Handbook of Dermatology

HANDBOOK OF DERMATOLOGY & VENEREOLOGY
(Social Hygiene Handbook, 2nd Edition)
TABLE OF CONTENT
DERMATOLOGICAL DISEASES
Introduction of Skin Diseases Dr. K.K. LO
Pruritus Dr. C.S. LEUNG
Eczema Dr. Y.M. TANG, Dr. H.F. HO & Dr. K.H. YEUNG
Psoriasis Dr. K.K. LO & Dr. L.Y. HO
Acne Vulgaris and Other Acneiform Eruptions Dr. C.Y. LEUNG
Urticaria Dr. C.Y. LEUNG
Vitiligo Dr. R. SU
Cutaneous Vasculitis Dr. R. SU
Collagen-vascular Diseases Dr. R. SU & Dr. Y.M. TANG
Blistering Diseases Dr. C.N. LOOK
Alopecia Dr. C.N. LOOK
Nail Diseases Dr. H.F. HO
Cutaneous Malignancies Dr. H.F. HO
Infection: Bacterial, Viral, Fungal Dr. W.K. FUNG
Infestations Dr. T.S. AU
Cutaneous Tuberculosis and Atypical Mycobacterial Infection Dr. L.Y.
CHONG
Leprosy (Hansen's Disease) Dr. N.R. HONEY & Dr. K.K. LO
Practical Guidelines for Phototherapy Dr. L.Y. CHONG
Health Nursing in Skin Clinics Ms. M. WONG, Mr. W. LEUNG, Mr. E. WAN
& Subordinates
Health Nursing in Special Skin Clinics Ms. M. WONG, Mr. W. LEUNG &
Subordinates
Cutaneous Laser Therapy Dr. L.Y. CHONG & Dr. H.H.L. CHAN
Cutaneous Manifestation of Internal Disease Dr. H.H.L. CHAN & Dr. W.K.
FUNG
Cutaneous Drug Eruptions Dr. L.Y. CHONG
SEXUALLY TRANSMITTED DISEASES
Introduction of STD Dr. L.Y. CHONG
Syphilis Dr. L.Y. CHONG
Gonorrhoea Dr. K.H. LAU & Dr. H.F. HO
Non-Gonococcal Urethritis and Non-Specific Genital Infection Dr. K.T.
CHAN
Chancroid Dr. Y.M. TANG
Lymphogranuloma Venereum Dr. N.M. LUK
Genital Warts Dr. C.Y. LEUNG
Genital Herpes Dr. C.N. LOOK
HIV Infection Dr. L.Y. CHONG
Molluscum Contagiosum Dr. S.Y. CHENG
Candidiasis Dr. L.Y. CHAN
Trichomoniasis Dr. C.S. LEUNG
Pediculosis Pubis Dr. W.M. CHEUNG
Balanitis, Bacterial Vaginosis and Other Genital Conditions Dr. T.S. AU &
Dr. K.H. YEUNG
STD in Pregnancy Dr. K.M. HO & Dr. W.S. LAM
Health Nursing in Social Hygiene Clinics Mr. W. LEUNG, Mr. S. LEUNG,
Mr. T. LAM & Subordinates
TOPICAL PREPARATIONS FOR
DERMATOLOGICAL & SEXUALLY TRANSMITTED DISEASES
Basic Pharmacology and Terminology of Topical Preparations
Dr. Y.M. TANG & Dr. R. SU
Principles of Prescribing Topical Preparations and Topical Steriods
Government Formulary
Commercial Dermatological Preparations and Sunscreens
Dr. K.M. HO, Dr. R. SU & Dr. Y.M. TANG
APPENDIX
Dermatology, Social Hygiene and Special Skin Clinics in Hong Kong
Medical staff of Social Hygiene Service
Publications from/Contributed by Social Hygiene Service
Annual Incidence and Trends of Disease
Suggested Books for Reading
Normal Laboratory Values
INTRODUCTION OF SKIN DISEASES

Dr. K.K. LO
CHAPTER 1
The art of diagnosis in dermatology in the past was particularly emphasized
by the visual experience of the skin and the skin lesions. The story of
arriving a dermatological diagnosis even when the patient has not the time to
sit down is less true nowadays for a careful dermatologist. It is a good way
to impress the neophyte dermatologist but it is not the rule. It is true that
some skin lesions can be diagnosed on sight with a high degree of
confidence but even in such cases a systematic approach is indispensable for
a good dermatologist not to miss other important skin lesions. When
dermatology first evolved from general internal medicine in the nineteenth
century, the principle of diagnosis in medicine still held valid till today even
in the highly specialized specialty: dermatology. Hence, detailed systematic
history with good physical examination, supplemented by appropriate
investigations will be the golden rule for the correct approach in the
diagnosis of skin conditions. The old days of when you can recognize the
lesion and so the lesion can recognize you will only be true for some senior
dermatologists but it will not be seen again in modern dermatology.
1. SKIN FUNCTION AND STRUCTURE OF SKIN

1.1. Skin Function
Skin is actually the largest organ in the body. Its wet weight can be as heavy
as 4 kg and covers an area of 1.4 to 2 sq metres. It also plays many
important functions in the body as summarized in Table I.
Table I: Function of the Skin
Function Structure
Protection from harmful agents of

external environment: biological germs, Epidermis
ultraviolet light & chemicals
Preservation of a balanced internal

Epidermis
environment
Shock absorber Subcutaneous fat

Blood vessels & eccrine sweat
Temperature regulation
glands
Insulation Subcutaneous fat
Sensation Nerve endings
Lubrication Sebaceous glands
Protection & grip Nails
Calorie reserve Subcutaneous fat
Vitamin D synthesis Epidermis
Body odour Apocrine sweat glands
Psychosocial Hair & Nails

1.2. Structure of Skin
Epidermis: Thickness varies from 0.1 mm at the eyelids to nearly 1 mm on
the palms and soles. The outermost is the horny layer (stratum corneum)
which is made up of flattened dead keratinocytes. It acts as the major
physical barrier in the epidermis. The granular layer, spinous layer or prickle
cell layer are composed of the living keratinocytes and the basal layer which
is the deepest, most active and single layer of the epidermis is the
germinative layer for the epidermis. There is a gradual differentiation from
basal layer to the horny layer.
Skin appendages: Hair, nail, eccrine sweat glands, apocrine sweat glands,
sebaceous glands.
Dermo-epidermal junction: At the interface between the epidermis and
dermis lies the basement membrane zone. Electron microscopy shows that it
can further be divided to basal cell membrane, lamina lucida (20-40 nm),
lamina densa (30-60 nm, Type IV collagen) and sublamina densa with
anchoring fibrils (Type VII collagen), dermal microfibril bundles and Types
I & III collagen fibres. The structures of the dermo-epidermal junction
provide good mechanical support, adhesion and growth of the basal layer
unless it is diseased.
Dermis: It is thickest at the palms, soles and back (3 mm) least at the eyelids
(0.3 mm) and penis. There are papillary dermis and deeper reticular dermis.
It contains many cells, fibres and amorphous ground substance. Fibroblast
for synthesis of collagen, reticulin, elastin, glycosaminoglycans is the major
cell in the dermis. The ground substance consists of two
glycosaminoglycans: hyaluronic acid and dermatan sulphate. Other
structures found in the dermis include: blood vessels, lymphatics, nerves,
nerve endings and receptors, dartos muscles in scrotum, appendageal glands
and their accessories e.g. arrector pili muscles.
Subcutaneous fat: It is absent from the eyelids and the male genitalia. It has
abundant blood and lymphatic supplies.
1.3. Cell Types
Epidermis: Keratinocytes (85% of cells in epidermis), Langerhans cells (800
per sq mm), Melanocytes (from neural crest, wedged between basal
keratinocyte in 1 to 10 ratio; 1 melanocyte supplies pigments to 36
keratinocyte), Merkel Cells.
Dermis: Fibroblast, mononuclear phagocytes, lymphocyte, Langerhans cell,
Mast cell.
1.4. Kinetics of Skin
Epidermis: Cell cycles of keratinocytes: 300 hours (from G1, S, G2 to M
phases); keratinocytes need 14 days to move from basal layer to horny layer
and another 14 days to slough off from horny layer (i.e. from the basal layer
to the environment requires 28 days).
Skin appendages:
Hair (scalp): growth rate: 0.37 mm/day, 80% in anagen at any one time;
anagen phase: 3 years, catagen phase: 3 weeks, telogen phase: 3 months.
Nail: fingernail growth rate: 1 cm/3 months (0.1 mm/day), toenail growth 1
cm/9 months
2. HISTORY TAKING IN DERMATOLOGY
2.1. General History
Race, geographical factors (especially for immigrants), occupation, sports,
hobbies, social background, ethnic tradition (dietary habits)
Past medical history: allergy to medication, hay fever, asthma, past major
illness or operation.
Social & occupational history: travel abroad, hobbies and details of the type
of work, substances in contact.
2.2. Special History (Dermatology)
History of present illness: duration, date & site of onset, details of spread,
evolution of rash & original morphology, symptoms such as itchiness, pain,
burning sensation, numbness, precipitating and relieving factors such as
climate, sunlight etc., treatment (topical & systemic medication) sought or
applied.
Past history of skin disorders, history of sunburn.
Family history of skin disorders (e.g. skin cancers) and atopic disorders.
Drugs: include herbs, topical, systemic, patient initiated or physician
prescribed.
Patient's own perception on the cause of the problem.
3. PHYSICAL EXAMINATION
3.1. General Examination
Good lighting, adequate privacy, light torch, spatula, magnifying glass and
transparent glass slide for diascopy. General impression on the patient is
very important especially for the general health, pallor, intellectual
assessment, queer personality etc. will be picked up by an observant doctor
when patient enters the consultation room.
3.2. Examination of Skin
Distribution of the rash, arrangement and morphology of individual rash.
Distribution of the lesion: symmetrical, asymmetrical, exposed area, sun
exposed area, scalp region, hand, extensor aspect, flexor aspect.
Arrangement and configuration of the lesion: grouped (as in insect bites,
dermatitis herpetiformis, herpes simplex, common warts), annular or
arciform (as in granuloma annulare, mycosis fungoides, tinea circinata,
erythema annulare centrifugum), linear pattern (as in Koebner phenomenon,
Psoriasis, lichen planus, plane wart, molluscum contagiosum; epidermal
naevus, sporotrichosis, lichen striatus, lichen simplex, morphoea, lichen
sclerosis, phytophotodermatitis).
Morphology of lesion: Individual lesion described with the help of
magnifying glass. To find out the early primary lesion and to inspect it
closely. Note the shape(geometric shape, oval), colour(salmon-pink,
erythematous, skin colour, yellow), size, margin (sharpness of edge, well-
defined, ill-defined), the surface characteristics (dome-shaped, umbilicated,
spike like), temperature and smell.
It is a good practice if affordable to have thorough examination of the whole
body especially for new consultation and for the elderly. Sometimes,
examination of the back and buttock of the elderly may pick up unexpected
lesions, even the patient himself or herself may not notice them e.g.
persistent chronic annular erythematous rash in the buttock found in a case
of tuberculoid leprosy. Do not skip examination of the nail, scalp and oral
mucous membrane because there may be valuable clues. Making it a habit to
examine these sites routinely is important.
3.3. Terminology Used in Dermatology
Macule: flat area of altered colour or texture (less than 0.5 cm)
Patch: large macule (more than 2 cm)
Papule: elevated solid lesion (less than 0.5 cm)
Nodule: elevated solid lesion (more than 0.5 cm)
Plaque: elevated area of skin of more than 2 cm in diameter, a disc shaped
lesion, formed by extension or coalescence of papules or nodules.
Vesicle: fluid filled blister (less than 0.5 cm)
Bulla: larger blister (more than 0.5 cm)
Pustule: collection of free pus
Abscess: localized collection of pus in a cavity (more than 1 cm)
Petechia: pinhead size extravasation of blood into skin
Ecchymosis: larger extravasation of blood into skin
Purpura: blood in skin up to 2 mm in diameter, may be palpable
Haematoma: large purpura
Wheal or weal: accumulation of dermal oedema
Angioedema: diffuse oedema of deep dermis extending to subcutaneous
tissue
Comedo (comedones): a plug of keratin and sebum wedged in a dilated
pilosebaceous orifice
Burrow: a small tunnel in the skin that houses scabies acarus
Telangiectasia: visible dilatation of small cutaneous blood vessels
Poikiloderma: combination of atrophy, reticulate hyperpigmentation and
telangiectasia
Sclerosis: induration of the subcutaneous tissues
Gangrene: death of tissue, usually due to loss of blood supply
Scale: flake from the horny layer
Crust: dried serum, exudate or tissue fluid
Ulcer: whole of the epidermis and part of dermis lost
Excoriation: linear erosion or ulcer produced by scratching
Erosion: partial loss of the epidermis
Fissure: slit in the skin
Sinus: channel that permits escape of pus or fluid
Scar: result of healing, normal structure replaced by fibrous tissue
Atrophy: thinning of skin due to diminution of the epidermis, dermis or
subcutaneous fat
Stria: linear, atrophic, pink or white lesions due to changes in connective
tissue
3.4. Special Techniques Used in Clinical Examination
Magnification with hand lens is important to note the fine details of skin
lesions: Magnification is essential to examine follicular plugging in lupus
erythematosus, Wickham's striae in lichen planus, telangiectasia and
translucence in basal cell carcinoma, changes in colour in malignant
melanoma.
Tangential shining of examination torch to the skin lesions will enhance and
detect elevated skin lesions with ease.
Diascopy consists of pressing a transparent slide or plastic spatula over a
skin lesion. Examiner will find this of special value to distinguish erythema
or purpura. It is useful to detect the glassy yellow-brown appearance of
papules in sarcoidosis, tuberculosis and other granuloma.
Darier's sign is positive when a brown macular or papular lesion of urticaria
pigmentosa becomes palpable wheal after being rubbed with the blunt end of
an instrument. Auspitz's sign is positive when slight scratching or curetting
of a scaly lesion reveals punctate bleeding points within the lesion which
suggests of psoriasis. Nikolsky's sign is positive when a new blister is
generated with ease by applying shearing force to skin.
3.5. Examples of Description of Skin Rash

"Examination revealed multiple firm, well-defined nodules and plaques
ranging from 1 to 4 cm in diameter. They were erythematous and were
distributed over the left cheek, shoulders, upper aspect of the back, buttocks
and thighs. The remainder of the examination was unremarkable." ---
Subcutaneous fat necrosis of the newborn.
"The physical examination revealed an alert, happy five year old girl with
perioral vesicles, pustules, and erosions. In addition, she had a bullous
eruption on a slightly erythematous base with erosions and crusts involving
the scalp, chin, umbilicus, suprapubic surface, groin, and scrotum. Some of
the lesions had a serpiginous border. No oral, ocular, hand or foot lesions
were present. Nikolsky sign was negative." --- Chronic bullous dermatosis of
childhood.
4. DERMATOLOGY INVESTIGATIONS
4.1. Skin Biopsy
Specimen is sent for Histopathology, direct Immunofluorescence study or
culture and smear for AFB, fungus. Try to sample a representative lesion,
avoiding sites where scar would be conspicuous, avoid keloid prone area i.e.
upper anterior chest, avoid legs where healing is slow and histology
modified, avoid over bony prominence, place in proper fixative or fresh (as
in immunofluorescence staining or culture) and make sure the correct
labeling with name, site, history, diagnosis. Discussion with the pathologist
is often helpful.
Punch biopsy: 3 to 4 mm tissue punch, specimen not to be crushed with
tooth forceps, skin hook may be good in handling the tissue.
Scalpel biopsy: elliptical excisional, incisional or shave biopsy. 3/0 non-
absorbable sutures for legs, 5/0 for face and 4/0 else-where. In general,
stitches are planned to be removed from the wound in face 4-5 days, from
the neck and the scalp in 7 days, from the anterior trunk and arms in 12 to 14
days, from back and legs in 14 to 28 days. Skin splints in the form of Steri-
Strips can be applied after stitches are removed. They can be kept for two to
six weeks after suture removal.
4.2. Wood's Lamp Examination
Ultraviolet light of 365 nm wavelength is obtained by passing the beam
through a Wood's filter composed of nickel oxide containing glass. The
examination has to be done in a dark room. Infected hair in tinea capitis
caused by Microsporum canis will fluoresce bright green, skin lesion of
active pityriasis versicolor will fluoresce yellow, fresh urine in porphyria
cutanea tarda fluoresces a reddish colour, erythrasma will fluoresce coral
red, vitiligo lesion appears more white and ashleaf macule in Tuberous
sclerosis is more apparent, coral red fluorescence of teeth in congenital
erythropoietic porphyria. Make sure that there are no artificial cream or
cosmetic are left in the area of skin examined by Wood's light because many
creams or dyes will fluoresce under Wood's light.
4.3. Patch Test
This tests the type IV hypersensitivity reaction and it is a confirmatory test
for allergic contact dermatitis.
Trolab standard patch test is used to screen and confirm allergic contact
dermatitis. Further breakdown of the test may require patch test with
different series e.g. fragrance series. The test materials are applied to the
back under aluminium discs with occlusion. The sites are inspected at 48
hours and test materials removed. The sites are re-inspected at 96 hours for
delayed reaction. The grading of the reaction will be as follows:
No reaction: 0
Doubtful: +/-
Weak (erythema, non-vesicular): +
Strong (vesicular or edematous): ++
Extreme (with ulceration): +++
Irritant reaction: IR
Not tested: NT
4.4. Mycology Examination
Superficial fungi can be identified by examination of the skin scraping, nail
or hair. The scales, nail or hair should be collected onto a slide and a drop of
10 to 20 percent KOH to dissolve the keratin. It can be hastened by gently
warming the preparation but never over warm to cause bubbles with
artefacts affecting microscopic examination. It takes 10 to 15 minutes to
prepare for scales, but it takes longer for nail clipping from 30 to 45 minutes
for best preparation. Then it can be examined under low power objective and
then the high power objective for detail. The tissue can also be sent for
mycology culture. The result may not be available for 3 weeks.
4.5. Mite Examination
To identify the burrow in common area e.g. finger webs. With the help of
magnifying glass, the acarus may be seen as a tiny grey dot at the end of
burrow. It can be removed by a sterile needle. If mites not seen, burrow will
be moistened with liquid paraffin or mineral oil and scraping with the
scalpel blade and transferred to slide for examination.
4.6. Blood & Urine Tests
Just like that in general internal medicine, appropriate tests e.g. muscle
enzymes to exclude dermatomyositis, urine sugar test to exclude diabetes
mellitus.
4.7. Radiology Examination
The commonest tests done are X-ray chest to exclude pulmonary
tuberculosis and X-ray joints for psoriatic arthropathy. CT scan is important
for exclusion of internal enlarged lymph nodes in cutaneous lymphoma and
to exclude brain lesions in a case of neurofibromatosis.
4.8. Other Tests
Prick testing is much less helpful in dermatology. It is not done or available
in Social Hygiene Clinics. Multiple positive skin tests to commercially
prepared diluted antigens may only imply the atopic tendency of the tested
subject. Dark-ground examination for suspected genital ulcer to look for
Treponema Pallidum can be easily done when equipped with a dark-ground
microscope. It is the interpretation of the wet smear which may require some
experience. Acetic acid test on genital or cervical papules facilitates
detection of subclinical condylomata acuminata. Gauze saturated with 5%
acetic acid is wrapped around area for 5 to 10 minutes and the use of
colposcope or magnifying hand lens to detect the lesional white papules.
Cell cytology (Tzank smear) is not available in the clinic because it requires
a good and well trained cytologist for the smear.
4.9. Clinical Photography
Clinical photo is the best to document any lesion. One picture worths
thousand words of description. Usually all medico-legal cases, biopsy cases,
complicated cases and skin cancer cases require the clinical photo as an
additional documentation. It is a useful investigation tool for follow-up of
lesions e.g. naevus sebaceous, pigmented naevus. Standard macro lens with
fixed magnification in good focus, appropriate flash-lamp (with good
battery) or good lighting, with good backgrounds (pure blue or green cloth
as background) will make the photo not a waste. Date, site of photo taken
and a good filing system are needed to make it a useful and interesting tools
for investigation in dermatology.
5. PATTERN OF COMMON SKIN DISEASES IN SOCIAL HYGIENE
CLINICS
1) The commonest 20 skin diseases in the statistical return in 1996 in
dermatology clinic of Social Hygiene Service.
Rank Condition Incidence (new cases)
1 Eczema 4,931
2 Tinea (all types) 1,577
3 Verruca 1,263
4 Acne 764
5 Contact Dermatitis 642
6 Psoriasis 560
7 Urticaria 421
8 Herpes infections 381
9 Pigmentary disorders 329
10 Alopecia 322
11 Naevi (all types) 310
12 Neurodermatitis 292
13 Pityriasis versicolor 210
14 Rosacea 195
15 Skin tags 162
16 Scabies 157
17 Seborrhoeic wart 154
18 Nail dystrophy 86
19 Keratosis (all types) 81
20 Cysts 55
21 Others 2,628
¡@ Total 15,520
2) Skin malignancies (biopsy confirmed cases) in 1992 to 1996.
Diagnosis 1992 1993 1994 1995 1996
Basal cell carcinoma 53 59 79 72 84
Squamous cell carcinoma 10 12 9 10 22
Malignant melanoma 3 4 0 9 3
Bowen's disease 22 18 16 23 23
Extramammary Paget's Disease 5 1 7 1 1
Adenocarcinoma 2 0 0 1 0
Lymphoma/Mycosis Fungoides 3 9 5 16 9
Kaposi's sarcoma 0 3 4 3 1
Baso-squamous carcinoma 0 0 0 0 0
Angiosarcoma & Metastatic carcinoma 0 0 1 2 3
Sebaceous carcinoma & Trichilemmal
0 0 0 0 0
carcinoma
Other carcinoma of skin 0 0 0 2 4
Solar keratosis 18 15 21 32 54
Total 116 121 142 171 204
PRURITUS
Dr. C.S. LEUNG
CHAPTER 2
1. PATHOPHYSIOLOGY
Itch receptors are unmyelinated, unspecialized free nerve endings, found
near to the dermal- epidermal junction. It was widely believed in the past
that pain and itch are transmitted by the same nerve pathway, and also low
intensity stimulation of unmyelinated polymodal C fibre results in itch
sensation whereas high intensity stimulation causes pain. However, in recent
experiments, when single unmyelinated C fibres are stimulated two sets of
fibres have been identified. Stimulation of most these fibres produce pain
sensation, whereas a small number of fibres produce the sensation of
itchiness upon stimulation. (Greaves)
2. PERIPHERAL MEDIATORS
1) Histamine
2) Neuropeptides, including substance P
- Substance P, together with neuropeptides, is localised in cutaneous sensory
nerve endings. They could be depleted by capsacin cream.
3) Other relevant periperhal mediators
Arachidonic acid transformation products
- Prostaglandin E potentiates itchiness caused by other mediators
Platelet activating factor
Other vasoactive peptides and proteases
Others
Finally, it is found that enkephalins, which are opioid pentapeptides, exert a
modulatory action on transmission of pain and itchiness.
3. Causes of itchiness
Understanding the various causes of pruritus is fundamental to its
management.
3.1. Localized Causes
Certain skin disease may select to affect a particular site of a body causing
localized pruritus. Some of the important examples of localized pruritus are
as follows:
Scalp: Seborreic eczema and neurodermatitis, psoriasis
Eyelid: Airborne irritants or allergens; allergic reactions to cosmetics and
nail vanish
Fingers: Eczema, scabies, fowl mite infestation
Legs: Gravitational and discoid eczema, asteatosis
3.2. General Pruritus

