Ultraviolet Radiation (UVR)

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INTRODUCTION, PRODUCTION, THERAPEUTIC

INDICATION, CONTRAINDICATION, PRECAUTION

& DANGERS.

Ultraviolet radiation (UVR) covers a small part

of electromagnetic spectrum lying between

the violet end of the VISIBLE LIGHT and X-RAY

REGION.

UVR are INVISIBLE to the human

eyes.

Natural source of UVR is SUN.

UVR provoke CHEMICAL CHANGES &

not simply heat at sites where they

are absorbed.

1. Reflection

2. Refraction

3. Absorption

4. Penetration

Snow Desert area

90%

5%15-30%

The longer the wavelength, the deeper the penetration

UVA (LONG UV) UVB (MEDIUM UV,

ERYTHEMAL UV)

UVC (SHORT UV,

GERMICIDAL UV)

WAVELENGTH 400 – 320nm 320 – 290nm 290 – 200nm

PENETRATION deeper dermis Deep Epidermis

only a small

proportion

reaches the upper

dermis.

absorbed or

reflected

predominantly in

the stratum

corneum and in

upper layers of

the epidermis.

EFFECTS development of

slow natural tan

Produces new

pigment

formation,

sunburn, Vitamin

D synthesis.

Responsible for

inducing SKIN

CANCER

Does not reach

the surface of the

earth so usually

does not affect

the human

Elevates mood and improves energy

1. High pressure mercury vapor

lamp – Air cooled.

2. High pressure mercury vapor

lamp – Water cooled ( Kromayer

lamp).

3. Fluorescent lamps

It used for GENERAL UV

IRRADIATION.

The spectrum contains a

large proportion of short UVR

which are undesirable for the

general treatment.

FLUORESCENT TUBES:

The modern treatment methods often require

the use of Long UV without short UV.

So to meet this criteria the fluorescent tubes

are used.

These are similar to the tubes used for

lighting.

It is made of a type of glass which allows long

UV to pass.

The output proportion of this is mainly of Long

UV, Few IRR & some Short UV.

It is mainly used for General Irradiation for

individual or in Group.

The UVR physiological effects

may be divided into 2 groups;

Local – Effects which produced

locally in the area.

General – Results from a systemic

effects of radiation.

In the presence of UVB, 5 to 20 minutes of daily

exposure.

UVB irradiation quickly converts

epidermal 7-dehydrocholesterol

into previtamin D3; the latter

then isomerizes to vitamin D3

(cholecalciferol), which is then

converted in the liver to 25-

hydroxyvitamin D3 and

subsequently in the kidneys

to 1,25-dihydroxyvitamin D3, its

active form. UVR-induced vitamin

D3 synthesis is maximal at

suberythemogenic doses.

APPETITIE & SLEEP BEING IMPROVED

NERVOUSNESS & IRRITABILITY

DECREASED

Acute and Subacute Effects1. Acute inflammatory erythema (sunburn)

2. Pigment darkening and delayed tanning

3. Epidermal hyperplasia

4. Desquamation

5. Immunologic changes

Chronic Effects

1. Photo-aging

2. Photocarcinogenesis

First observable effect of UV Irradiation.

UVR exposure leads to the acute inflammatory

reaction of sunburn.

Wavelengths around 300 nm are the most

erythemogenic, with those between 260 and

280 nm a little less so.

It cause chemical action which result in

IRRITATION & DESTRUCTION of cells. This

causes liberation of “H”-substance which

produce the TRIPLE RESPONSE.

The triphasic response to the firm stroking of the skin

characterized by sharply demarcated erythema, a

brief blanching of the skin, and release of histamine

from the mast cells, followed by arteriolar dilation

causing an intense red flare that extends beyond the

margins of the affected site, and ending with the

appearance of a wheal having the configuration of the

original stroking.

1.

In a few individuals, brief immediate erythema occurs within seconds of UVR exposure and lasts for minutes.

Otherwise, the typical delayed bright red appearance of a sunburn develops confluently on all sufficiently exposed skin, beginning within 30 minutes to 8 hours, peaking at 12 to 24 hours and diminishing over hours to days in the case of UVB exposure.

