nm
Visible light has little biologic Virtually no UVC reaches
activity, except for the earth’s
stimulating the retina surface, because it is
absorbed by the ozone
Infrared radiation is layer
experienced as radiant heat Exception:
Australia, welders

31. UVB is 1000 times more
erythemogenic than UVA
Amount of ultraviolet
UVA is 100 times greater
than UVB radiation during exposure increases
the midday hours at higher altitudes, is
greater in tropical
Most solar erythema is regions, and
temperate climates
cause by UVB
in summer
UVA is more melanogenic
and reflected from sand,
snow, or ice to a greater
degree than UVB

32. Sunburn 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

33. Cool compresses 
Topical steroids 
Topical remedy: 
Indomethacin 100 mg
Cooling agents:
*Absolute ethanol
*Propylene glycol
spread widely over burned
area with palms and let dry

34. 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)

35. In 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