3.2.1. External Causes
1) Climatic: low humidity e.g. due to cold weather or central heating may
renders the skin brittle, and allows minor irritant such as soap to penetrate,
causing mild inflammation and pruritus. The dry skin of the old aged
causing itchiness is common. Excessive dry skin associated with atopic
eczema will also lead to itch. High humidity can also cause pruritus
secondary to sweat retention in some individuals.
2) Particulate matter: foreign body e.g. glass fibre, hair; industrial exposure
to powdered alumina or fibreglass (curtains, draperies, plastic furniture) can
cause pruritus.
3) Chemical: some detergent (e.g. optical brighteners in certain washing
powders) may cause pruritic dermatosis with little sign.
4) Parasite contact or infestations: scabies or due to mites of pets etc. can
cause marked pruritus.
5) Aquagenic pruritus: the condition may be a premonitory symptom of
polycythaemia vera, myeloproliferative diseases or even histocytic
disorders.
6) Excessive bathing
3.2.2. Skin Diseases
Pruritus is a feature of many of skin diseases. Some common skin diseases
causing itchiness is listed as follows:
Severe Moderate
Scabies, pedulosis Psoriasis
Insect bites Seborrhoeic eczema
Contact dermatitis Fungal infection
Atopic eczema Dry skin
Urticaria Sunburn
Miliaria
Lichen planus
Dermatitis herpetiformis
Generalized pruritus can precede some skin disease such as pemphigoid.
3.2.3. Systemic Causes
A wide variety of systemic disease can cause generalized pruritus without
diagnostic skin lesions. The incidence of the association of generalized
pruritus with significant internal disease is difficult to assess, but it has been
estimated to range from 10-50%.
1) Infectious causes (including tropical and intestinal parasites)
a) Rubella
b) Varicella
c) HIV infection
d) Trichinosis, tapeworm infection
e) Onchocerciasis
f) Schistosomiasis
g) Fungal infection
Generalized pruritus has been associated with localized fungal
infection.
2) Endocrine disease
a) Diabetes: general pruritus is not a manifestation of diabetes mellitus
(Greaves) and the pruritus is usually localized (e.g. itchiness of genitalia or
perianal area due to candidiasis; and pruritus of scalp.)
b) Hyperthyroidism, hypothyroidism (due to skin dryness)
c) Disorders of the parathyroid gland
d) Carcinoid syndrome
3) Hepatic disease
a) Pregnancy: intrahepatic cholestasis
b) Obstructive jaundice (in biliary tract or extrahepatic, e.g. carcinoma of
Ampulla of Vater)
c) Primary biliary cirrhosis
d) Drug induced cholestasis: intrahepatic biliary obstruction
e.g. chlorpromazine, contraceptive pills, testosterone
4) Renal disease
Pruritus is common among patients with chronic renal failure. In patients on
maintenance dialysis, over 80% are affected.
5) Haematological diseases (including lymphoproliferative disorders)
a) Polycythaemia vera: pruritus may occur after contact with water or after a
hot bath (the pruritus after a hot shower is not specific for polycythaemia, as
it can occur in Hodgkin's Disease, myeloid metaplasia, or other disorders,
not to mention the vasodilatation produced by heat may enhance itchiness of
almost any causes).
N.B.: Aquagenic pruritus may precede the development of polycythaemia
vera by several years
b) Iron deficiency: Iron deficiency has been often regarded as a cause for
pruritus, or even in the absence of anemia. The itch may be due to factors
other than the iron deficiency itself.
c) Hodgkin's Disease: (about 30% patients feel itchy)
Pruritus can be the early or presenting complaint. It can be severe (which
may imply a worse prognosis.) Excoriations, papules, prurigo nodules from
continuous scratching may be present. Therefore periodic reinvestigation or
revaluation of p.u.o. is important.
d) Mycosis fungoides
e) Lymphosarcoma
f) Chronic leukaemia: pruritus is an uncommon presentation of chronic
leukaemia, and is more often encountered in the lymphatic than the
granulocytic form.
g) Myleomatosis
h) Paraproteinaemia
i) Mast cell disease
6) Occult malignancy
a) Haematological and lymphoproliferative disorders as mentioned.
b) Pruritus is an important but uncommon manifestation of carcinomatosis.
Among the tumors reported to present with generalized pruritus,
adenocarcinoma and squamous cell carcinoma of various organ are most
common. Though generalized, the itching may be more marked on the legs,
upper trunk and the extensor surfaces of the upper limbs.
c) Tumor of brain: associated with pruritus of nostril
7) Autoimmue disease
SLE, 'Sicca syndrome'
8) Neurological
Tabes may give rise to segmental pruritus.
GPI
Multiple sclerosis
Brain tumor
Paroxysmal unilateral pruritus has been recorded with central nervous
system disease
9) Psychiatric/Psychogenic Causes
Emotional stress and psychological trauma intensifies all form of pruritus
and neurosis may be the cause for pruritus.
Delusion e.g. delusional parasitosis (a manifestation of monosymptomatic
hypochondrical psychosis) of course can be a cause for complaint of
pruritus.
To make a diagnosis of pruritus (localized or generalized) as psychogenic
or psychiatric in origin, cutaneous and systemic causes have to be excluded.
10) Drugs or as a result of therapy
Pruritus can be a side effect of a wide variety of drugs. This include the
opium alkaloid, CNS stimulant/depressant, niacinamide, cimetidine, aspirin,
quinidine, chloroquine. Drugs can also cause pruritus via the mechanism of
hepatic cholestasis (e.g. chlorpromazine, testosterone, contraceptive pills).
Subclinical sensitivity to any drug may cause pruritus. Pruritus may be a
side effect of PUVA.
To help in memorizing these systemic causes, the word BLINKED can be
remembered.
B = Blood disease
L = Liver disease
I = Infection, immunological or autoimmune disease
N = Neoplastic disease, neurological disease
K = Kidney disease
E = Endocrine disease
D = Drug
Of course psychiatric or psychogenic cause should not be forgotten.
* Pruritus ani deserves mentioning here as the symptom could be due to
primary pruritus or associated colonic or anorectal diseases. Common
anorectal disease are haemorrhoids and anal fissures. Neoplasia associated in
descending order of frequency are rectal cancer, anal cancer, adenomatous
polyp and even colonic cancer, also the pruritus associated could be present
longer than that due to primary pruritus or benign anorectal disease.
4. Evaluation
4.1. A, B, C
The patient must be evaluated for the A (external causes), B (skin diseases),
C causes (systemic causes: which in turn include the BLINKED causes) as
mentioned. The evaluation consists of taking a detailed history, physical
examination and laboratory investigations.
4.2. History: Detailed History of the Present Illness
Besides, the following questions concerning the features of pruritus is
relevant:
1) Is the pruritus localized (external cause) or generalized (internal cause)?
2) Is only the exposed skin affected? If yes, this implies an exogenous cause.
3) Are any other family members affected?
4) Is there relationship with occupation? e.g. exposure to fibre glass.
5) Is there any recent history of travel? (tropical infestations?)
6) Is there exposure to plants, animals or chemical?
Characteristics of pruritus:
1) Site, whether localized or generalized.
2) Precipitating and relieving factors: e.g. any relation to hot bath such as
found in aquaenic pruritus?
3) Severity: the influence on daily activities/sleep.
4) Time relationship: most itchiness are worse at night, esp. scabies.
5) Seasonal variation: asteatotic eczema is usually worse in winter.
The history should include assessment of personality, current emotional
stress.
Past medical history
Family medical history
4.3. Physical Examination
A complete physical examination is performed with the various possible
differential diagnosis (the A, B, C causes) in mind. During the physical
examination, particular attention should be paid to vital signs,
lymphadenopathy and enlargement of organs etc., with special alertness to
any possible connection between cutaneous sign and disease of other organ
system. In the absence of obvious localizing signs or symptoms indicating
systemic disease, rectal and pelvic examination should be included in the
full physical examination.
Patient with P.U.O. (pruritus of unknown origin) must be considered for any
underlying disorder, e.g. "occult carcinoma" may need to be ruled out in
elderly patient presenting with persistent pruritus.
4.4. Laboratory Investigation
1) Haematological: CBP, ESR
2) LFT, RFT, acid phosphatase, serum iron, serum protein electrophoresis,
immunoelectrophoresis
3) Thyroid function test/glucose
4) CXR
5) Stool for occult blood, ova/cyst
6) Urine for R/M
7) Skin biopsy
8) Others: e.g. test for HIV antibody, Pap smear, further radiological
examination if indicated
Further investigations may be necessary depending on the situation.
5. Treatment
1) Treat the underlying cause.
2) General symptomatic treatment
a) To reduce or avoid any provocative factors, e.g. dryness of the
environment, wearing irritating fabric, overheating, stress, vasodilatation
from hot food.
b) Topical applications: Emollient, menthol in calamine lotion can be used.
3) Commonly used oral medication: Antihistamine are most useful in
conditions in which antihistamine clearly plays a role, e.g. urticaria.
Histamine is the most consistent itch mediator known, but it is not always
useful as other mediators may also be involved.
* Tricyclic antidepressants may be of help in some patients with intractable
itching.
4) For treatment of the pruritus of some of the specific disorders, the
following measures have been reported to be useful. (Some of these
treatments may need further studies and trial for evaluation.):
a) Aquagenic pruritus +/- polycythaemia vera (PV)
Topical capsacin treatment
PUVA (maintenance therapy may be necessary), UVB
regional sponging at bathing may be helpful in aquagenic pruritus with PV.
Interferon alpha: not only controls the pruritus, also helps to contain the
increased haemopoiesis in PV, and lead to better haemopoietic control. Yet
some patients may not be able to stand the side effect.
Phlebotomy reported to be useful in a case of PV.
N.B.: The pruritus usually responds poorly to antihistamine
b) Obstructive jaundice
cholestyramine is helpful, but is associated with a high incidence of side
effects.
new anion resin, BR 350
rifampicin
antihistamine
naloxone infusion, opiate antagonist
Ondansetron, a specific serotonin type 3 (5-HT3) receptor antagonist
Flumecinol used in pruritic patients with primary biliary cirrhosis
propofol (an intravenous anesthetic induction agent) employed in a
subhynotic dose, for short term use.
c) Chronic renal disease: Some patients with hyperparathyroidism
secondarily to renal failure improve dramatically after subtotal
parathyroidectomy. However, only a minority of patients respond and the
improvement may only last a few months.
Phototherapy by UVB for moderate to severe cases.
Emollients may relieve those with a dry skin.
Activated charcoal or cholestyramine orally may be helpful.
Capsacin cream topically.
Ketotifen.
Azelastine hydrochloride (an anti-allergic drug/antihistamine) orally.
Talidomide for difficult cases.
Other treatments including heparin, mexiletine, ion-exchange resin and
intravenous lignocaine have been advocated but are of uncertain
effectiveness and usually impractical to use.
Low protein diet was reported to be useful.
Antihistamine and topical steroids are usually not helpful.
d) Psychological/psychiatric diseases: psychiatric advice should be sought.
After careful consideration, antidepressant and anxiolytic drugs including
doxepin and hydroxyzine can be tried.
Pimozide has been advocated for delusions of parasitosis.
e) Atopic eczema:
Doxepin cream.
f) Myeloproliferative disorders and other disease:
Danazol has been tried in the treatment of refactory pruritus associated with
myeloproliferative disorders and other disease e.g. autoimmune disease etc.
5) Other medication/measures that has been employed to treat generalised
pruritus:
Odansetron (5 HT3 antagonist)
transcutaneous nerve stimulation
ECZEMA
Dr. Y.M. TANG, Dr. H.F. HO & Dr. K.H. YEUNG
CHAPTER 3
1. INTRODUCTION
1.1. Terminology
ECZEMA: Use as a clinical descriptive term, it describe a process that is
clearly superficial in form and that, early, is erythematous, papulo-vesicular,
oozing and crusting and, later, red-purple, scaly, lichenified and possibly
pigmented. Epithelial disruption and non-sharp margination are its
characteristics.
ECZEMA can be defined histologically by the presence of a predominantly
lymphohistiocytic infiltrate around the upper dermal blood vessels,
associated with varying degrees of spongiosis and acanthosis.
The terms 'ECZEMA' and 'DERMATITIS' are regarded as synonymous.
1.2. Table 1: Stages of Eczematous Inflammation
Stage Morphology of Symptoms Examples Treatment

Lesions
acute contact cold wet
intense itch, dermatitis, acute compresses,
vesicles, blisters,
Acute stinging, nummular eczema, steroid,
intense red
burning stasis dermatitis, antihistamine,
pompholyx, antibiotics
red, scale, contact allergy,
slight to
fissuring, irritation, atopic topical steroid
moderate
parched dermatitis, stasis emollients,
Subacute itch,
appearance, dermatitis, nummular antihistamine
stinging,
scalded eczema, asteatotic antibiotics
burning
appearance eczema
atopic dermatitis,
thickened skin, lichen simplex topical steroid
lichenified moderate to chronicus, fingertip antihistamine
Chronic
excoriation, intense itch eczema, antibiotics,
fissuring hyperkeratotic emollients
eczema
1.3. Table 2: Common Types of Eczema
Exogenous Endogenous
Irritant Dermatitis Atopic
Allergic Contact Dermatitis Seborrhoeic Dermatitis
Photoallergic Contact
Asteatotic Dermatitis
Dermatitis
Eczematous Polymorphous
Discoid Eczema
Light Eruption
Infective Dermatitis Pityriasis Alba
Dermatophytide Hyperkeratotic Eczema
¡@ Gravitational Eczema
¡@ Juvenile Plantar Dermatosis
Eczema Associated With