In the case of UVA, the reaction is deeper red in color, is usually more persistent, and often begins during irradiation, before fading over hours to days.

After excessive exposure, edema and blistering may occur, which, if widespread, may lead to associated systemic symptoms such as chills and malaise. Such reactions are generally followed by pruritus and desquamation over a period of days to weeks.

Photoprotection is the best prevention.

Once excessive UVR exposure has occurred, only symptomatic treatment can be offered (e.g. increased fluid intake, emollient creams or lotions); topical or oral nonsteroidal or steroidal anti-inflammatory agents must be administered as soon as possible after irradiation, or they will not help.

If the sunburn is severe or life-threatening, hospitalization and treatment as for thermal burns are necessary.

1

It is thought that the UVR stimulates

MELANOCYTE & ACCELERATES the

production of MELANIN PIGMENT.

Pigmentation commonly follows an

erythemal reaction.

It varies with the dosage of UVR & the

different individuals.

Following a single exposure to UVR:

Immediate pigmentary darkening

- occurs within minutes and fades over 6–8 hours.

- most obvious in darkly pigmented skin as greyish coloration

- representoxidation & redistribution of pre-existing melanin

or melanin precursors

• Delayed tanning

- develops in genetically competent individuals over hours to

days and persists for weeks to months

• - tyrosinase activity → new pigment production

- the size and number of melanocytes,

- transfer of melanosomes to keratinocytes,

Repeated exposures to UVR:

number of stage IV melanosomes transferred to keratinocytes

number of active melanocytes.

UVR provokes an increased reproduction of

KERATINOCYTES.

This leads to thickening of epidermis which

acts does acts a PROTECTION AGAINST THE

RAYS.

So longer doses are required to repeat an

ERYTHEMAL reaction.

Hyperplasia lasting a month or so occurs over a

period of hours to days following UVB, but

generally not UVA, exposure.

This results from a markedly increased

cellular mitotic rate and DNA, RNA and

protein synthesis.

Hyperplasia of the viable epidermis and

thickening of the stratum corneum result

in several-fold protection against later

sunburning; this adds to, and may

exceed, that simultaneously provided by

delayed tanning, particularly in fair-

skinned individuals.

It is the shedding of dead cells from

the surface of the skin.

The desquamation is proportional to

the intensity of the erythema.

Cutaneous UVB, UVC, and, to some extent,

UVA irradiation

Exerting both pro- and anti-

inflammatory responses

I. Alters epidermal Langerhans cell

function.

II. Generates regulatory T lymphocytes.

III. changes the cutaneous cytokine profile.

refers to cutaneous changes secondary to

long-term exposure to sunlight.

Photoaging is much less pronounced and has

a delayed onset in individuals with more

darkly pigmented skin

1. Solar elastosis

2. Nodular elastosis

3. Weathering nodules

4. Cutis rhomboidalis nuchae

5. Colloid milium

6. Wrinkling (coarse > fine)

7. Favre-Racouchot syndrome

8. Actinic comedonal plaque

9. Poikiloderma of Civatte

10.Solar purpura and hemosiderin

deposition

11.Fragility /photo-onycholysis

12.Pseudoscars

13.Erosive pustular dermatosis

14.Grover’s disease

15.Dyschromia/melasma

16.Solar lentigines,

17.Ephelides (freckles)

18.Actinic keratoses

19.Squamous cell carcinoma

20.Basal cell carcinoma

21.Cutaneous melanoma, especially

lentigo maligna

22.Acquired elastotic hemangioma

Cutis rhomboidalis nuchae

Favre-Racouchot syndrome

Favre-Racouchot syndrome

Colloid milium

Poikiloderma of Civatte

Grover’s disease

1. DERMATOLOGICAL CONDITIONS – Psoriasis,

Acne, Sub acute & Chronic Eczema.