¡@
Systemic Disease
¡@ Eczematous Drug Eruption
2. ATOPIC ECZEMA
Atopic eczema (AD) is a characteristic type of chronic dermatitis frequently
associated with atopy and an elevated IgE level. There are no single
distinguishing features of AD; however, the diagnosis can be made on a
combination of history, and morphological findings.
2.1 Epidemiology
AD has a world-wide distribution and affects all races. About 3% of children
under age 5 years had AD with a male to female ratio of 1.2 : 1. Majority of
patients presents within the first 5 years. AD runs in family. About 75% of
patients have a personal or family history of other atopic diseases, e.g.,
allergic rhinitis, asthma, hay fever.
2.2. Aetiology and Pathogenesis
The aetiology is unknown and the pathogenetic mechanisms are speculative.
However, a number of clinical, pathological and immunological
abnormalities are frequently observed in these patients and are briefly
discussed below:
1) Elevated IgE
Occur in about 80 percent of AD patients and are directed against a wide
variety of antigen like pollens, molds, foods, house dust mites (HDM) and
bacterial antigens etc. A high IgE level is not a unique feature of AD but
appears to correlate with the clinical severity and falls with remission.
2) Skin Prick Test and RAST
Patients with AD often show positive Prick test and RAST to common
household allergens like egg, milk, wheat, fish, soy, peanut, pollens, HDM
and animal danders etc. However, avoidance of such allergens does not
necessarily bring about a clinical response.
3) Bacterial Antigens
Staph. aureus colonization occurs in over 50% of AD patients and compared
to less than 5% in normal individuals, and is frequently isolated (> 90%)
from acute exudative lesions and lichenified plaques. The density of the
organism correlates with the severity of eczema and antibiotics that clear
Staph. aureus improve eczema.
4) Impaired Cellular Immunity
This includes a reduced CD8+ suppressor T cells, a reduced natural killer
cell function, a reduced IFN-g production, a reduced response to mitogens;
peripheral eosinophilia in some and abnormal neutrophil chemotaxis.
5) Inflammatory Cells and Mediators
A very characteristic feature of AD is intense pruritus. It has been shown that
an increased population of mast cells occurs in the skin of AD patients
which releases histamine, leukotrienes and cytokines much more readily
compared with normal subjects.
6) Abnormal Vascular Responses
Disturbed vascular reactivity like white dermographism, nicotine blanching,
and delayed blanch with methacholine are well documented.
7) Sweat and Sebum Production
AD patients tend to produce more sweating than nonatopic controls. It has
been suggested that an increase in transepidermal water loss, and a possible
deficiency of lipids in the epidermis account for the skin dryness.
2.3. Clinical Features
1) Pruritus
Is the hallmark of AD. It is more severe at night and is attributed to the
absence of distraction, capillary dilatation, and increased skin temperature. A
natural response to itch would be scratching, and scratching results in
erosions, weeping, crusts, secondary infections, prurigo papules and
lichenification.
2) Dry Skin (Xerosis)
Manifests as scaling, chapping and a feeling of skin roughness. It is worse in
winter times due to reduced ambient humidity and coldness. Dry skin is
enhanced by frequent use of detergents or defatting substances.
3) Eczematous Lesions
The most typical skin sign of infantile AD. They are polymorphic, with an
erythematous, papulovesicular, erosive and crusted appearance.
4) Prurigo
Is a dome-shaped papule, sometimes with a tiny vesicle on top. Excoriation
is frequent. Prurigo papules vary in number and distribution.
5) Lichenification
A lichenified plaque is a poorly demarcated, slightly tan to red plaque with
grossly accentuated skin markings. Lichenified plaques take long time to
resolve. The antecubital and popliteal fossae and the neck are predilected
sites.
6) Dennie Morgan Fold
Is an extra infraorbital eyelid fold. About 80% is bilateral. Some consider
this is a consequence of scratching of the eyelids.
7) Hand and Feet Ivolvement
Dry, nonpruritic plaques and recurrent hyperkeratosis and fissuring of the
finger pulps (and soles) are common. Linear furrows running across thenar
and/or hypothenar eminences referred to as hyperlinearity of palms occurs in
about 1/3 to 1/2 of AD patients. Coarse pitting and ridging of nails may
occur.
2.4. Four Phases of AD
1) Infantile Phase
Lesions first appear on the cheeks, forehead, and scalp, but may occur on the
trunk, neck, hands and feet. Eczema with oozing and crusts are more typical.
Nocturnal restless, irritability and crying are prominent. When the child
begins to crawl, the exposed areas especially the extensor aspects of knees
are affected.
2) Childhood Phase
At about 18 months, the eczematous lesions tend to be replaced by
lichenification. Prurigo papules occur and are very itchy. Elbow and knee
flexures, wrists and ankles and neck are commonly involved. The neck may
show striking reticulate repigmentation (dirty neck). Hands may be dry and
lichenified; sole involvement may mimic juvenile plantar dermatosis. The
face is less frequently affected. Problems with schooling may occur.
3) Adolescent/Young Adult Phase
Predominant features are pruritus, lichenification, prurigo papules, scratch
marks, and crusting. Lesions occur mostly on the face, neck, flexures, and
upper trunk. Localized patches of eczema around the nipple or vermillion of
the lips can occur. Psychological difficulties occur in some.
4) Adult Phase
AD resolves spontaneously in most patients after age of 20. Majorities of the
patients, however, still have sensitive, unstable skin and a higher tendency to
develop dermatitis. Full blown AD occurs in only a small percentage of
patients throughout adulthood.
2.5. Associations
The association of AD with allergic rhinitis, asthma and conjunctivitis is
well documented. Eczematous conditions like contact dermatitis, discoid
eczema, pityriasis alba, lip-stick eczema and follicular eczema are more
frequently seen in atopic subjects. Others like ichthyosis vulgaris, keratosis
pilaris, Netherton's syndrome, alopecia areata and vitiligo etc. also have
linkage.
2.6. Complications
1) Infection
Bacterial especially Staph. aureus, viral, and fungal infections are common,
and so as scabies. Eczema herpeticum, which is herpes simplex infection in
eczematous skin is characterized by multiple, painful, vesiculopustular
lesions; and often become haemorrhagic, eroded and crusted. Affected areas
may be very edematous; regional lymphadenopathy occurs and secondary
bacterial infection is common. Diagnosis can be established by Tzanck
smears or electronmicroscopy from scarping of the skin lesions.
2) Exfoliative Dermatitis
This is severe and requires hospitalization.
3) Eye
An increased incidence of anterior subcapsular cataract may be due to
extensive use of systemic steroid, and to topical steroid applying around the
eyes. Keratoconus is corneal degeneration characterized by increasing
conicity of the cornea resulting from a raised intraocular pressure. Visual
disturbance occurs.
4) Retarded Growth
May be attributed to a combination of reduced exercises, infections, and
malnutrition secondary to inappropriate dietary restriction; however,
frequent use of systemic/topical steroid is perhaps a more important
contributing factor.
¡@
2.7. Criteria for Diagnosis of Atopic Eczema
Major criteria Minor criteria
Pruritus Dryness
Typical morphology and distribution Hyperlinearity of palms/Keratosis
. pilaris
of skin lesions. Increased IgE
Chronic and relapsing course Early age of onset
Personal or family history of atopy Tendency to cutaneous infection
Cheilitis
Dennie-Morgan infraorbital folds
Pityriasis alba
Keratoconus/anterior subcapsular cataracts
White dermographism etc.
There is no single diagnostic feature for AD. However, it has been suggested
that a diagnosis of AD can be established with 3 or more major criteria plus
3 or more minor criteria.
2.8. Differential Diagnosis
Infantile seborrhoeic dermatitis has an earlier onset than AD. The presence
of family history, scratching, possible food intolerance, and high IgE level in
AD is absent in seborrhoeic eczema. Allergic contact dermatitis with
autosensitisation, psoriasis, candidiasis, dermatophytosis, pityriasis rosea,
scabies, nutritional deficiency may at times cause confusion.
2.9. Treatment
1) General Measures
a) Explanation
Explanation on the nature and management of AD improves compliance and
efficacy of treatment. AD runs a long course that can be controlled but not
cured. AD improves with increasing age, but patients often have a dry,
sensitive skin and avoidance of irritants and trigger factors is always
necessary. Good medical compliance is important. Scratching of skin should
be discouraged in order to disrupt the itch-scratch cycle; keep nails short.
Immunization is given as non-atopic subjects but should be cautious for
vaccines derived from eggs if patient is egg-sensitive. Defer vaccination if
the child has an acute flare of eczema. Career advice emphasizes the
selection of a 'clean' job. Occupations like barber, chef, laboratory
technician, car mechanic, nurse and jobs that require contact with chemicals
are not suitable.
b) Environmental Modification and Avoidance of Trigger Factors
Woolly underclothes irritate skin and should be avoided Woolly toys tend to
house allergens so as carpets. Pets have the similar problem; their hair and
excreta can be allergenic and pets are a source of infestation. Avoid
excessive heating in the bedroom as this increases dryness and itchiness.
Regular once daily bathing is not strictly required. Over-bathing or over-use
of soaps is detrimental to the sensitive skin. Avoid bathe with hot water, use
soap substitutes, avoid vigorous rubbing at the skin and keep the bathing
time short. The skin should be mopped dry immediately after bathing and
emollients applied. Swimming is permitted but chlorinated water irritates
skin and hence immediate showering is required afterwards. Many cosmetic
products have the potential to trigger a flare. Foods implicated as allergenic
include eggs, milk, wheat, legumes, seafood and peanuts. Few young
patients do have a clear relationship between food and eczema flares. In such
case, they can try a 3-4 week's period of suspected food elimination. One
should aware that unsupervised food restriction in the young may lead to
malnutrition. Avoid unnecessary physical and emotional stress.
2) Management of Dry Skin - Emollients and Soap Substitutes
Dry skin is more prone to itch and chapping and hence risk of infection and
subsequent perpetuation of eczema. A good dry skin care can be achieved
by:
a) Keep bathing time short and to a minimum necessary
b) Use lukewarm water not too hot
c) Use soap substitute e.g. emulsifying ointment
d) Avoid vigorous rubbing and cleaning at the skin
e) Pat dry, and
f) Apply emollients e.g., aqueous cream, as soon as after getting out of the
bath.
Emollients minimize dryness and is the mainstay in treating mild AD. Some
emollients are also humectants, e.g. urea cream. Humectants attract water
into the skin, and are useful on unbroken skin but can cause stinging.
Emollients should be applied as frequently as possible according to patient's
need. It is believed that regular and frequent use of emollients can reduce
10-20% of the amount of topical steroids used in the maintenance treatment
of AD. Some emollients contain lanolin that may sensitize skin e.g., Alpha
keri, oilatum etc. Chapters 35 and 37 give further description on the property
and use of emollients.
3) Ichthammol and Tar Preparations (0.5-1%)
Ichthammol impregnated bandages are old remedy but are still used for
treating childhood eczema in UK. Tar can reduce itch. Tar/steroid-
impregnated bandages are useful for chronic lichenified eczema. Tar bath is
a useful bath additive in reducing itchiness. Tar compounds can induce
folliculitis and photosensitisation; and because of its smell and colour,
patient compliance is a poor.
4) Topical Steroids
Is the mainstay of treatment for inflammatory aspect of atopic eczema. The
strength and the base used will depend on the stage and location of the
eczema. Acute weeping eczema should first be treated with potassium
permanganate (KMnO4) compresses followed by a steroid lotion or cream.
In chronic eczema, creams and ointments are both suitable. Twice daily
application is usually sufficient. Prolonged use of a potent corticosteroid
e.g., clobetasol propionate 0.05% over 50 g per week may result in systemic
and local side effects. Fear of side effects, however, should not limit the use
to a weaker but ineffective corticosteroid. Potent corticosteroids can be used
as a short-term measure aiming to obtain initial control, this is then changed
over to a weaker steroid suitable for the situation. Chapter 41 gives an
overview on topical corticosteroids.
"Wet-Wrap"is a newly developed way of using topical steroid under the
occlusion of wet tube gauze. It has the combined advantages of applying
steroid under occlusion, maintaining moisture and prevent scratching. It is
indicated in the chronic, dry, thickened and lichenified type to atopic
dermatitis especially in young children. Exudative lesions in acute and
subacute eczema is not suitable.
5) Control of Infections
Staph. aureus infection is a frequent cause of eczema flare requiring
systemic antibiotics, e.g., erythromycin or cloxacillin. Sometimes, a
prolonged course of antibiotics may be required. Topical mupirocin twice
daily to nasal vestibules and chlorhexidine massaging onto body during
bathing can reduce the number of Staph. aureus in a carrier. Systemic
antibiotics for treating large area of infected eczema are superior than using
large amount of topical antibiotics that carry risk of hypersensitivity and
inducing bacterial resistance. Eczema herpeticum needs systemic acyclovir.
Molluscum contagiosum, warts and fungal infections should be treated
accordingly.
6) Systemic Corticosteroid
It is not a routine management of atopic eczema and it should be avoided at
times of puberty. Sometimes, a short course of systemic corticosteroid is
effective in gaining control of a severe eczema flare. Whenever systemic
steroid is used, any infection must be looked for and treated promptly.
7) Systemic Antihistamines
Recommended doses can be given during periods of excessive scratching.
Avoid excessive doses as hyperexcitability may be quite marked in young
children.
8) PUVA
It is useful in chronic lichenified eczema where pruritus is intractable and a
useful adjunct to leaving off topical steroids at the time of pubertal growth
spurt. Patient selection is important. No PUVA should be given to children
under the age of 12 because of risk of cataract in the immature lens and
difficulty in co-operation and understanding with the PUVA regime. The
same precautions and procedures as PUVA for other conditions should be
undertaken. The response of AD to PUVA is not as good as compared with
that for treating psoriasis and the total dose required is often larger. The
experience in UK showed that approximately one-third showed remission or
significant response, one-third remit and relapse, and one-third no response.
9) Immunosuppressives
Azathioprine or cyclosporin are helpful in severe cases. Nevertheless, drug
toxicity and long-term hazards are a definite risk. They should only be
considered for chronic severe AD with poor response to the usual treatment.
10) Hospitalization
In severe cases, it can be very helpful. Remove the patient from his
environment and potential trigger factors, institute regular and intensive
treatments can lead to resolution of the eczema.
2.10. Alternative Treatments
1) Evening primrose oil
Which contains linoleic acid and gamma linolenic acid, was found to be
effective in some cases in reducing erythema and pruritus; but it may take 2-
3 months to see effect. It is also costly. The precise indications are not clear
and it cannot be predicted which patients will respond. It may be tried for
patients who failed with conventional therapy.
2) Chinese herbs
Recent studies in UK using a certain formulary of Chinese herbs for patients
with long-standing, widespread, and non-exudative AD have shown a
statistical significant improvement in symptoms and skin signs. At this stage,
Chinese herbs do seem to have a therapeutic potential in the treatment of AD
but its palatability, efficacy and its safety need further evaluation.
3) Sodium cromoglycate
It is given as 100-200 mg qid orally. In general, it is not effective.
4) Behavioral therapy
May be a useful adjunct for patients who cause excessive self-mutilation in
their families.
2.11. Prevention
There is no definite evidence that breast feeding is protective against
development of AD. It has been suggested that the early introduction of solid
foods (before age 4 months) does have a deleterious effect, and that a greater
variety of foods correlated with an increased probability of developing AD.
2.12. Prognosis
Studies investigating the long-term outcome of AD have been unsatisfactory.
In general, patients with a family history of AD, associated asthma, hay
fever, later-onset disease and the presence of severe dermatitis have higher
rates of persistent disease. Many quote 40-50 percent of recovery by age 15
years.
3. OTHER TYPES OF ECZEMA
3.1. Irritant Contact Dermatitis
1) Diagnostic features
The affected sites characteristically conform to history of specific contact to
a susceptible contactants. Some non-exposed areas are also susceptible to
irritant contact dermatitis, e.g., body folds and flexural areas, due to a
combination of friction and direct contact with sweat or urine. Once
exposure to the irritant ceases, improvement start to occur.
2) Clinical presentation
Strong irritant contact dermatitis can occur after a single brief exposure. The
latent period is short. Examples are acid and alkaline burns, thermal burns
and frost bites. The offending irritant is usually obvious. Weak irritant
contact dermatitis develops after multiple exposures, latent period is long.
3) Management
The offending irritant should be identified and removed. Soap and detergents
should appropriately be minimized. Cool water is less detrimental than hot
water. Advice on the use of protective barriers whilst at work, e.g., gloves,
protective clothes etc. should be strictly followed by the patient. Restoration
of the lipid layer can be accomplished by frequent application of emollients.
In case of maceration, wet clothing should be changed frequently, non-
porous clothing to be avoided. Inflammatory element can be controlled with
topical steroid.
3.2. Allergic Contact Dermatitis
1) Diagnostic features
The characteristic distribution of the lesions can often gives a clue to a
particular allergen (Table 3). Removal of the suspected allergen leads to
resolution of the dermatitis. A positive patch test to a suspected offending
contactant support the clinical diagnosis.
a) Both allergic contact dermatitis and irritant contact dermatitis bear similar
clinical signs. In acute cases weeping and crusting will be present, while in
chronic cases scaling and fissuring are the dominant findings. Sometimes,
allergic contact dermatitis differs from irritant contact dermatitis in that
erythema and edema may be more prominent and pruritus more troublesome
in the former.
b) Systemically induced allergic contact dermatitis: Patients who have been
sensitized to topical allergens may develop generalized eczematous
inflammation if these allergens or chemically related substances are
ingested. e.g. Patient with a history of nickel allergy may get a widespread
flare when he takes food rich in nickel; patient sensitized to topical
ethylenediamine may develop generalized inflammation following treatment
with aminophylline.
c) Airborne allergic contact dermatitis and photodermatitis have a similar
distribution. Look for sparing in the upper eyelids, areas below the chin, and
the Wilkinson's triangles behind the ear.
Table 3: Distribution of Allergens
Location Material
Scalp and
Shampoo, hair dyes, topical medicaments
ears
Nail polish, cosmetics, contact lens solution, metal

Eyelid
eyelash curlers, topical medicaments
Airborne allergens, cosmetics, sunscreen, acne

Face
medications, aftershave lotion
Necklaces, airborne allergens, perfumes, aftershave

Neck
lotion
Topical medicaments, sunscreens, plants, clothing,

Trunk undergarments (e.g., elastic waist band, spandex
bra), metal belt buckles
Axilla Deodorant, clothing
Arms Watch and watchband
Hands Soaps and detergents, foods, poison ivy, industrial

solvents and oils, cements, metal, topical
medications rubber gloves
Genitals Rubber condom, allergens transfers by hands
Anal
Haemorrhoid preparations, antifungal preparations
region
Lower
Topical medicaments, dye in socks
legs
Feet Shoes, cements spilling into boots

3) Management
a) The first step is the identification and removal of the contactant. A
detailed history and a careful examination is usually sufficient. Patch
testing* is indicated for cases in which inflammation persists despite
avoidance and appropriate topical therapy.
b) For acute inflammation with blisters and intense erythema, cold wet
compresses e.g. KMnO4 are highly effective. They should be used for 15 to
30 minutes several times a days until blistering and severe itching is
controlled. Prednisolone, in dosage of around 30-40 mg a day in divided
doses is used for extensive inflammation. Topical steroids for reduction of
local inflammation.
* Patch Testing
1) 23 materials in the European Standard Screening Series are employed in
Social Hygiene Service (Table 4). More description about Patch test is
available in Chapters 1 and 18. Whether or not the allergy demonstrated by
the patch test is relevant to the patient's dermatitis must be determined by the
critical judgment of the physician.
2) Contraindications to patch testing:
a) Acute widespread dermatitis.
b) Ongoing systemic steroid therapy. Defer till at least 1-2 weeks after
steroid therapy.
Table 4: European Standard Screening Series and Examples of
Common Sources
¡@ Potassium dichromate cement
¡@ Neomycin sulphate topical medicaments

rubber products (shoes,
¡@ Thiuram mix
balloons), pesticides
Paraphenylenediamine hair dyes, azo dyes, fur dyes,

¡@
free base leather dyes, photodeveloper
in all almost all trades and

¡@ Cobalt chloride, 6H2O industry, nickel and cobalt
often occur together
¡@ Benzocaine topical anaesthetics
glues, paper, clothing,

¡@ Formaldehyde
cosmetic e.g. shampoo
adhesive plasters, paper,

¡@ Colophony
plaster, polishes and waxes
antiseptics in topical
¡@ Quinoline mix
therapeutics
¡@ Balsam of Peru cosmetics (perfumes, flavours)
¡@ Black rubber mix rubber products
¡@ Wool alcohols lanolin, vehicles
¡@ Mercapto mix shoes, rubber products
glues, pastes, insulator,

¡@ Epoxy resin
building material
preservatives and vehicles in

¡@ Paraben mix
medicine and cosmetics
Paratertiarybutyl phenol leather, adhesive and rubber

¡@
formaldehyde resin systems
¡@ Fragrance mix stabilizer in medical products
Ethylenediamine
¡@ medicaments
Dihydrochloride
¡@ Quaternium 15 cosmetics
earrings, metal tools, clothing

¡@ Nickel sulphate
accessories, cheap ornaments
the allergen in P obconica,

¡@ Primin which mingle with house dust
causing dermatitis.
¡@ Mercaptonbenzothiazole plant
Sesquiterpene lactone
¡@ ¡@
mix
3.3. Common Patterns of Hand Eczema

3.3.1. Pompholyx
1) Recurrent eruptions of minute, non-inflammatory, vesicles on fingers,
palms and soles is characteristic. Pruritus is common, sometimes lesions can
be painful or it may be asymptomatic. Scratching of vesicles leads to
weeping and crusting.
2) Management
KMnO4 soaks, oral antihistamines and application of mid to high potency
steroids for mild cases. A short course of oral steroid is required for severe
cases. Psychological factors are important. Counselling, behavioral
modification may be necessary.
3.3.2. Keratolysis Exfoliativa
This is a common chronic asymptomatic non inflammatory bilateral peeling
of the palms and soles. Its cause is unknown. The eruption is most common
during the summer months and often associated with sweaty palms and
soles. Scaling starts simultaneously from several points on the palms or soles
with 2 or 3 mm in diameter round scales that appear to have originated from
ruptured vesicles; however, such vesicles are never seen. The scales continue
to peel and extend peripherally, forming larger roughly circular areas that
resemble ringworm, while the central area become slightly red and tender.
The condition resolves in 1 to 3 weeks and requires no therapy other than
lubrication.
3.3.3. Fingertip Eczema
A very dry chronic form of the palmar surface of finger tip. Usually of
unknown cause, but may be the result of an allergic reaction. One or several
fingers may be involved. Initially the skin is moist; gradually becomes dry,
cracked and scaly. The process usually stops shortly before the distal
interphalangeal joint is reached. Fingertip eczema may last for months or
years and is resistant to treatment. Treatment is by avoiding irritants and
frequent lubrication. Topical steroid with or without occlusion may give
temporary relief. Tar is an alternative treatment. Allergy and psoriasis may
have to be excluded.
3.3.4. Ring Eczema
An irritable patch of eczema under a ring and tends to spread to adjacent
area. This affects mainly young women soon after marriage or childbirth. If
the ring is transferred to the other hand, the eczema will appear at the new
site. The cause is due to concentrations of detergent beneath the ring and
repeated friction. Removal of the ring often brings remission.
3.3.5. Hyperkeratotic Eczema
Plaques of yellow-brown dense scale increase in thickness and form deep
interconnecting cracks over the surface, similar to mud drying in a river bed.
Occurs on the palms and occasionally soles. Hyperkeratotic eczema may
result from allergy or excoriation and irritation, but in most cases the cause
is not apparent. Differential diagnoses may be psoriasis and lichen simplex
chronicus. They may respond to potent steroid and occlusion, but recurrence
are frequent.
3.4. Nummular Eczema
Nummular eczema (discoid eczema) is characterized by circular or oval
plaques of eczema with a clearly demarcated margin . The typical
lesions are coin-shaped, 1 to 5 cm in diameter itchy plaques. There are
commonly distributed on the extremities and can become generalized. Acute
lesions may be vesicular; chronic lesions may become scaly, cracked and
confluent.
2) Differential diagnoses
Allergic or irritant contact dermatitis have primary lesions conform to area
exposing to allergens/irritants, and a contact history is often present.
Ringworm infection presents as annular, scaly erythematous patches or
plaques with central clearing. Psoriatic plaques are well marginated with
prominent scales. Irritation is variable. Lesions of chronic superficial
dermatitis are dry, indolent patches.
3) Management
Treatment is similar to other forms of eczema and depends on the stage of
activity. A course of mid to potent topical corticosteroid combined with
topical or systemic antibiotic is effective since infection is commonly
associated; however, relapse is not uncommon.
3.5. Asteatotic Eczema (xerotic eczema, eczema craquele)?
1) Diagnostic feature
Lesions are mainly distributed over the hands and legs; and consist of
minute, thin fissures, with minimal inflammation.
It commonly occurs in the elderly and people with dry skin especially in
winter times when the humidity is low. The condition is thought to due to a
reduction of in skin surface lipid. Distal parts of the extremities especially
the legs are affected. The skin is dry, slightly scaly and criss-crossed on the
surface to produce a reticulate pattern. The borders of this reticulation can
become erythematous and slightly raised, and finally eczematous. The
patient feels itchy, sting and burnt.
3) Management
The mainstay of treatment is to reduce moisture loss and to maintain the
surface lipid layer. Reducing the bathing frequency to an acceptable level;
avoiding hot bath, restricting soap are good measures. Ordinary soaps should
be replaced by soap substitute and emollients should be used as frequently as
appropriate. Inflammation can be controlled by application of mid potency
topical steroid ointment.
3.6. Stasis Dermatitis (Gravitational eczema, Varicose eczema, Venous
eczema)
A history of preceding non-inflammatory swelling, distributed over the
ankles and association with varicose veins.
Acute inflammation is characterized by a red, superficial, itchy plaque with
weeping and crusting on the lower limbs especially the medial side of lower
legs, ankles and calves. This is due to a combination of eczematous changes
and cellulitis. A vesicular eruption (id reaction) on the palms, trunk,
extremities sometimes accompanies this acute inflammation. In subacute
and chronic stages, an increased hydrostatic pressure lead to extravasation of
red blood cells from the leg veins. Disintegration of these red blood cells
lead to haemosiderin deposition. The skin looks dry, scaly, hyperpigmented
and accompanied with white atrophic changes ('atophie blanche'). Ulceration
is common in the late stage and is a serious consequence.
3) Aetiology
Venous insufficiency is a major factor but not all patients with venous
insufficiency develop stasis eczema. Allergic response to an epidermal
protein antigen created through increased venous pressure, susceptibility to
minor trauma and irritation are the contributing factors. Patients with stasis
eczema are more prone to develop hypersensitivity reaction to topical
medicaments. Topical medicaments that contain potential sensitizers such as
lanolin, benzocaine, parabens and neomycin should be avoided by patients
with stasis disease.
4) Management
The dry eczematous inflammation can be managed with lubricants and
topical corticosteroids. Moist exudative inflammation and moist ulcers
respond to tepid wet compress of KMnO4 solution several times a day. Any
infection should be identified and treated promptly. Oral antibiotic
appropriate to the organism is more preferable than topical antibiotic which
should be avoided. Physiotherapy, elevation of legs and compression
stocking are helpful. Patients with varicose veins should be referred to the
vascular surgeons for early assessment and prompt treatment.
3.7. Lichen Simplex (Circumscribed Neurodermatitis)
1) Definition
Lichenification denotes a cutaneous response to repeated rubbing or
scratching. It is characterized clinically by a thickened appearance of the
skin, with accentuation of the surface markings so that the affected skin
surface resembles tree bark. Lichen simplex is a circumscribed area of
lichenification resulting from repeated rubbing and scratching occurring on
some predilected sites. This term is used when there is no known
predisposing skin disorder.
2) Clinical features
Women are more common affected than men. Pruritus is the predominant
symptom and is often out of proportion to the extent of the objective
changes. During the early stages the skin is reddened and slightly
oedematous, and the normal markings are exaggerated. The redness and
oedema subsided and the central area becomes scaly and thickened and
sometimes pigmented. Almost any sites are affected, but the commonest
sites are those that are conveniently reached. The usual sites are the nape of
the neck, the lower legs and ankles,. the sides of the necks, the scalp, the
upper thighs, the vulva, pubis or scrotum and the extensor forearms.
3) Management
A search for a causation should be made before the lichenification is
considered to be primary, then a careful psychological history should be
taken and the patient given some assistance in reducing her tensions. Topical
steroid is the treatment of choice, sometimes with occlusion to enhance
absorption and prevent further scratching. Intralesional triamcinolone is
useful for circumscribed chronic lesions. Topical antibiotic may be
prescribed if secondary infection is present.
3.8. Seborrhoeic Dermatitis
Seborrhoeic dermatitis is characterized by a distinctive morphology (red,
sharply marginated lesions covered with greasy looking scales) and a
distinctive distribution (scalp, face and upper trunk) which are areas rich in
sebaceous glands.
2) Clinical patterns
a) Adult (may be associated with Parkinsonism and HIV infection)
Scalp Dandruff is usually the earliest manifestation. In chronic cases, there
may be hair loss which is reversible when the inflammation is controlled.
Ears are a common site of involvement.
Face Medial sides of the eyebrows, glabella, nasolabial fold, are predilected
sites . Blepharitis is a feature.
Trunk Petaloid form is commoner than the pityriasiform. Follicular papules
with greasy scale that may become confluent, and commonly found over the
sternum and interscapular region.
b) Infantile
The eruptions in infants frequently first appear between the third and eighth
weeks of life. It may start in the napkin area, the face and scalp, and
occasionally on the trunk outside the napkin area. The rash comprises well-
defined areas of erythema and scaling with tiny vesicles. Papular and
lichenified lesions are not seen. Typically the infant is well and not irritable
(c/w atopic dermatitis). The prognosis is usually good. Most uncomplicated
cases clear in 3 to 4 weeks.
3) Differential diagnoses
Psoriasis, pityriasis rosea, pityriasis versicolor, drug eruption and lichen
simplex in adult. Intertrigo, irritant contact dermatitis, atopic dermatitis,
psoriasis, histocytosis X and eczematous eruptions in immunodeficiency
disorders in infants.
4) Management
a) Adults
Ketoconazole shampoo is very effective in removing dandruff. Shampoos
that contain salicylic acid, selenium sulphide, zinc pyrithione and tar are
alternatives. For thick scalp scale and crust, sulphur salicylic emulsion can
be applied before bed and shampooed next morning. Steroid lotion applied
twice daily provides symptomatic relief but may relapse.
Lesions on face, chest can be treated by weak topical steroid and
antiseborrhoeic shampoo. Washing the affected areas with soap can be a
useful adjunct. 2% Ketoconazole cream once a day is highly effective in
difficult cases.
Scaling of blepharitis may be suppressed by frequent washing with zinc or
tar containing antidandruff shampoos. Prolonged use of steroid lotion on the
eyelids causes glaucoma and should be avoided. 2% ketoconazole cream
once a day should be tried in resistant cases.
b) Infants
Cradle cap should be oiled regularly with warm olive oil and washed off few
hours later with 5% cetrimide shampoo. Erythema and scaling on the body
can be treated with weak topical corticosteroid cream +/- topical antibiotic if
infection is present. Shampoo that contains salicylic acid or selenium
sulphide should be avoided in neonates for the risk of systemic absorption.
PSO RI ASI S
Dr. K.K LO & Dr. L.Y. HO
CH APTE R 4
1. INT RO DU CTI ON
Psoriasis is a chronic inflammatory disease of unknown cause. It is now
considered to be due to T-lymphocytes mediated disease of abnormal
keratinocyte proliferation in genetic predisposed subject. In 1995, Psoriasis is the
sixth commonest skin condition found in all new cases attending dermatology
clinics of Social Hygiene Service (4.18% of all new cases) and it is one of the
common skin diseases worldwide. Although there is no study in the
documentation of the exact number of psoriatic patients or prevalence of the
disease in Hong Kong, the disease is commonly presented even in the primary
care setting. There had been analysis in the figure of some local dermatology
clinics of Social Hygiene Service in 1974 to 1976 and comparison with some of
the larger cities in China, Taiwan and Japan claiming the number of psoriasis in
the Mongoloid race to be around 0.3% or well below 1%.
2. CL INI CAL FE ATU RE
Psoriasis is a chronic erythemato-squamous condition characterized by sharply
circumscribed salmon pink patches, plaques covered with silvery scales. The
onset of the disease is usually gradual and becomes noticeable by the patient
from 30 years onwards. However, in patient with family history positive for
psoriasis, there may be earlier onset at teenager or even below ten. In these
cases, the prognosis is worse. From a study in China, the majority (97.98%) of
the types of psoriases is the psoriasis vulgaris or chronic plague type. We have
similar experience in Social Hygiene Service with over 91% of the psoriasis are
chronic plaque type (see Table 1).
The classification of psoriasis may vary with different author's preference but for
simplicity and practicability, we take the following classification for psoriasis: I)
Non-pustular psoriasis II) Pustular psoriasis III) Psoriasis with arthropathy. They
can be subclassified further into:
2. 1. No n- pu st ula r Pso ri asi s
Chronic Plague type
Acute Guttate
Inverse, flexural
Erythrodermic
Regional: Scalp, palms & soles, nails
Unstable nummular
Sebo-psoriasis
2. 2. Pu st ul ar P so rias is
Generalized Pustular psoriasis (von Zumbusch)
Localized pustular psoriasis of palms & soles
2. 3. Ps or iasi s w ith Ar th ro pa th y
5 Types of arthropathy found: oligoarticular asymmetrical arthritis, symmetrical
involving small joints of fingers likes rheumatoid arthritis, classical distal
arthropathy involving distal interphalangeal joints, destructive arthritis mutilans
and psoriatic spondyloarthropathy which is similar to ankylosing spondylitis.
Two interesting phenomena occur in Psoriasis. They are mutually exclusive:
Koebner and reverse Koebner responses. Any form of trauma may result in
psoriasis appearing in the traumatized areas which is known as Koebner
phenomenon or isomorphic response. A degree of healing may occur when a
psoriatic plague is traumatized which is the reverse Koebner phenomenon. It also
explains why some patient found cryotherapy is useful to suppress psoriasis.
The commonest form of psoriasis is the chronic plague type which usually
presents as brightly erythematous scaly plagues at the predisposed areas i.e. the
extensor aspect, the tip of elbows, knees, sacral area, the scalp. They may be
associated with no symptoms to moderate pruritus. Excessive dandruff and
scaling from the lesional area may be an early complaint. Family history is not
very commonly found in this group because the other family members may not
have the disease at all or if possess, usually in a very mild degree. Patient may
have history of acute guttate psoriasis before but it either never clears or
reappears as plague form. The most useful form to confirm the diagnosis is to
use the wooden spatula to scrape the surface of the suspected lesion, profuse
silvery scaling can easily be generated

. The well demarcated border of the plague, the prominent scaling, other
associated findings such as symmetrical distribution with scalp involvement,
Auspitz¡¦s sign (to forcibly remove the superficial scaling of top of the psoriatic
plague will reveal the fine dots of bleeding points) and the characteristic colour
which is also quite obvious in Chinese patients will lead to the diagnosis of the
disease without difficulties. The course of the disease is very chronic. We
seldom see a case of persistent, sustained long term remission because either
remission may not be common (it had been quoted from 20 to 50% when
following the psoriatic patient long enough e.g. 50 years), or remitted patient
will not turn up in the clinic to thank you, or patients seen by different doctors
every time attending Social Hygiene Clinic. It usually waxes and wanes, tend to
improve in summer and worsen in winter. However, with correct therapy,
majority can lead normal life and there is definitely a chance of spontaneous
remission though the younger the onset of the disease, the more likely it will
persist till elderly. The presence of a strong positive family history will be
another poor prognostic factor.
However, other forms of psoriasis though much rare, they do present diagnostic
problem occasionally. The erythrodermic psoriasis may be mistaken as other
causes for erythroderma such as seborrhoeic eczema, drug eruption, pityriasis
rubra pilaris. Flexural psoriasis may lack the prominent silvery scaling because
the flexural areas affected usually appear as brightly erythematous, homogenous,
well defined and sharply demarcated plaque or patch with or without super-
infection with Candida.
Acute guttate psoriasis is often preceded by a history of sore throat 10 days to 2
weeks ago. It may be a streptococcal infection. The small guttate maculopapular
scaly lesion still have the characteristic feature of psoriasis and hence there will
be no diagnostic problem. Occasionally, pityriasis rosea, pityriasis lichenoides
have to be excluded. The course of the disease initially will go into remission in
few months time but it can reappear after another attack of infection and many
do gradually become a chronic plaque type case.
Regional psoriasis involving scalp, palm and soles are relatively common. They
are often misdiagnosed as seborrhoeic dermatitis, keratoderma or chronic
eczema of hand and feet before the more definite sign of psoriasis appear.
Fortunately, the types of treatment do not differ much. Unstable nummular
psoriasis can occasionally be seen and they have tendency to change from time
to time, to either erythrodermic psoriasis or pustular psoriasis. There is low
erythema threshold in this group of patients. Usually they are found in patients
with psoriatic arthropathy. Topical irritants or sudden withdrawal of topical
steroid may prone this group of patients flaring up of their diseases and they may
be required hospitalization for stabilization.
Localized pustular psoriasis of palms and soles usually present as symmetrical,
monomorphic eruption of small sterile pustular eruption on hands and feet. They
are painful rather than pruritic. Very often, brownish thick wall pustules are
found. They are resistant to treatment and will be quite disabling. Another form
of local pustular psoriasis is asymmetrical involvement affecting distal phalanx
with nail destruction. It is called acrodermatitis continua. It may change to
generalized pustular form.
Generalized pustular psoriasis can present in a psoriatic prone patient who is
given systemic steroid for other conditions and upon sudden withdrawal of the
steroid, generalized pustular psoriasis will be precipitated for the first time.
Occasionally, it develops from the unstable nummular psoriasis or acrodermatitis
continua after inappropriate irritant therapy or withdrawal of extensive topical
steroid. Pregnancy can sometimes associate with the generalized pustular
psoriasis. There are low grade fever, pain and burning sensation over the
pustules. Systemic and constitutional upset may be severe. This requires in-
patient management with bed-rest and institution of transient systemic therapy.
Many doctors may not consider the existence of this condition: sebo-psoriasis or
seborrheic psoriasis. Very often, we can encounter conditions in which both
psoriatic and seborrheic eczema features are present. We consider this a separate
entity because it is not rare. Genetically constituted psoriatics can develop
seborrhoeic eczema lesions at the scalp, eyebrows and regions of ears with
characteristic morphology of psoriasis at these sites.
Nail involvement is commonly seen in all types of psoriasis which can

affect the nail matrix and nail bed leading to pitting, discoloration, subungual
hyperkeratosis, onycholysis, splinter hemorrhage. Circular area of discoloration
of nail bed resembling an oil drop underneath the nail - oil drop sign is most
characteristic for psoriatic nail.
Patients with AIDS develop severe recalcitrant form of psoriasis and psoriasis
related disease such as Reiter¡¦s disease. The use of etretinate and anti-viral
therapy such as zidovudine are necessary to control this type of psoriasis.
The clinical features of psoriasis especially chronic plaque type is so obvious
and unique that seldom requires further investigations. However, differential
diagnosis should be remembered especially for other types of psoriasis. Eczema,
psoriasiform drug eruption, lichen planus , discoid lupus erythematosus,

lichen simplex chronica, pityriasis rubra pilaris, secondary syphilis, Bowen¡¦s
disease, Paget¡¦s disease and superficial fungal infection will mimic chronic
plague type psoriasis. Pityriasis lichenoides chronica, pityriasis rosea can
resemble guttate psoriasis. Candidal intertrigo, Hailey disease may be mistaken
as flexural psoriasis. The keratoderma blenorrhagica (palmoplantar lesions) of
Reiter's disease will be indistinguishable from localized pustular psoriasis.
3. IN VESTI GAT ION

Skin biopsy is the most useful investigation e.g. in erythrodermic psoriasis. The
typical histopathology of psoriasis (non-pustular form) is characterized by: 1)
regular elongation of the rete ridges with thickening in their lower portion. 2)
elongation and edema of the papillae. 3) thinning of the suprapapillary portions
of the stratum malpighii with the occasional presence of a very small spongiform
pustule. 4) the absence of granular layer 5) parakeratosis 6) presence of Munro
microabscesses.
Radiological examination of the affected joints may confirm the psoriatic
arthropathy. The following findings are characteristic signs of psoriatic
arthropathy: 1) destructive distal interphalangeal arthropathy with bony ankylosis
of the interphalangeal joints 2) abnormally wide joint spaces and well
demarcated adjacent bony surfaces 3) bony proliferation of distal phalanx in
great toe 4) resorption of tufts of distal phalanges of hands & feet.
4. MA NA GEMENT I N S OC IAL H YG IENE SE RV ICE