2. Calcium / Phosphorus disease –

Osteomalacia

3. Non pulmonary tuberculosis

4. Local Ulceration – Ulcers, Pressure sores,

Surgical incision

5. Counter Irritant Effect.

The principle therapeutic uses of UVR are of SKIN

DISEASES

1. PSORIASIS:-

In this state the aim of UVR irradiation is to decrease the

DNA synthesis in the cells of the skin & to improve the skin

condition

Acne is also a skin condition which presents PUSTULES,

PAPULES formed by blocking of sebaceous pores & hair

follicles affecting mainly the face, chest & back.

The more severe & long lasting forms cause disfiguring &

serious distress.

Using UVR is aiming to produce desquamation to open the

blocked pores and hair follicles.

E2 dose is given to the face, chest and neck.

It is an INFLAMMATORY RESPONSE in

the skin associated with OEDEMA.

The patient suffers marked ITCHING

with REDNESS, SCALING, VESCILES &

exudation of serum on the skin.

A mild UVR treatment will help. (Sub

acute & Chronic stage)

It is a condition in which destruction of

MELANOCYTES in local areas causes WHITE

PATCHES to appear on the skin.

Both UVA & UVB stimulate melanocyte activity.

UVA seems to provoke a DARKER & LONGER

LASTING TANNING.

UVB provokes more THICKENNING.

Infected wounds such as

1. ULCERS

2. PRESSURE SORES

3. SURGICAL INCISIONS are often treated with HIGH

DOSES of UVR.

The aim of UVR irradiation is to destroy the surface

bacteria, remove the (SLOUGH) infected material

& promote repair.

E3 dose is sufficient, the dose is may be given daily

and is not being applied to normal skin.

The aim of UVR mainly UVA is to

stimulate the GROWTH of

GRANULATION TISSUE & SPEED

UP REPAIR.

Example for non infected wounds

are – Venous / Arterial ulcers.

It is used to produce a strong

counter irritation effect over

the site of DEEP SEATED PAIN.

E4 dose is given to cause

discomfort and producing mask

of pain.

1. Pulmonary Tuberculosis

2. Severe cardiac disturbances

3. Systemic Lupus Erythematosis

4. Severe Diabetes

5. Known Photosensitivity.

7. Photosensitizing medication.

8. Deep x – Ray therapy.

9. Acute Febrile illness

10. Recent skin grafts.

Porphyria

Sarcoidosis

Xeroderma pigmentosum

Acute psoriasis

Generalized dermatitis

Acute eczema

Herpes simplex

Hypersensitivity to

sunlight

1. Shock

2. Eyes - UVR may produce conjunctivitis,

iritis or cataract.

3. Over Dosage – UVR burn can occur.

Mainly E4 reaction

4. Ozone – Important to ensure adequate

Ventilation in the area.

Proper patient education should be given:-

1. Wear Goggles

2. Observe & monitor the skin condition

3. Keep skin moisture following exposure to UVR

4. Pigmentation changes are to be expected &

are a normal response.

5. Prolonged & repeated exposure leads to

premature aging.

It is used to assess the individual patients (ERYTHEMAL) reaction to UVR irradiation.

The basis for any calculation of any UVR dosage is the MED (MINIMAL ERYTHEMA DOSE)

This MED refers to the response of erythema for the dose to be given

The patient must understand that the purpose of the MED test is to DETERMINE just how much EXPOSURE TIME is necessary based on their skin sensitivity.

It is a slight reddening

(erythema) of the skin

which takes from 6 – 8hrs

to develop & which is still

just visible at 24hrs.

1. The area chosen for the test is of importance.

2. Because the patient is to inspect at regular

intervals a convenient, visible site is essential.

3. It should be clear of skin disease.

4. The FLEXOR SURFACE of the FOREARM is the most

usual site.(Other sites are – Abdomen, Medial aspect

of arm / thigh)

5. The selected site should be cleaned with soap &

water to remove surface grease.

6. Cover the patient other areas leaving only the

forearm exposed to UVR.

7. Three to Five holes of at least 2cm² & 1cm

apart are cut in a piece of

lint/paper/cardboard is taken for irradiation of

UVR along with a slide cover – to pull up to

reveal one opening at a time.