4. 1. Ge neral
Management of psoriasis requires a complete thorough history not only for the
disease activities but also to include information about how the patient perceive
and handle this condition in the past, the past treatment, the failed treatment and
possible the cause of failure of the treatment. The sex, occupation and social
background are all important factors to consider in the management and it will
be very true that every patient will present an entirely different problem. The
degree of acceptance of the condition by the patient and the knowledge on the
condition will also affect the management plan.
Dietary manipulation has no place in management of psoriasis. Stress is one of
the factor contributory to flare up of the condition though not agreed by all and
stress can also be one of result of deteriorating psoriasis. Chinese herbs are not
recommended because no single good control study have proven these to be
effective alone without using the traditional western anti-psoriatic medication
simultaneously. Many harmless placebo have been tried on this condition and it
will not be surprising to read one or two reports claiming good effect on
psoriasis, the progression of which can be affected by so many factors.
Alcohol intake should be discouraged because there is a positive correlation
between psoriasis and alcohol intake and alcohol induced liver problems may
preclude patient from receiving effective systemic therapy in future. Medications
such as lithium, salicylates, iodine, beta blockers, naprosyn and penicillin have
been implicated in exacerbating psoriasis. 80% of patients with psoriasis find
that sunlight improves their conditions but the rest may find no change or even
exacerbation. However, sunburn is always a precipitating factor because the
scalded area will heal with new crops of psoriasis (the Koebner's phenomenon).
Streptococcal infection if persistent or carried in the deep tonsil crypts should be
eradicated with a course of antibiotics.
Some of the known aggravating factors if correctable should be removed or
avoided. Climatotherapy can only be afforded by the rich and retired patients.
4. 2. To pi cal
4.2.1. Emollient
It is indeed very useful to decrease fissure, cracking and scaling. Aqueous cream,
Ung Emulsificant and 10% urea cream are commonly used by Psoriatics.
4.2.2. Tar
Pinetar, Coal tar are all useful. They can be in the lotion, shampoo, cream, paste,
ointment forms. The commonly used items in Social Hygiene Service are: 3% tar
paste, Ung 2-4-2 or Ung 1-2-1, 1% crude coal tar. They are good for the stable
chronic plaque type. However, slow action, messy and sticky, poor smell,
staining properties are all factors for its low acceptance in patients. Education
and persuasion to patients are necessary to insist using the cream for few months'
time before giving it up. It is an adjunctive component in the Goeckerman's
regimen.
4.2.3. Sulphur and salicylate
2% sulphur salicylate emulsion is a very common prescribed item to thick scalp
psoriasis for its keratolytic effect.
4.2.4. Topical steroid
It is widely used not only by dermatologists but by the primary care doctors.
Moderate potent steroids have to be used to suppress the psoriasis. Good
examples are Synalar, Betnovate, Dermovate creams or ointments. However,
only careful dermatologists will know when to stop them to avoid tachyphylaxis
and rebound of the condition and what to control during the period of
withdrawal. The combination of topical corticosteroid and other topical agents,
such as tar and salicylic acid is often effective in refractory areas. The use of
liposome packaging to increase the delivery of corticosteroids to the epidermis is
under clinical trial in psoriasis.
4.2.5. Topical calcipotriol (Daivonex) cream
It has similar efficacy as that of potent steroid but lacks the local adverse effect
of skin atrophy, rebound phenomena and tachyphylaxis. The main indication is
for chronic plague psoriasis. Its main drawback is irritant dermatitis especially
over flexural and face area. New calcipotriol formulations, gel and lotions, cause
less irritation than ointment. Cutaneous absorption is probably the most
worrisome side effect. The 50 m g/g ointment formulation can be used twice
daily. 100 gm of this ointment used per week is the maximum safety dosage so
as not to induce hypercalcaemia. An arbitrary pulse topical therapy can also be
adopted. Topical Calcipotriol ointment or cream is used in weekdays but it is
switched back to potent topical steroid in weekend and off all medication on
Sunday. It will help to reduce tachyphylaxis of steroid.
4.2.6. Dithranol
0.25% dithranol in Lassar paste can be tolerated by some patients with plaque
type psoriasis at the shins, elbows and knees and with good therapeutic result.
However, careful instruction of how to use and olive or mineral oil to remove
the paste have to be prescribed as well. In-patient will be a good chance of
giving a trial of this preparation. Adjunctive phototherapy as in Ingram regimen
will be very helpful but only is possible in in-patient or day care centre. The
commercial preparation of 1 to 4% Dithranol ointment is good for the SCAT
(Short contact Anthranol therapy). It is because the staining and stinging
sensation that most patient dislike this regimen.
4. 3. Sy stem ic T herap y
The indications of systemic therapy will vary from one patient to the other
because the degree of severity will be perceived differently by different patients
with some correlation to the need or occupation of the patient. The choice of
treatment depends on a number of factors such as:
severity, extent, site of disease
compliance, intelligence of patient
sex (chance of conception), age of patient
presence of other systemic illness or skin conditions
financial and time factors, motivations
limiting factors from available treatment facilities
distance from treatment centre to home or working place
the type of psoriasis
4.3.1. Etretinate (Tigason)
Avoid using the medication in reproductive female in order to prevent pregnant
patient receiving the drug which is teratogenic. Absolute contraception must be
practiced in some difficult case and this must be continued for two years after
stopping the medication (because of high lipophilic property and long
elimination half-life of 80 days). The newer acitretin was found to be of much
shorter half life (elimination half-life of 50 hours) but because of some
conversion back to etretinate was detected, its enthusiastic future is jeopardized.
Avoid treating patients with overt symptoms of ischaemic heart disease or
patients that are at definite risk for developing atherosclerosis. Handle patients
with preexisting hyperlipidaemia carefully, it is a relative contraindication.
Dietary regulation and recommendations about increase physical activity should
be given. Low fat, low calorie diet, avoidance of alcohol intake and increasing
physical activity are effective in reduction of hyperlipidaemia induced by the
drug. Hyperostoses can be induced after several years of continuous treatment
with etretinate.
Minor side-effects are unavoidable and dose related. Dryness of the lips, nasal
mucosa, eyes, mouth, throat or vagina, painful exfoliative cheilitis, urethritis,
balanitis, gingivitis, peeling of finger tips and corneal ulceration, burning
sensations in the skin, diffuse alopecia, epistaxis, widespread erythema will be
present to various degree. Slight elevation of liver enzymes may be found. Toxic
hepatitis may occur especially when it is combined with methotrexate. The long
term effect of hyperlipidaemia, hyperostosis resembling diffuse idiopathic
skeletal hyperostosis (DISH) will be problematic in psoriatic patients on long
term etretinate therapy.
The initial dose will be between 0.5 mg and 1 mg/kg/day. The response is very
often dose related. Dose reduction is possible when it is used in combination
with phototherapy or photochemotherapy. They are one of the most effective
combination in clearing psoriasis. Etretinate alone seldom can control psoriasis
perfectly and useful adjunctive therapy with phototherapy, PUVA, steroid cream
will be very synergistic. It may also be used in generalized pustular psoriasis
although methotrexate works as good or better.
Etretinate is indicated for moderate or extensive psoriasis, pustular psoriasis and
psoriasis resistant and poorly controlled with all forms of topical therapy. Patient
should be excluded for the following conditions before initiating treatment: liver
disease, hyperlipidaemia, pregnancy or potential pregnancy, previous history of
hypersensitivity to retinoid and history of elevate cerebrospinal fluid pressure.
Monitoring with fasting lipid level and periodic liver function are required
monthly initially and then every few months when stabilized.
4.3.2. Methotrexate
It is a magic drug for psoriasis provided adequate monitoring is provided. It is
given as once weekly to once biweekly doses. An initial test dose of 2.5 mg was
given and complete blood picture and liver function test should be monitored for
a few days before the full planned dose is given. Usually 7.5 to 25 mg per week
as a single dose can be given according to body weight of patient and response
of disease. Before initiating treatment, renal (renal function tests), hepatic
function (history, liver function tests and if feasible a preliminary liver biopsy),
and complete blood picture should be taken to ensure no contraindication. Peptic
ulcer and infection must be treated before starting therapy. Impaired renal
function must be accompanied by dose reduction. Continuous recording of the
cumulative dose in a chart together with liver, marrow and renal function will be
very helpful. Complete blood picture and liver function test should be taken
regularly every month initially and then every 3 to 6 months for monitoring.
When the cumulative dose reach 1.5 to 2.0 gm, a liver biopsy is advised and this
investigation at present is not replaceable by other methods, e.g. hepatic or CT
scan. Early fibrosis and cirrhosis found in biopsy are indications for stopping the
therapy whereas fatty change and mild inflammatory changes can allow
continual therapy if the condition is compelling. If patient refuse to have the
liver biopsy, no more methotrexate should be give. For those who have normal
result on liver biopsy, another cumulative dose of methotrexate of 1.5 to 2.0 mg
reached before the second biopsy done to monitor the liver function. This usually
takes 2 to 3 years.
The guidelines for liver biopsy of patients receiving methotrexate is now
controversial. Low dose (< 15 mg weekly), long term methotrexate may be less
hepatotoxic than previously thought and liver biopsy is not entirely without risk.
Therefore risks and cost effectiveness should be carefully balanced.
Methotrexate is teratogenic and conception is not advised within 3 months of
stopping treatment. Other side effects include: anemia, leukopenia, anagen
alopecia, cutaneous erosions, ulceration, reactivation of tuberculosis, septicemia,
gastrointestinal bleeding, oligospermia, anorexia, nausea.
Despite all these side effects, methotrexate is highly effective for many forms of
psoriasis and also psoriatic arthropathy. It is available as 2.5 mg tablets and
injection form (for intramuscular injection).
4.3.3. 5-Hydroxyurea
Hydroxyurea causes short term reversible marrow suppression and hence
complete blood picture must be monitored closely. It is given from 500 mg daily
to 1,500 mg daily with a modest fall in hemoglobin expected. Mild GI upset may
be associated. It is unfortunately not very effective in many psoriatic patients and
it is of slow onset. The therapeutic effect may not be apparent after 2 months of
therapy. It can be tried for patient with impaired liver function.
4.3.4. Cyclosporin A (Sandimmun-Neoral)
This is a powerful medication. Improvement may be seen within few days with a
dose of 3 mg/kg/day. If there is no improvement within 2 weeks, the dose may
be increased by 0.5 to 1 mg/kg/day at a 2-weekly interval to a maximal dose of 5
mg/kg/day. Maintenance dose should be reduced to the smallest dose that allows
adequate control. Relapse is inevitable after cessation of treatment but
fortunately rebound is not a problem.
The most important side-effects are dose related hypertension and
nephrotoxicity. Hence blood pressure and renal function (creatinine clearance)
should be closely monitored in the first few weeks, then monthly. Other side-
effects include gum hyperplasia, hypertrichosis, acral paraesthesia or
hyperaesthesia, tremor and dyspepsia.
Cyclosporin should not be given to patients with renal dysfunction, uncontrolled
hypertension, past or present malignancy, acute infections, pregnancy, lactation
and known hypersensitivity. Cyclosporin is expensive but this low dose regimen
for psoriasis is the last resort for patients with resistant psoriasis to other
therapies or contraindicated for one reason or another. Even if the patient can
afford to purchase the medication himself, it should not be used indiscriminately
because the theoretical risk of prolonged immunosuppression and possible risk
of lymphoproliferative malignancy.
4. 4. Ph ot oth era py a nd P ho toc hemo the rap y
4.4.1. UVB Phototherapy
Suberythemogenic doses given 2 to 3 times weekly can clear psoriatic lesions in
a few weeks. The compliance of patient depends very much whether the patient
can afford to spare time for this form of treatment. The power of Phototherapy
unit varies one from the other. In old models, the irradiation time may well be
over 10 to 20 minutes but newer models will deliver the MED (minimal
erythema dose) within 100 seconds.
At the first visit, a test area is needed with increasing doses of UVB to find out
the optimal doses. Usually the darker the skin, the greater dose is required for
reaching the MED (similar the skin types in Caucasian). It has been estimated in
the West temperate regions, the annual UVB dose an outdoor worker receives is
500 MEDs, while an indoor worker receives 200 MEDs. A psoriatic patient on
maintenance therapy receives more than 700 MEDs. The long term life-time
incidence of non-melanoma skin cancer in patients receiving long term UVB
phototherapy is estimated to be three times to eight times that of normal. Long
term follow up later in life is necessary in order to pick up skin cancer. The other
side effects include pruritus secondary to xerosis, sun burnt and flare up of
Herpes Simples infection.
Emollient applied on the skin before irradiation will enhance the therapeutic
effect and it will antagonize the drying effect of UVB phototherapy. Cumulative
dosage of UVB should be recorded clearly in patient¡¦s record. The addition of
etretinate will help to lower the dosage or frequency of UVB phototherapy. In
pregnant psoriatic woman, phototherapy may be the best to control psoriasis and
least effect on the fetus.
4.4.2. Goeckerman Regimen
This is mainly a regimen for in-patient or day care centre patient. It is a time-
consuming but effective methods. The combination of rest, tar, phototherapy all
contribute to the success of this form of therapy.
Patient is treated either in day care centre or dermatology wards. Experienced
dermatology nurse will be essential to carry out this form of therapy. 1% crude
coal tar will be applied in the morning and again at afternoon. In the later part of
morning the residual tar is removed by bathing with Liquor Picis Carbonis and a
suberythemogenic dose of UVB is administered, follow which the tar is
reapplied. Tar is best applied with a paintbrush or a wooden spatula covered with
layers of tubular cotton gauze. Dressings maybe applied before the tar dries. No
powder is needed. The removal of tar is best done by softening the tar with an
application of coal tar and salicylic acid ointment, followed by the tar bath. The
main complication of this treatment is folliculitis. Majority of the patient will
have extensive plaque psoriasis cleared, thinned or controlled after 3 weeks
treatment.
4.4.3. Ingram Regimen
It is similar to that of Goeckerman regimen except that 0.25% Dithranol in
Lassar Paste is applied instead of 1% crude coal tar. It is applied once daily
usually after the UVB therapy. It is difficult to spread in applying the paste to
the lesions. Since dithranol is a strong irritant and stains linen, accurate
localization of the medication is needed to prevent burning of the normal
surrounding skin which may be protected by using some barrier cream e.g. zinc
cream surrounding the psoriatic lesions. It is not used in pustular psoriasis and
unstable psoriasis. Dusting with talcum powder and covering with old nylon
tights helps to prevent the spread of dithranol especially if a modern ointment
form is used instead of the lassar paste product. Olive or mineral oil may be
needed to remove the stiff paste before going to take the tar bath prior to UVB
therapy. It has similar efficacy as that of Goeckerman regimen.
4.4.4. PUVA (Systemic and Topical)
0.6 mg/kg of 8-methoxypsoralen is taken orally by patient 2 hours before
irradiation with UVA (320-400 nm). New model of PUVA machine can irradiate
the whole body while patient has to stand upright in the chamber. Old model
machine can only radiate one side of body at a time but with the advantage that
patient can lie down comfortably. Eye protection is important. During irradiation
and after taking the drug that day, patient must wear UVA opaque goggles to
prevent cataract and acute photosensitivity of the eyes. Patient is required to
have treatment at the day care centre two to three times a week. In Chinese
patient, the initial dose can be 2 J/cm2 and then step up the dosage carefully by
0.5 J/cm2 each visit till the optimal dose is reached which may be as high as 8 to
15 J/cm2. Acute PUVA burn can result from a too high initial dose for sensitive
patient. Usually 15 to 25 treatment will complete one course and maintenance
treatment can be given with weekly or biweekly PUVA for 3 more months. If
the psoriasis remains quiet, it can be managed with topical therapy only. In later
phase, if there is flare up of condition, a new course will be given again. The
duration to complete each course will require 2 to 3 months. When cumulative
dose of 2,000 J/cm2 reached, PUVA is usually not advised to be continued
because of the substantial increase risk of skin cancer. Patients with cutaneous
malignancy potential are excluded for PUVA e.g. Arsenic ingestion,
radiotherapy. PUVA is of value in generalized pustular psoriasis, erythrodermic
psoriasis, chronic palmoplantar pustular psoriasis.
The topical PUVA can be given applying similar principle except that the
psoralen is given not in oral form but in the form of topical lotion (the
Meladinine Paint) which is particularly convenient for local palm and sole
psoriasis. However, phototoxic reaction is more common. The UVA is given as
soon as 10 to 15 minutes after the application of the paint. It is commonly used
to treat Vitiligo which is limited to the face. Very extensive application of the 8-
MOP paint is not advisable because of the phototoxic effect and absorption of
enough 8-MOP requiring protection of the eyes as in systemic PUVA. However,
topical PUVA requires no systemic medication and patient with gastrointestinal
upset of 8-MOP will tolerate topical PUVA and smaller dose of UVA delivered
with fewer side effects to normal skin.
The adverse effects of PUVA are: Erythema, nausea, pruritus, gross freckling
(PUVA lentigines), hyperpigmentation, onycholysis, cataract, increase non-
melanoma skin cancer risk, cutaneous pain and burning sensation, precipitate
photosensitive condition such as lupus erythematosus, reduction of delayed
hypersensitivity and flare up of herpes.
4. 5. Co nc lu si on i n t he Trea tmen t Mo da lit ies i n S oci al Hy gi ene
Ser vi ce
The commonest form of treatment for mild psoriasis is topical steroid. For
moderate plaque type psoriasis, the topical therapy is usually an adjunctive
therapy and the combination of etretinate and phototherapy of
photochemotherapy usually have the best result. For severe cases, admission to
hospital is necessary for management because bed rest and away from work can
already lead to more stable condition. Moreover, the trial of in-patient regimen
will work at most time. The last resort is Cyclosporin A. All the systemic
therapies have to some extent harmful to the body. They should be selected and
supervised by experienced dermatologists. Systemic steroid is very effective in
controlling psoriasis but it is deliberately not listed because it will do more harm
than good in the long term management. Very often, you may find that there are
more problems than before when starting a psoriatic patient with systemic
steroid. However, systemic steroid will be given to the poorly controlled pustular
psoriasis of pregnancy, life threatening erythrodermic or generalized pustular
psoriasis. Very rarely, bullous pemphigoid can be associated with psoriasis.
Systemic steroid is needed to treat the bullous pemphigoid and psoriasis will also
benefit at the induction high dose. However, a steroid sparing agent has to be
started early to prevent flare up on reducing the steroid dose after control of
bullous pemphigoid. All these conditions should only be given in in-patient
under the supervision and advice of consultant dermatologist.
5. OTHE R TRE ATMENT