8. This cutting is fixed to the forearm with adhesive

plaster.

9. The cuttings are of different sizes & shapes in-

order to make IDENTIFICATION OF THE ERYTHEMA

EASIER for the patient.

10. Allow the lamp to warm up according to the

manufacturer instructions.

11. Place the lamp PERPENDICULAR to the area being

tested (Forearm) & a DISTANCE of 60 to 90cms from

the site.

12. Expose the 1st opening for 30sec, then expose the

2nd opening for another 30sec & go on till the last

opening

13. So the 1st opening would receive the longest

exposure time & the last opening would receive the

least amount of exposure time.

14. Switch off the lamp

15. Instruct the patient to MONITOR the forearm

every 2hrs & note which opening or shape appeared

pink / red first & when it faded / disappeared.

16. The patient is also given a card similar to the

opening to make a note.

Degree

of

Erythe

ma

Laten

t

perio

d

In HRS

Appearance

color

Duration

of

Erythema

Skin

Oedema

Skin

discomfort

Desquam

ation of

skin

Relation

to

E1 Dose

E1

(MED)

6-8 MILDLY PINK <24hrs NONE NONE NONE E1

E2 4-6 Definite PINK

RED. Blanches

on Pressure

2 Days None Slight

Soreness,

Irritation

POWDE

RY

2.5% of

E1

E3 2-4 Very red,

Does not

blanch on

pressure

3-5 Days Some Hot &

Painful

IN THIN

SHEETS

5% of

E1

E4 <2 Angry Red A Week BLISTER Very

Painful

THICK

SHEETS

10% of

E1

The skin response to UVR depends on;

1. The quantity of UVR energy applied to unit area

of the skin.(Depends on);

a) The output of lamp – Make, Type, Aging

b) Distance between the lamp & the skin – Inverse

square law

c) Angle at which radiations fall on the skin – cosine

law

d) Time for which radiations are applied

2. The sensitivity of the skin

1. An E1/MED – Given to the total body area

(Whole body)

2. An E2 - May not be given to up to 20% of

total body area

3. An E3 – May not be given to up to 250cm² of

normal skin

4. An E4 – May only be given to an area up to

25cm² of normal skin.

Key points

Gilaberte Y, González S. Actas Dermo-Sifiliográficas. 2010; 101: 659-72

Gilaberte Y, González S. Actas Dermo-Sifiliográficas. 2010; 101: 659-72

Sunscreen doesn’t offer 100% protection.

SPF(Sun Protection Factor) 30+ sunscreen blocks 96% of UV; SPF 15+ blocks out 93%.

In addition to sunscreen, wear a hat, sunglasses, more clothing, and seek shade.

Most cotton and cotton/polyesterfabrics protect against 95% of UV, but are less effective if wet, faded, or aged.

Sunscreens are photochemical systems thatabsorb or reflect UV radiation.

Frequently use of sunscreens is the bestphotoprotection strategy.

The first sunscreen was marketed in 1930 Actually there are 28 chemical filters in

Australia, 26 in Europe and 14 in USA.

Kockler J, Oelgemoller M, Robertson S, Glass B. Journal of Photochemistry and Photobiology. 2012; 1-17

Dispersion

UVR

Chemical or physical filters

Reflection

La capacidad de eritema depende◦ Longitud de onda de radiación

◦ Fotosensibilidad del individuo

◦ DEM uso estudios observacionales

SPF = ----------------MED protected

MED unprotected

Kockler J, Oelgemoller M, Robertson S, Glass B. Journal of Photochemistry and Photobiology. 2012; 1-17

20 min before and 2 - 3 hours

SPF 30 (97.5 UVB)◦ 370nm

High UVA protection

SPF 30 UVA highprotection

50- 80% solar damage isbefore 18

Correct solar protection

Walker D. Journal of Pediatric nursing. 2011 Article in press

Beyond the violet UV and Skin Karen Zapata Montenegro Dermatology and Dermatologysurgery CSS

Bolognia 2nd & 3rd ed.

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