There are some other forms of treatment for psoriasis not practiced in Social
Hygiene Service. They are not used because they are either not gaining
consistent results or their limited experience with one or two reports of success
or requiring special treatment facilities. Some of the initial improvement may be
solely placebo effect. These are mentioned because they signify how
disappointing the treatment to some form of psoriasis and that we are always
trying to seek new treatment breakthrough for psoriasis.
The treatment of psoriatic nail do place a dilemma for dermatologists.
Intralesional corticosteroids injecting to the nail matrix may control some nail
dystrophy but it is painful and the control is not complete and not always
successful. Avulsion of grossly deformed nail will not correct the deformity.
Occasionally, methotrexate or PUVA for extensive psoriasis may also improve
the nail.
Topical treatment: Occlusive dressings with hydrocolloid dressings. Topical
methotrexate, cyclosporin, and retinoids, capsaicin have been studied as potential
topical treatment of psoriasis. It is hoped that new effective topical treatments
allow dose reduction of potent topical steroids and often systemic modalities,
therefore reducing potential toxicities.
Systemic treatment: Sulphasalazine, ketoconazole, acitretin, Fumaric acid, Fish
Oil supplements, Zinc sulphate, Razoxane (withdrawn because of increase
incidence of acute myeloid leukaemia), Azathioprine, Colchicine, Antibiotics,
Piritrexim (withdrawal because of unexpected high incidence of liver damage),
rifampicin, propylthiouracil, benoxaprofen, topical lonapolene, azaribine and
zidovudine for AIDS associated psoriasis.
Selective UVB phototherapy (UV sources with peak effective output in the 300-
320 nm range): Psoralen-311 nm therapy: a narrow-band UVB source emitting
311 nm (compared with conventional PUVA: peak emission at 352 nm) are
shown to be effective. The 311 nm UVB phototherapy alone is also effective.
This source of UVB light has avoided the non-therapeutic but erythemogenic
UVB (of wavelengths of less than 300 nm). Low intensity selective UVB
phototherapy (LISUP) has been designed for home use but they are probably less
effective than conventional phototherapy. The Dead Sea Clinic treatment (helio-
therapy) is basically a form of phototherapy: sun exposure followed by bathing
in mineral rich sea. (It is claimed to be cost effective and pleasant treatment. As
a result, some Scandinavian countries health clinics prefer to fund Dead Sea
Therapy over the expensive in-patient care for chronic psoriatics.)
Others: Alternative medical treatment such as acupuncture, dietary manipulation
programmes, biofeed back, Chinese herbal treatment, homeopathic remedy.
Dialysis, Extracorporeal photophoresis, Propylthiouracil Cryotherapy, Yellow
light laser, carbon dioxide laser, dermabrasion, Grenz ray therapy
Tab le 1 : T ype o f P so ria si s in 1 99 5 ( Derma to log y C lini cs o f S ocia l

Hy gie ne Ser vice )
Conditions Incidence %
Chronic plaque 558 91.6
Guttate 45 7.39
Flexural 0 0
Erythrodermic 1 0.16
Generalized pustular 3 0.49
Localized pustular 2 0.33
All Psoriasis (all new skin cases) 609 (14,569) 4.18
ACNE AND OTHER

1.4. Management
Apart from general measures, topical treatment alone is usually adequate for
patients with mild acne. For more severe acne, combination of a topical
agent and an antibiotic, or with hormonal therapy for female patient, is
required. It is better to combine agents having different mode of actions - for
example a keratolytic with an antimicrobial. For acne conglobate,
isotretinoin is the treatment of choice.
1.4.1. General Measures
Educating the patient on the nature of the disease and daily skin care is
important. The latter should be in form of face cleansing with ordinary soap
and water twice daily. Expensive soap or strong detergent are not necessary.
'Facial' treatment (facial sauna, heat and massage) is not only useless but
may also worsen the condition by precipitating the development of inflamed
lesions. Oily cosmetics and hair greases are comedogenic and causes
prommade acne and should not be used. Squeezing lesions and excessive
cleansing should also be avoided. The psychological aspect of the patient
must not be overlooked especially for those with acne excoriee.
1.4.2. Topical Therapy
1) Benzoyl peroxide
It is an effective antibactericidal and has some anti-inflammatory action as
well. Various strengths (2.5%, 5% and 10%) are available. Since it can cause
irritation of the skin patients should be warned and advised to start with the
weakest strength. The frequency and duration of exposure can then be
stepped up gradually.
2) Retinoic acid
It is a comedolytic, and can increase the basal cell mitosis and epithelial
turnover. Various strength are available in the gel and cream base (Retin A
gel 0.01% and 0.025% ,and cream 0.05 and 0.1%) As it is also an irritant, the
same principle of application like benzoyl peroxide is employed.
3) Topical Isotretinoin
Isotretinoin for topical application is available recently. Its effect is
comparable to topical retinoic acid though it is much less effective than
systemic isotretinoin (see below).
4) Azelaic acid
It is available as 20% azelaic acid in cream base. It act by both inhibition of
the growth of the propionibacteria and decreasing the ductal
hypercornification, and is indicated for comedonic, mild to moderately
severe papulopustular acne. It is a safe topical agent and can be given to
pregnant woman. The cream should be applied twice daily. Although minor
degree of irritation is very common, it is generally well accepted by most
patients.
5) Topical Antibiotics
Although topical antibiotics are less effective than benzoyl peroxide in
inhibiting P. acnes, they are less irritant and better tolerated. Both topical
erythromycin and clindamycin appear to be safe and effective for the
treatment of mild to moderate inflammatory acne. However there is concern
on the possible epidemiological consequences of transferred bacterial
resistance resulting from the use of topical antibiotics.
6) Other topical agents
Sulphur, salicylic acid and resorcinol are agents commonly used in
commercial preparations, probably act as keratolytic and are useful in mild
acne. Topical steroids are sometimes added into proprietary preparations.
Although they are anti-inflammatory and may help to reduce the
inflammatory effects of keratolytics, long-term use is not advisable in acne
patients (c.f. perioral dermatitis).
1.4.3. Systemic Therapy
1) Antimicrobials
Antibiotics act by inhibition of the follicular bacterium, Propionibacterium
acnes. Tetracycline and erythromycin have additional anti-inflammatory
actions. They should be given for 6 months to exert the full effect, though
noticeable improvement may be observed earlier. If the response to one
antibiotic is not satisfactory another one can be tried. These drugs can safely
be continued on a long-term basis if indicated. However, patients should be
made to understand that the treatment is only suppressive and not curative,
and relapse may follow withdrawal of the drug. A pustular folliculitis of the
face due to Gram-negative superinfection is a rare complication of long-term
antibiotic therapy and must be looked out for in case of 'resistance' to
treatment. Culture of the pustules should be done in case of doubt.
a) Tetracycline
This is still the drug of choice, being cheap and effective. It is a
bacteriostatic agent which acts mainly by reducing the acne bacteria
population on the skin. The usual dose is 1 gm/day in divided dosage and
should be taken with an empty stomach. Milk and dairy products should be
avoided. Side effects include GI upset, drug eruption (especially fixed drug
eruption). This group of antibiotic is absolutely contraindicated in pregnancy
and extra caution should be taken in prescribing it to young female patients.
b) Minocycline and doxycycline
Minocycline is more lipid soluble and penetrates the sebaceous glands better
than tetracycline. It has a more persistent effect and bacteria resistance is
less common than tetracycline. Both minocycline and doxycycline are
probably more effective and better tolerated, but more expensive, than
tetracycline. They can be given as a single daily dose (100 mg/day) or in a
divided twice daily dosage. Both drug can cause GI upset and drug eruption
like tetracycline. Other side effects of minocycline include dizziness and
various types of pigmentary change. There is also a recent report revealing
that minocycline is more frequently associated with immunologically
mediated reactions like chronic active hepatitis and lupus erythematosus
than other anti-acne antibiotics.
c) Erythromycin
This is as effective as Tetracycline but resistance develops more rapidly. The
drug is safe in pregnancy, and is preferred to tetracycline for married
woman.
d) Dapsone: previously very useful for treating cystic acne before
isotretinoin is available. Dosage is 100 mg daily. This may cause haemolytic
anemia in G6PD deficiency patients.
e) Septrin: this has been proven effective for acne that does not respond to
conventional therapy. The dosage is one to two tablet twice daily. Because it
can produce severe allergic reactions such as erythema multiforme as well as
blood dyscrasia, it is only recommended for use in refractory patients for
relatively short periods (6 months or less).
f) Ampicillin is used mainly for gram negative folliculitis.
2) Hormonal therapy
This is indicated for women with acne especially for those patients with
features of androgen excess like hirsutism and androgenic alopecia.
Possibilities of androgen excess secondary to diseases like polycystic
ovarian disease should not be overlooked.
Diane 35 (Dianette): is a combination drug of an anti-androgen, cyproterone
with an estrogen, ethinyl estradiol. It is indicated only for women and
especially for those who would consider oral contraceptive pill for
contraception. Cyproterone is teratogenic and the drug is contraindicated in
pregnancy. It is also not used for patients with other risk factors like familial
history of cardiovascular diseases or diabetes mellitus. Patients on dianette
should be followed up regularly for pap smear and blood pressure.
Spironolactone: is an effective competitor of androgen receptor as well as an
inhibitor of 5-a-reductase. The dosage range from 50 mg to 200 mg per day.
Polymenorrhoea may be a problem when high dose is given.
Others: Keotconazole has antiandrogen activity but is limited by its serious
side effects. Cimetidine is a mild antiandrogen and is not clinically useful.
Administration of gonadotropin releasing hormone agonist as a form of
medical castration should only be undertaken by endocrinologists or
gynecologists.
3) Retinoid
13 Cis-retinoic acid (Roaccutane) is a vitamin A derivative with a potent
effect on sebaceous glands. The drug is the treatment of choice for
nodulocystic acne, for acne that is unresponsive to adequate conventional
therapy, and particularly for acne causing scarring. It is given in a dosage of
0.5-1 mg/kg/day orally. Studies have been shown that optimal long-term
benefit can be achieved by using the higher dosage regime especially in
younger patients and in patient with predominantly truncal disease. There is
also evidence that when patients have received a total cumulative dose of
more than 120 mg/kg, they have a better chance of achieving long-term
remission. In practice the cure rate approaches 90% if given for 4 months
with the 1 mg/kg dosage. Occasionally longer duration of therapy may be
needed for resistant cases. This drug is teratogenic and it is unwise to
prescribe the drug to female patients without concomitant adequate
contraception, and contraception should be continued for at least 1 month
after cessation of therapy. Its side effects include dryness of the skin and
lips, epistaxis, arthralgia and myalgia, and temporary hyperlipidemia and
abnormal liver function test. Headaches can occur, and benign intracranial
hypertension has been reported.
1.4.4. Other Specific Therapy
1) Surgery
Unsightly scars and persistent cysts, when they are no longer inflamed, may
be excised. Dermabrasion may be of value for depressed scars and can be
considered when the disease is inactive. Pigmentary changes after
dermabrasion is a problem in colored race. Laser surgery has also been used
to improve acne scars and pigmentation.
2) Treatment of Comedones
Blackheads can be removed with a comedones extractor. The use of light
cautery after the application of EMLA as a local anaethestic has been shown
to help patients with multiple macro-whiteheads.
3) Collagen injection of scars
Purified bovine dermal collagen injection can give good cosmetic results for
some acne scars. This is an expensive procedure and injection need to be
repeated to maintain the improvement. There is also a small risk of
hypersensitivity reaction.
4) UVB irradiation: UVB irradiation to the face in sufficient doses to
produce mild erythema and desquamation of the skin can improve acne in
some patients, but response to treatment is variable.
5) Systemic steroids: very useful in arresting the inflammatory lesions
before isotretinoin is available. Now rarely used except for treatment of acne
fulminans.
6) Chemical peeling: superficial peel with glycolic acid has been claimed to
useful in treatment of acne. Deeper peel can be employed to alleviate acne
scars. Chemical peeling should only be performed by dermatologists
experienced in the technique.
7) Intralesional kenacort A: for individual cystic lesion, can reduce the
inflammation quickly but there is a risk of leaving a pitted scar. Injection for
keloidal acne is another indication.
8) Zinc: Oral zinc therapy had been very popular before but failed to
demonstrate significant benefit in many clinical trials. Dosage is Zinc
gluconate 200 mg/day. The addition of zinc to topical erythromycin has been
shown to enhance the therapeutic efficacy especially on inflammatory
lesions. This preparation has been marketed in USA.
URTICARIA
Dr. C.Y. LEUNG
CHAPTER 6
1. DEFINITION
Urticaria is characterized by transient itchy pale dermal swellings secondary
to the release of histamine and possibly other vasoactive agents from mast
cells.
2. AETIOLOGY
The release of histamine, and possibly other vasoactive mediators from mast
cells leads to a sudden increase in vascular capillary permeability allowing
the escape of fluid from the circulation into the tissues. Mast cells may
degranulate in response to a number of stimuli including physical, chemical,
pharmacological and immunological.
Different mechanisms may be operating in different types of urticaria. The
type I hypersensitivity is mediated through the IgE attached to the mast cell
which will degranulate on exposure to the specific antigen. Patients suffering
from this type of allergic urticaria frequently have a personal or family
history of atopy. Mast cells can also degranulate by other non-
immunological stimuli. Certain drugs, for example morphine, codeine,
ethanol, polymyxin B, and bacterial, plant or invertebrate toxins can
stimulate mast cells to degranulate directly. Other drugs like salicylates and
NSAIDs on the other hand act on the mast cell through its action on the
cyclo-oxygenase pathway. It has been postulated that food additives such as
tartrazine, azo dyes, benzoates and sulphites can provoke urticaria through a
similar mechanism. Recently some research workers have demonstrated the
presence of IgG auto-antibodies directed against IgE receptor Fc epsilon RI
of mast cells and basophils in some patients with chronic idiopathic
urticaria, which can activate the mast cells to degranulate. This autoimmune
hypothesis of idiopathic chronic urticaria has led to the use of various
immune therapies for treatment of the condition (see below).
Vasodilatation, dermal oedema and a mild perivascular infiltration of
lymphocytes and eosinophils are seen in a typical lesion of urticaria.
However in a small number of patients repeated biopsies may show a
predominance of neutrophils and eosinophils infiltrate and absence of
endothelial damage, representing a late phase reaction. This picture would
suggest that other cellular elements and mediators may operate in the
pathogenesis of urticaria in some cases.
3. CLASSIFICATION OF URTICARIA
Various types of classifications exist, the following classification adopts a
more practical approach.
3.1. Acute Urticaria and Urticaria with an Identifiable Cause
In acute urticaria, a self evident precipitating factor is usually present (table
1). Some patients with chronic urticaria may also have a well defined cause
although this is uncommon.
3.2. Chronic Idiopathic Urticaria
Defined arbitrarily as urticaria that persisted for six weeks or more without
any identifiable cause.
3.3. Physical Urticaria
cholinergic urticaria
symptomatic dermographism
delayed pressure urticaria
solar urticaria
cold urticaria
aquagenic urticaria
vibratory urticaria
3.4. Angio-Oedema
May accompany any types of urticaria. Hereditary angioedema is due to C1
esterase inhibitor deficiency. An acquired form of this enzyme deficiency is
also known. ACE inhibitors can provoke angio-oedema through inhibition of
the kinin system.
3.5. Others: hereditary urticaria, contact urticaria, papular urticaria,
urticarial vasculitis, and urticaria pigmentosa.
Table 1: Common Causes of Urticaria
salicylates, penicillin, ACE inhibitors, NSAID,
Drugs
allopurinol and many others.
fish, nuts, egg, strawberries, milk, cheese, wine

Foods
and many others.
Food
azo dyes, benzoates, sulphites and yeast.
additives
hepatitis B, infectious mononucleosis, candidosis

Infections
and focal sepsis.
Inhalants grass pollens, moulds, housedust mites, etc.
Infestation enterobius, filariasis, ascariasis.

Immune
transfusion reaction, drugs
complex
4. CLINICAL FEATURES
The lesions in urticaria are usually not difficult to recognize. They are
intensely itchy, with a white palpable centre of oedema and a variable halo
of erythema . The size and shape can be highly variable and

individual lesion usually lasts for several hours, except in urticarial
vasculitis and angio-oedema where the lesion may persist longer. Frequently
patients do not have any lesion during the visit to the clinic and one has to
rely on the description from the patient to diagnose a prior attack of
urticaria.
The history is very important for the diagnosis of different types of urticaria
in particular for physical urticarias. The frequency, duration, severity, and
timing of the attacks may give clues to the diagnosis and are essential for
subsequent management. A thorough food and drug history should be
elicited. The characteristic rash of physical urticaria, if present on
examination, together with the typical history would usually allow the
diagnosis to be made. In case of doubt, simple tests can be done to confirm
the diagnosis (table 2).
After making the diagnosis, one should always try to look out for any
underlying causes and associated involvements. Focal sepsis, such as dental
abscess and urinary tract infection have been reported to cause chronic
urticaria. Urticaria can also be the presenting symptom of connective tissue
diseases and other features of the disease would usually be evident. Acute
urticaria can be just part of the manifestation of serum sickness with
systemic symptoms like fever, arthritis and nephritis. Similarly systemic
symptoms are also seen in patients with urticarial vasculitis.
Table 2: Tests for Physical Urticaria

Cholinergic
exercise test, whole body warming
Urticaria
light stroke on the skin,

Dermographism
dermographometer
cold urticaria ice cube test

solar urticaria phototesting
aquagenic water at 25oC compresses
5. INVESTIGATION
In most patients suffering from urticaria, the correct diagnosis can be made
after history taking and physical examination. A complete blood count
together with ESR is adequate for the majority who has no other abnormal
physical finding. Other investigations should be done when necessary.
1) complete blood count and ESR: look for eosinophilia
2) Liver function test
3) complement C3 and C4
4) C1 esterase inhibitor level
5) Investigating underlying infections: chest radiograph, urine for culture,
stool for ova, throat swab, HbsAg, viral study etc.
6) ANF, RF etc. in suspected connective tissue disease
7) Skin biopsy: urticarial vasculitis, urticaria pigmentosa
8) RAST: controversial as to its usefulness
9) Skin prick test: useful for contact urticaria. Difficult to interpret for
chronic idiopathic urticaria
6. ACUTE URTICARIA
Patients with acute urticaria are usually seen by their family doctors or by
doctors in the A&E department. The cause of the acute attack is often
obvious and there may be a history of similar attack. Initial investigations
should include the differential white cell count and ESR measurement. The
presence of eosinophilia points to parasitic infestation. Other possible
causative factors listed above should be sought for.
Since the causal factor can usually be withdrawn, subsequent attack can be
avoided and long-termed treatment is usually not required. Challenge test is
not advisable since acute urticaria is frequently IgE mediated and there is a
definite risk of anaphylaxis during the test. Though the prognosis is good in
most cases, those with persistent symptoms for weeks may actually be
suffering from chronic idiopathic urticaria with an acute onset.
Most of these acute episodes can be successfully controlled with
antihistamine. In acute urticaria of serum sickness type hypersensitivity, a
short course of systemic steroid may be necessary. Parenteral adrenaline is
life saving in case of anaphylaxis and bronchial constriction. Resuscitation
procedures should be carried out as indicated.
7. CHRONIC IDIOPATHIC URTICARIA
Chronic idiopathic urticaria is defined as urticaria lasting longer than 6
weeks, for which no obvious cause can be found. This is the commonest
type of urticaria in a dermatology clinic and a study by Champion reported
that 80% of urticaria is chronic idiopathic urticaria. Although symptomatic
relief can be achieved with drug therapy, a certain percentage of patients
may suffer from continuous symptoms for years without true remission.
Numerous factors have been suggested for causing this disease including sea
food, azo dyes, food preservatives, candida in the gut and trace of penicillin
in dairy products. Some patients may benefit from elimination of one of
these factors, but for most others the cause of the disease remains obscure.
Recently an autoimmune aetiology has also been proposed.
By definition, no obvious aetiological factor is apparent and special
investigations are nearly always unhelpful. For most patients with chronic
idiopathic urticaria, a complete blood count, ESR for screening may be
adequate. Stool for ova is indicated if there is eosinophilia. Other tests
detailed above should be performed for individual patient as directed by the
history and examination. Prick test and intradermal skin test are often
positive but are difficult to interpret. Challenge tests with food coloring
agents and preservatives if available, are helpful in the management.
Although no underlying cause can be found, for the majority of patients their
symptoms can be well controlled by drug with minimal disturbance to their
daily life. Depending on the patient's tolerance, a sedating or non sedating
antihistamine can be prescribed during daytime. Because most patients have
more severe attack at night time, an additional nocte dose of more sedating
drug like promethazine is helpful. The patient should be encouraged to keep
a food diary. Food containing tartrazine dye and preservatives as well as
drugs that known to aggravate urticaria should be avoided. In suitable cases,
elimination diet can be carried out with the help of a dietitian.
Tolerance to antihistamine therapy may develop in a patient whose
symptoms are previously under control. This tolerance cannot be overcome
by increasing the dosage or by changing to another antihistamine. The cause
of tolerance is thought to be due to the down regulation of the H1 receptors.
Ketotifen and sodium cromoglycate can be tried and responsiveness to
antihistamine may return. Hospital admission may be required for alternative
therapy in difficult cases.
8. CHOLINERGIC URTICARIA
A common condition in young adults with intensely itchy and short-lived
eruption developing in response to sweating, exercise, emotion and hot
foods. It is postulated that an increase in blood temperature triggers a neural
reflex which releases acetylcholine from sympathetic nerve endings, in turn
activate the mast cell to degranulate. Characteristic small wheals, less than 2
mm in diameter with surrounding red halo are more profuse on the upper
trunk and proximal parts of the upper limbs. Thus it is also called
micropapular urticaria. Associated systemic symptoms include faintness,
headache, wheezing and palpitation.
Diagnosis is established from the history and the finding of characteristic
rash during an attack. The rash can also be brought up on exercise or whole
body warming. These lesions can often be reproduced by intradermal
injection of cholinergic drugs, e.g., metholyl or acetylcholine.
Treatment is unsatisfactory. Patients, especially those with associated
systemic symptoms, should be told to avoid situations that can precipitate an
attack. Some patients improve with antihistamine therapy. This can be taken
regularly or at times when they anticipate attacks. Fortunately for most
patients the condition tends to improve spontaneously.
9. PRESSURE URTICARIA
This rather rare condition is not a true urticaria. Delayed cutaneous erythema
and oedema and subcutaneous oedema occur in response to the sustained
application of pressure to the skin. The lesions itch and burn. They appear
between 30 min to 9 hours after the stimulus. A large proportion of these
patients have associated chronic idiopathic urticaria.
The lesions characteristically occur after certain activities: sitting on hard
chairs, carrying bags, leaning against furniture, wearing seat belts and lying
on hard mattresses. Swelling of the feet and hands, often indistinguishable
from angio-oedema, occurs after walking, jogging, running, climbing ladder
and using a screwdriver. During severe attacks, arthralgia and a flu-like
illness may accompany the rash.
The pathogenesis of pressure urticaria is not known. Histamine is probably
not an important mediator of this disease and treatment with antihistamine is
useless. Other forms of treatment including the use of NSAIDs and
colchicine have been tried with varying results. Systemic steroid is an
effective agent but is limited by its side effects.
10. SYMPTOMATIC DERMOGRAPHISM

Dermographism means whealing after direct pressure on the skin. The
patient notices that the skin itches with linear wheals appearing after
scratching . The itching and whealing reach their maximum in 5-10
minutes after the stimulus and disappear 30-60 minutes later. It is an
exaggerated response of the skin to trauma.
Lesions frequently appear in areas where clothing is tight and at sites of
scratching. Patients can be of any age group but young adults are more often
affected. No associated systemic disease has been recognized and no
increased incidence in patients with chronic idiopathic urticaria is noted. The
diagnosis can be confirmed by using the more sophisticated
dermographometer. Any patient who itches and wheals at or below a
stroking pressure of 3.5 x 105 Pa has symptomatic dermographism. The
tendency to dermographism may last for years but ultimately improve in
most cases.
11. SOLAR URTICARIA

Solar urticaria is a rare photodermatosis of unknown aetiology. It is
occasionally associated with polymorphic light eruption, other urticarias,
lymphocytoma cutis or lupus erythematosus. It may also be symptomatic of
porphyria cutanea tarda.
Patients notice erythema, burning, and urticarial wheals within minutes
following exposure to sunlight or other visible light source. Wheals can
develop anywhere on the body, mostly in the sun exposed skin. If the whole
body is irradiated, severe generalized solar urticaria can occurred with
haemodynamic disturbance. The action spectrum of solar urticaria is broad,
ranging from UVC, UVB, UVA to visible spectrum. The diagnosis can be
confirmed by phototesting with monochromator on areas of the body that are
normally covered e.g. the buttock. If monochromator is not available, lesions
of solar urticaria can be reproduced outdoor by direct exposure to sunlight or
visible light.
Avoidance of sunlight is essential in the management. The body should be
covered with clothing and the patient should be advised to use an
appropriate sunscreen. Antihistamines can produce symptomatic relief.
Other treatment modalities that have been used include hardening with
UVB, UVA, or visible light, PUVA, and plasmapheresis.
12. COLD URTICARIA

Patients with cold urticaria develop whealing on exposure to cold. Wheals
typically appears on exposed areas on a cold day. Handling of cold objects
also causes immediate local reaction. There may be swelling of the mouth
and oesophagus after drinking cold water. If whealing is extensive, cold
urticaria may be associated with systemic symptoms like faintness,
wheezing and palpitations. Diagnosis is established by placing an ice cube
(wrapped in plastic bag) on the skin for 30 seconds to 10 minutes. Wheals
form on rewarming. In some cases, water at 7o C is more effective in
bringing out the wheal.
It is important to warn patients against swimming in cold water or
immersing in cold water as syncope may occur. Antihistamine treatment is
partially effective in suppressing symptoms. Cyproheptadine is generally
considered to be the drug of choice. Salbutamol and aminophylline can
relieve the pruritus of cold urticaria. Unlike antihistamines these drug act by
suppressing histamine release from skin mast cells. Doxepin and ketotifen
may also be useful.
Desensitization to cold has a place in the management of this condition. This
should be carried out in the hospital under antihistamine cover. The
procedure begins with putting one limb in water at 15 ?C for 5 min, hourly
at first and then at longer intervals up to 24 hours. Other limbs and the face
can then be treated. The exposure needs to be repeated indefinitely at 24
hours intervals to maintain the effect.
It should be remembered that occasionally cold urticaria is secondary to the
presence of cryoglobulin, cold hemolysin and cryofibrinogen in the
circulation. These condition should be ruled out accordingly.
13. AQUAGENIC URTICARIA

This is a rare type of physical urticaria in which brief contact of the skin
with water of any temperature causes an immediate urticarial eruption at the
site of contact, the morphology of which closely resembles that of
cholinergic urticaria. This condition may persist for many years. Aquagenic
pruritus is a related but distinct condition in which brief contact of skin with
water evokes intense local pruritus without any skin lesion. Patients with this
disorder, which is probably quite common in the elderly, are often wrongly
labelled as psychoneurosis or senile pruritus. Complete blood count should
be checked as this condition may be symptomatic of polycythemia rubra
vera. Both disorders involve histamine release from skin mast cells and
respond well to antihistamine. UVB therapy is also helpful.
14. VIBRATORY ANGIOEDEMA

Vibratory angioedema is an acute short-lived itchy swelling of the skin that
occurs within minutes of application of a vibratory stimulus to the skin. This
condition is rare and is probably genetically transmitted. It is benign and the
familial form is not associated with any other physical urticaria. Affected
patients generally limited their activities to avoid symptoms. The lesions
tend to appear after low frequencies vibration (about 10 Hz) like handling a
power lawn mower and running, and wheals can be seen within minutes
after the stimulus and disappears within an hour. Clapping and riding a
motor bike may also produce lesions. The severity of symptoms is
proportional to the intensity of the provoking stimulus. If the stimulus is
sufficiently strong, facial and/or generalized erythema may occur. Systemic
symptoms like headache and dizziness are also reported. Treatment with
antihistamine is usually effective.
15. ANGIOEDEMA
This is a variant of urticaria where massive oedema involves subcutaneous
tissues rather than the dermis. It may involve any part of the body surface
like the lips, eyelids, tongue and larynx. This condition can be associated
with urticaria of any cause. The hereditary form is caused by a quantitative
or functional deficiency of C1 esterase inhibitor and is inherited as an
autosomal dominant trait. An acquired form of C1 esterase inhibitor may
develop in patients with lymphoproliferative disorders and systemic lupus
erythematosus.
Hereditary Angioedema
In hereditary angioedema attacks are infrequent in childhood, common in
adolescence and early adult life and may subside later. It is precipitated by
trauma and the lesions may affect the skin, mucosal surface and intestine.
Subcutaneous swelling is not itchy and typically persisted for a few days.
Intestinal oedema may causes symptoms simulating acute abdomen.
Laryngeal oedema may lead to upper airway obstruction and death. The C2
and C4 level are low in between attacks and C3 is normal. There is a low C1
esterase inhibitor level. In acute airway obstruction, subcutaneous adrenaline
may be life saving. Fresh frozen plasma should be administered by
intravenous infusion or, alternatively a purified C1 esterase inhibitor
concentrate can be given. For long term management attenuated androgens
stanozolol or danazol can be used for prophylaxis. They act by stimulating
hepatic synthesis of C1 inhibitor. Antifibrinolytic agents like tranexamin
acid and epsilon aminocaproic acid are less effective as prophylaxis but can
be tried in patient who cannot tolerate androgenic steroids.
16. CONTACT URTICARIAS

Contact urticaria is a local immediate or delayed erythema or urticarial
reaction at the site of epidermal or mucosal contact with a causative agent. It
may be associated with generalized cutaneous reactions, rhinitis, asthma, or
anaphylaxis. It is commonly an IgE mediated immediate reaction and non
immunological mechanism is also possible.
Probably the most important cause of contact urticaria is natural rubber latex
present in gloves and other rubber products. Latex contact urticaria
symptoms vary from mild itching to bronchial asthma, anaphylaxis, and
death. Up to ten allergenic proteins have been isolated from latex. Small
molecular wight chemicals may cause contact urticaria. Chemicals like
ethylene oxide, isocyanates, chloramine-T, epoxy resins and nickel sulphate
can act as hapten and initiate IgE-mediated allergies. This can be confirmed
by using skin prick testing.
17. URTICARIAL PIGMENTOSA

This condition is in fact not urticaria but is a disorder of mast cell
proliferation commonly seen in early childhood. Clinically there is multiple
guttate or larger pigmented macules on the trunk and limbs of the baby and
urticated lesion may appear on rubbing the pigmented lesions. The biopsy of
the skin shows increase in the number of mast cells.
18. URTICARIAL VASCULITIS (refer to the Chapter of Vasculitis)
19. THERAPEUTIC MODALITIES FOR URTICARIA

19.1. Antihistamines
This group of drugs has H1 receptor blockers action and is the mainstay of
therapy for urticarias. There are many antihistamines available. While the
classical ones have been used for many years and are effective and cheap,
they have more anticholinergic action and can cause more sedation. The
newer antihistamines are more expensive and less sedating. In general there
is little difference in the efficacy between the two groups of antihistamines
and there is a lot of individual variations in response to treatment.
As a guideline one should prescribe an antihistamine that one is familiar
with and gradually titrate the dosage according to the response. It is
worthwhile to switch to an antihistamine of another class if the response to
the first choice is not satisfactory when the maximum dosage has already
been given. Alternatively, in order to select out the most suitable agent for
the patient, an antihistamines self-assessment questionnaire can be
employed.
The classical antihistamines (see table 3) can be grouped into 6 classes
according to their chemical structures, but the introduction of the newer
drugs has greatly complicated this.
Table 3: Commonly Used 'Classical' Antihistamines
Generic (Proprietary)
Class Usual Adult Dose
Name
Dimenhydrinate
50-100 mg qid
Ethanolamines Diphenhydramine
25-50 mg qid
(Benadryl)
Chlorpheniramine
(Piriton) *1 4 mg tid
Alkylamines Dexrochlorpheniramine 2-4 mg tid
(Polaramine) *2 75 mg bid
Pheniramine (Avil)
Phenidenes Mebhydrolin (Incidal) 50-100 mg tid
Promethazine
(Phenergan) 10-25 mg bid
Phenothiazines Trimeprazine 10-30 mg qid
(Vallergan) 5 mg bd
Mequitazine (Primalan)
Piperazines Hydroxzine (Atarax) 10-25 mg tid
Cyproheptadine
4 mg tid
Piperidines (Periactin)
1-2 mg tid
Azatadine (Zadine)
*1 a short acting, good general purpose drug

*2 dextro-isomer of chlorpheniramine
*3 causes sedation, suitable for use at night time, e.g. 25 mg
nocte
*4 with addition antiserotonin action, very useful for cold
urticaria
Unwanted effects are common with these antihistamines, the commonest
being sedation, dizziness, fatigue, insomnia and dry mouth. Paradoxical
increase irritability may be seen in children. Alcohol can potentiate the
sedative effect and patient should be advised to abstain from drinking while
on antihistamine therapy. The anticholinergic action may cause urinary
retention and precipitate glaucoma. All antihistamines are not proven safe in
pregnancy and one should balance the risk and the possible benefit before
prescribing antihistamines to pregnant woman. Newer antihistamines should
always be avoided.
Table 4: Low Sedating Antihistamines
Duration of
Usual Adult Dosage Onset
Action
Terfenadine 60 mg bd 1-2 hours > 12 hours *1
Astemazole 10 mg daily days 4 weeks *2
Loratadine 10 mg daily 1-2 hours 24 hours
Cetirizine 10 mg daily 1-2 hours 24 hours
Acrivastine 8 mg tid 30 minutes 12 hours
Notes: 1. Fatal ventricular arrhythmia has been reported with

larger than normal dose, in patients with liver disease and when
it is administered with erythromycin or ketoconazole.
2. Very long duration of action. Ventricular arrhythmia
reported. Cautious in the elderly. Weight gain may occur during
prolonged therapy.
Other antihistamines and related drugs:
Ketotifen: Antihistamine-like drug with mast cell stabilising effect, worth a
try in difficult urticaria and when tolerance to antihistamine therapy appears.
Adult dosage: 1-2 mg bd
Oxatamide: properties comparable to ketotifen, dosage is 30 mg bd.
Doxepin: a tricyclic antidepressant with antihistamine activity. Suitable for
administration at night. There is drug interaction with MAOIs, and can cause
cardiac arrhythmia. Dosage: 10 mg nocte
19.2. H2-Receptor Blockers
The exact mode of action of H2 antagonist in urticaria is still uncertain. In
many stubborn cases addition of an H2 antagonist with an antihistamine may
be helpful, but there is no ground to give an H2 antagonist alone.
Cimetidine: 400 mg bd
Ranitidine: 150 mg bd
19.3. Beta-stimulants
This is considered as a second line treatment for patients with resistant
chronic urticaria and antihistamine tolerance. They act directly on the mast
cell and prevent degranulation. Although they are effective, their use is
limited by their side effects, including tremors and tachycardia.
Salbutamol: 2-4 mg tid
Terbutalin: 0.5 mg tid
19.4. Calcium Channel Blocker
Only nifedipine is useful for stubborn urticaria. It acts by stabilising mast
cell and inhibit degranulation. Side effects include hypotension and flushing
attacks.
Nifedipine: 5-10 mg tid
19.5. Anabolic Steroid
This has been used in patients suffering from hereditary angioedema. It is
also used in cholinergic urticaria.
Danazol: 100-600 mg daily
Stanozolol: 2.5-10 mg daily
19.6. Systemic Corticosteroid Therapy
This is an effective form of therapy for urticaria but long term therapy
should be used only in exceptional cases because of its side effects. Systemic
steroid therapy is indicated for anaphylaxis and acute urticaria of serum
sickness. For chronic urticaria, this should be avoided unless it is given for a
short duration to tie over an acute episode.
19.7. Mast Cell-Stabilising Agents
Disodium cromoglycate which stabilized mast cell membrane has been
found to be useful in atopic asthma when administered via an inhaler.
Because the drug is not absorbed in the gastrointestinal tract they are
generally not effective for patients with chronic urticaria. However, it may
be helpful in cases of urticaria caused by food allergy. Two antihistamine,
ketotifen and oxatamide, have additional mast cell stabilising effect but it is
not certain whether this additional property is of any clinical significance.
19.8. Immune Modulation
Based on the autoimmune hypothesis for chronic idiopathic urticaria,
various immune modulation therapies had been investigated for treatment of
the condition: plasmapheresis, cyclosporin A and intravenous
immunoglobulin. These treatment modalities are still experimental and not
yet suitable for routine clinical application.
Vitiligo
Dr. R. SU
CHAPTER 7
1. Definition
An area of acquired cutaneous depigmentation characterized by well-
circumscribed milky white macules devoid of identifiable melanocytes.
2. Aetiological Hypothesis
Various theories are suggested as the aetiology of vitiligo; the same
mechanism may not apply to all cases.
2.1. Autoimmune Hypothesis
Autoimmune destruction of cutaneous melanocytes with total loss of
melanocytes and melanin pigment in the skin of the affected area.
Lymphocytic infiltration on skin biopsy indicate lymphocytes are involved
in the destruction process. Frequently associated with other autoimmune
diseases; such as alopecia areata, autoimmune thyroid disorders, Addison¡¦s
adrenal disease, atrophic gastritis and pernicious anaemia, diabetes. Serum
autoimmune antibodies against melanocyte, thyroid, adrenal, islet-cell,
gastric parietal cell, and intrinsic factor have been demonstrated.
2.2. Neurogenic Hypothesis
A compound is released at peripheral nerve endings in the skin which is
toxic to melanocytes and inhibits melanogenesis. It is postulated that in the
dermatomal variant, the affected area shows sympathetic nerve dysfunction.
Catechol neurotransmitters probably destroy the melanocytes instead. There
is little support for this hypothesis.
2.3. Self-destruct Theory of Lerner
Defect of a natural protective mechanism in melanin synthesis within
melanocytes, leading to accumulation of toxic precursors (phenolic
compounds) which destroy melanocytes. This hypothesis is based on the
lethal effects produced by chemical compounds (phenols) on functional
melanocytes; the resulting leukoderma is indistinguishable from idiopathic
vitiligo.
3. Clinical Presentation
Affects around 1% of the population in all races, but more troublesome in
dark skin where there¡¦s marked contrast between normal and depigmented
areas. Hence the incidence may be apparently higher in pigmented races
where the social impact is also greater. Family history of the condition is
found in one third of the affected patients. Sex ratio is equal. Half the
patients first present before 20 years old. It may be precipitated by injury or
sunburn. In light skin individuals, vitiligo may only be discernible in
summer, when the vitiliginous area becomes sunburnt.
The main symptom being cosmetic and presents when the patient notices
that the affected area fails to tan after sun exposure, unlike the surrounding
normal skin. It is an essentially clinical diagnosis, based on the morphology
and distribution of the lesions as well as the exclusion of other
hypopigmented skin lesions.
Vitiligo may rarely be associated with premature greying of hair, retinal
pigmentary loss, uveitis, deafness, CNS involvement (Vogt-Koyanagi
syndrome). Other associations include: halo naevus, malignant melanoma,
alopecia areata, autoimmune thyroid disorders, Addison's adrenal disease,
chronic atrophic gastritis, Pernicious anaemia and diabetes mellitus.
4. Diagnostic Hallmarks
4.1. Distribution
Localized: Sun exposed areas such as dorsal surface of hands and
the face, including peri-orificial and peri-orbital areas.
Hyperpigmented areas such as axilla, groin, genitalia,
flexures, and nipple.
Sites of friction and bony prominences like elbows
and knees.
Generalized: Widespread
Unilateral variant: unilateral segmental pattern seen in children occurs
(linear/dermatomal) occasionally.
4.2. Individual Lesions
Sharp margin
No scale
Normal texture and intact sensation
Typical: milk white colour
Atypical:
Trichome vitiligo
- an intermediate uniform tan colour
- naturally evolves to a typical vitiligo macule
Quadrichrome vitiligo
- macular peri-follicular or marginal hyperpigmentation seen in
repigmenting vitiligo
Inflammatory vitiligo
- erythematous, raised border similar to that seen in tinea versicolor.
5. Differential Diagnosis of vitiligo and other Hypopigmented lesions
Generalized hypomelanosis albinism
hypopituitarism
Patchy hypomelanosis vitiligo
piebaldism
tubero-sclerosis
chemical leukoderma
Patchy hypomelanosis tinea versicolor
with inflammation and scaling leprosy
pityriasis alba
Patchy hypomelanosis with morphea
atrophy or induration lichen sclerosis
post-inflammatory
hypopigmentation
6. Investigation
Skin biopsy will show absence of melanocyte and melanin in the affected
area, but this is often not necessary as the diagnosis is clinically obvious.
Other investigations are considered to exclude associated autoimmune
disorders. The extent of the investigations may depend on the history and
physical findings.
7. Treatment
Educate and encourage relatives, friends and society to overcome the
stigma that this is infectious.
Acceptance of patient by physicians setting an example (e.g. shaking
hands) should be supportive to patient and help to overcome stigma.
Reassurance that this is a cosmetic problem and does not affect the patient's
health directly.
Educate the patient about the nature of the disease, that treatment may be
difficult and prolonged, and the results may not be predictable. While the
patient should not have unrealistic expectation they need not be discouraged.
More important is to take good care of their own skin, concentrate on what
can be done even if the condition can not be cured at present.
1) Sunscreen (SPF 15-30)
These are recommended for three reasons: 1) Vitiliginous areas are more
susceptible to sunburn, 2) Sunburn injury can further extend area of
depigmentation (Kobner response). 3) Sun-induced darkening of the
surrounding normal skin causes accentuation of the cosmetic disfigurement.
Sunscreens which shield both UVB and UVA light should be used.
For the same reason, avoiding outdoor activities under the strong mid-day
sun, together with protective clothing, will reduce ultraviolet damage to
depigmented skin which is devoid of protective melanin.
2) Camouflage Cosmetics (Covermark, Dermablend etc.)
Covermark and Dermablend are cosmetic that can be used to match most
skin hues.
Quick-tanning preparations containing dihydroxy-acetone may be used to
tan the vitiligo a more acceptable colour. It can produce different shades.
Instructions and guidance from a cosmetic instructor are required to give the
best cosmetic results and safety. These preparations are especially useful on
the eyelids where potent topical corticosteroids and ultraviolet-light should
not be used.
3) Repigmentation therapies
Moderately potent to potent topical corticosteroids
e.g. Sicorten Cream (0.5% halometasone)
This may be applied to affected area twice daily as a trial. Therapy should be
discontinued if repigmentation has not begun after six to twelve months. The
patient needs to be seen every 1-2 months to check for signs of cutaneous
atrophy from treatment. Caution is needed when applying it to the face and
flexures (once daily/alternate day). It should not be applied to eyelids and
periorbital areas to avoid the risk of steroid-induced glaucoma and cataract.
PUVA Therapy: Topical or systemic (Refer to chapter 17)
Topical PUVA involves ultra-violet A irradiation 30 minutes after application
of meladinine (topical methoxasalen) to the localized vitiliginous area.
Systemic PUVA involves ingestion of methoxasalen (0.6 mg/kg) two hours
before irradiation.
Treatment should be attempted under the supervision of a dermatologist or
those experienced in its use. In inexperienced hands PUVA may carry the
risk of phototoxic reaction, ocular damage etc.
Careful patient selection is also required. Within the Social Hygiene Service,
predominantly facial lesions (except eyelids) of recent onset are considered
for PUVA, because they tend to give better results. Some degree of
repigmentation occurs in 50-75% of cases compared with 15-20% in
controls.
The patient undergoes treatment 2 times per week, and needs to avoid
sunlight for 2 days after each treatment, using sunscreens both indoor and
outdoor. It takes at least 2-3 months to begin having an effect and therapy
needs to be continued for at least one year (100-200 treatment sessions)
before maximum benefit is reached. Hence a long term commitment to
therapy is required, and this must be appreciated by the patient before
embarking on therapy. The physician also needs to take into consideration
the patients¡¦ age, sex and disease severity, medical, social, occupational and
psychological factors.
If perifollicular pigmentation has not appeared after three months of therapy,
it is unlikely to occur; treatment might as well be stopped. But once
repigmentation has begun, it tends to persist and spread with continuous
treatment. However complete repigmentation occurs in 15-20% only.
Systemic PUVA is less often used than topical PUVA in vitiligo.
Contra-indications for systemic PUVA include:
Pregnancy, children <12 year old, photosensitivity, cardiac, hepatic and renal
disease, aphakia, and cataracts, and history of skin cancers.
4) Depigmentation therapies using bleaching agents such as 20%
monobenzyl ether of hydroquinone (Benzoquin 20%) once or twice daily is
indicated when vitiligo is extensive (>50% involvement or near universal).
Benzoquin may cause a contact dermatitis, hence as a test before generalized
therapy, it should be applied to a single pigmented spot daily for 1 week.
Thereafter large pigmented areas are treated twice daily for up to 6 months.
The compound is cytotoxic to melanocytes and destroys them. This process
which removes pigment from the remaining normal skin is irreversible. The
skin becomes albinoid, but the cosmetic appearance is improved
substantially. The patient must remember they are sun-sensitive and need
protective sunscreen.
Experimental Repigmentation modalities:
These can be tried in stationary vitiligo which are not extending any further.
They have achieved variable success in different individuals.
Grafts from uninvolved skin containing viable melanocytes; punch mini-
grafting using autologous pigmented donor sites is the simplest least
invasive surgical approach. Alternatives include growing melanocytes in
vitro from the patients¡¦ normal skin, and injecting them into artificially
induced blister cavities in the depigmented areas. Repigmentation by
tattooing has also been tried with some success.
8. COURSE AND PROGNOSIS

Variable and some what unpredictable. May remain static, spread or
repigment. But usually the condition is gradually progressive, sometimes
extending rapidly over a period of several months and then remaining
quiescent for may years. Spontaneous repigmentation is noted in about 10-
20% of patients.
Factors indicating good prognosis for regimentation are: Recent onset < 6
months, in a young individual on the facial area.
Conversely factors which indicate an unfavorable prognosis are: Late onset
in life, long-standing persistent lesions, located on the extremities and on the
lips.
Repigmentation begins within the affected area from the hair follicles where
there may be residual melanocytes; or else they occur from the normal
pigmented skin immediately adjacent to the vitiliginous area. Once
repigmentation begins it tends to continue, albeit slowly and sometimes
trivial.
CUTANEOUS VASCULITIS
Dr. Pedro Sá Cabral
CHAPTER 8
1. Introduction
Vasculitides compromise heterogeneous entities with diverse aetiologies and
manifestations. Vasculitis is strictly defined as a process through which
inflammatory destruction of the blood vessel wall occurs. Nowadays, most
clinicians use the term vasculitis in a broad sense to mean any condition or
process in which the blood vessel wall is inflamed and destroyed. The
process may be confined to the skin or involve other organ systems, such as
kidney, gut, nerves and joints.
2. AETIOLOGY
A causative agent can sometimes be implicated in small and medium vessel
vasculitis. Examples include: 1) Drug e.g. Aspirin, NSAID, penicillin etc. 2)
Infection, e.g. Hepatitis B, Streptococcus etc. 3) Blood disorder, e.g.
essential mixed cryoglobulinaemia. 4) Neoplastic, e.g. multiple myeloma,
lymphoma. In large vessel vasculitis, a causative agent is not identified yet.
e.g. Temporal arteritis, Takayasu's disease. 5) Connective Tissue Disease e.g.
rheumatoid arthritis, Sjogrens, lupus erythematosis, dermatomyositis.
3. HISTOPATHOLOGY
3.1. Major Features
The main histopathological features are fibrinoid necrosis of the affected
vessel wall and inflammatory cells within the vessel wall. Accompanying
extravasation of red cells are frequent and responsible for palpable purpura
observed clinically.
3.2. Minor Features
The minor histopathological features that often but not invariably
accompany vasculitis include: 1) thrombosis occluding the vessel lumen; 2)
associated inflammation and damage to surrounding tissue (e.g. panniculitis,
ischaemia, necrosis); 3) direct immuno-flourescence staining showing
immunoglobulin IgG, IgM, IgA and C3 deposition within the vessel wall*.
3.3. Vessel Size
The small vessels (post-capillary venules) are involved in leukocytoclastic
or hypersensitivity (allergic) vasculitis. The medium size vessels are
involved in polyarteritis nodosa. The large arteries are involved in giant cell
arteritis.
PS: Pitfall - Perivascular lymphocytic infiltration without involving the
vessel wall itself is commonly seen in many conditions but should not be
regarded as vasculitis.
3.4. Type of Inflammatory Cells
The type/s of inflammatory cells present differ in different types of vasculitis
and differ at different age of the lesion. The different types of inflammatory
cells and the clinical conditions in which they are found are outlined below:
Leucocytoclastic vasculitis:
Neutrophils are predominant. Examples include Henoch-Scholein Purpura,
drug-induced vasculitis, erythema elevatum diutinum, granuloma faciale,
hypo-complementaemic vasculitis, polyarteritis nodosa.
Lymphocytic vasculitis:
Lymphocytes are predominant. Examples include: erythema nodosum, lupus
erythematosus, lymphoma, pityriasis lichenoides.
Eosinophilic vasculitis:
Churg-Strauss is an example. Eosinophils are predominant.
Granulomatous vasculitis:
Wegener¡¥s granulomatosis and Churg-Strauss Angiitis**. Cells include:
histiocytes, plasma cells, lymphocytes and occasional giant cells.
Giant cells arteritis:
This occurs cranial and temporal arteritis and polymyalgia rheumatica.
Multinucleated giant cells are predominant.
* The optimum specimen selected for biopsy should be a lesion between 18-
36 hours old.
** Churg-Strauss (Granulomatosis) Angiitis has features of a necrotising
granulomatous (with eosinophils) vasculitis.
4. PATHOGENESIS
4.1. Immune Complex Deposition
Following exposure to an antigenic stimulus, antibodies (usually IgG or IgM
class) are formed and complex with the antigen in the circulation. These
complexes circulate without any difficulty until reaching certain sites, where
local factors (e.g. antigen excess in gravitational dependent areas) cause
them to deposit and bind to the vessel wall.
4.2. Complement Activation and Consumption
The Fc portion of the immunoglobulin molecule binds complement and
initiates the complement cascade. Subsequent elaboration of the potent
chemotactic factor C5a attracts neutrophils into the vessel wall. Tissue injury
occurs as the activated neutrophils phagocytise the immune complexes and
thereby release destructive proteolytic enzymes. The resulting inflammation,
necrosis, and haemorrhage appear clinically as palpable purpura when they
occur on the skin.
4.3. Lymphocytic Infiltration
Following exposure to antigenic material, tissue lymphocytes and histiocytes
become activated to produce various cytokines and inflammatory mediators.
Their interaction with intercellular adhesion molecules on cell surfaces will
initiate and regulate cell mediated immunity, leading to further lymphocyte
proliferation and macrophage aggregation at the site of inflammation.
4.4. Granulomatous Inflammation and Giant Cell Formation
Failure to clear the antigen will perpetuate the inflammatory processes and
eventually lead to epitheloid giant cell and granuloma formation.
5. CLINICAL PRESENTATION
5.1. Cutaneous Features
Morphology of skin lesions:
Persistent urticated lesions, tender palpable purpura, papules, nodules,
haemorrhagic bulla, ulcers, atrophie blanche, livedo reticularis, nail fold-
telangiectasia, infarct, digital gangrene.
Distribution of Skin lesions:
Often start on dependent areas initially (e.g. lower legs, buttocks, back)
before becoming generalized. This is due to the effect of hydrostatic force on
the post-capillary venules, leading to the preferential deposition of immune
complexes in these sites.
Course of skin lesions:
Occur in successive crops, evolving from papules, nodules to palpable
purpura which resolve leaving pronounced post-inflammatory
hyperpigmentation. Depending on the aetiology, the course may be acute,
resolving within few days to few weeks; or it may be chronic and recurrent,
persisting from months to years.
5.2. Extra-cutaneous Features
General: fever, malaise, mucous membrane ulcers
Renal: glomerulonephritis - proteinuria, haematuria, hypertension
Pulmonary: pneumonitis and haemorrhage - haemoptysis, dyspnoea
GI tract: malaena, abdominal pain
Musculoskeletal: joint pain, myalgia
Neurological: mononeuritis multiplex, myelopathy, CVA
Eye: iritis, uveitis
Cardiac: pericarditis, endocarditis, myocarditis and infarct
6. INVESTIGATION
Investigations are performed to: 1) Confirm the diagnosis of vasculitis and
determine the predominant cell infiltrate by skin biopsy. 2) Screen for any
extra-cutaneous organ involvement and hence the systemic nature of
vasculitis. 3) Exclude an offending causative agent and remove it if possible
e.g. drug. 4) Screen for and treat any underlying disease processes that may
be responsible for the vasculitis e.g. infection, connective tissue disease or
malignancy.
1) Skin biopsy for histopathological studies, including immunoflourescent
staining.
2) Blood Tests for
Complete blood count & Erythrocyte sedimentation rate
Antinuclear Factor Screen
Rheumatoid Factor
Complements C3, C4
Liver and Renal biochemistry profile
C-Reactive Protein
Anti-streptolysin O titre
Cryoglobulins
Anticardiolipin Antibody (Quantitative VDRL)
Immunoglobulin pattern and Serum protein electrophoresis
Hepatitis B Antigen
Anti-Neutrophil Cytoplasmic Antibody
3) Throat swab for culture
4) Urinalysis for proteinuria, Red blood Cell, White cell, and Casts
5) Stool for Occult Blood
6) Chest X ray
7) Nerve Conduction Studies and/or Nerve Biopsy
N.B.: More invasive investigations like renal or lung biopsy may be relevant
but should not be taken lightly unless clearly indicated and in conjunction
with the physician.
7. TREATMENT
7.1. Cutaneous
1) Supportive:
Bed rest, elevation of dependent parts and avoidance of trauma and cold
2) Anti-inflammatory agents:
Include topical steroids, non-steroid anti-inflammatory drug e.g.
indomethacin, colchicine 0.5 mg bd or tds, dapsone 50-100 mg qd (esp
erythema elevatum diutinum), sulphapyridine, Minocin.
3) Antiplatelet agents:
Such as aspirin or dipyridamole are sometimes used.
4) Systemic corticosteroids given as a short course may be useful in an acute
severe episode to reduce morbidity and produce early resolution of lesions
7.2. Systemic
Systemic vasculitis with widespread involvement of internal organs (e.g.
renal, heart, lung) may result in life-threatening complications (e.g. acute
renal failure). Prompt treatment with high dose systemic steroids and
immunosuppressives, e.g. cyclophosphamide are required to reduce
morbidity and are often life-saving. Monitoring of electrolytes,
haematological picture, and hepato-renal function is necessary during
treatment.
7.3. Life-Threatening Systemic Vasculitis
IV Pulse Methylprednisolone, 1 g QD for 3-5 days
IV Cyclophosphamide 2 mg/kg/day, for 5-7 days
Plasmapheresis, plasma exchange
These agents are indicated in emergency situations where immediate control
of the disease activity is imperative to prevent mortality and preserve organ
(e.g. renal) function. IV Cyclophosphamide may cause haemorrhagic
cystitis. Careful monitoring of fluid and electrolyte balance is necessary
during administration. Any infection should be identified and treated
promptly.
8. APPENDIX: Examples of vasculitis with significant skin involvement

8.1. Leucocytoclastic Vasculitis
This is a heterogeneous disorder with hypersensitivity reaction and immune
complex deposition, following exposure to an antigen, foreign (e.g.
infectious agent, drug) or endogenous. The small vessels (post-capillary
venules) are infiltrated with neutrophils and their nuclear debris (leuco-cyto-
clasis) in the acute stages. Skin lesions occur on gravitational dependent
areas: lower extremities of ambulatory patients or sacral area of bed-ridden
patients. These include palpable purpura, macules, papules, vesicles, bulla,
subcutaneous nodules, ulcers, recurrent or chronic urticaria. The ankles and
lower limb may be swollen. Extra-cutaneous symptoms include fever,
malaise, arthralgia, myalgia, haematuria, GI bleeding and neuropathy.
Investigations reveal mild leucocytosis and elevated ESR; cryoglobulins and
rheumatoid factor may also be detected.
Henoch-Scholein purpura (anaphylatoid purpura) is a variant that occurs in
children and young adults after an upper respiratory infection. It is
characterized by purpuric skin eruptions on the extensor surface of lower
limbs and buttocks, arthritis, abdominal pain, and glomerulo-nephritis with
haematuria. Raised serum IgA and IgA immune deposits are found on the
affected vessel walls. Platelet count is normal and distinguishes this
condition from thrombocytopenic purpura.
Treatment:
1) Bed rest and elevation of the dependent parts.
2) NSAID to control inflammation and relief joint pain.
3) Monitor for systemic involvement like blood pressure and urinalysis,
stool for occult blood etc.
4) Screen and treat the underlying cause if possible.
Only when the function of vital organs (e.g. renal) are compromised should
systemic steroids be necessary.
8.2. Necrotising Vasculitis
8.2.1. Classic Polyarteritis Nodosa (PAN)
This is a multi-system, necrotising vasculitis of small and medium sized
muscular arteries with characteristic involvement of renal and visceral
arteries. 30% are HBsAg +ve. The mean age of onset is 45 years with a male
preponderance (M/F 2.5 to 1). Systemic features include fever, malaise,
arthralgia, myalgia, abdominal pain, malaena, CVA, neuropathy,
hypertension and renal failure. Cutaneous lesions occur in 50% of cases with
painful subcutaneous nodules, purpura, ulcers, infarct and gangrene along
the course of arteries and a livedo reticularis pattern. Microscopic PAN is a
variant with small vessel vasculitis and focal segmental glomerulonephritis.
Investigations include skin biopsy of nodular lesions, sural nerve biopsy and
nerve conduction study. Blood tests showed raised ESR, leucocytosis with
neutrophilia, anaemia of chronic disease, hypergammaglobulinaemia, and
positive Hepatitis B surface antigen. Renal and visceral artery involvement
can be demonstrated by small aneurysmal dilatations on visceral
angiography. Classic PAN does not involve pulmonary arteries; granuloma
and significant eosinophilia are not part of the syndrome.
Treatment and course:
The clinical course is characterized by progressive deterioration with
intermittent acute flare ups. Death usually results from renal failure. The 5
year survival of untreated patients is 13%, but with combined systemic
steroid and cyclophosphamide therapy there may be a 90% long term
remission rate even after discontinuing therapy.
8.2.2. Cutaneous Polyarteritis Nodosa
A more benign form of PAN where vasculitis is chiefly confined to the skin
only. Cutaneous manifestation is similar but milder than classic PAN;
nodules and livedo, with accompanying fever, arthralgia and neuropathy
occasionally.
Treatment includes low dose systemic steroids. The prognosis is good with
no significant mortality even without treatment.
8.2.3. Churg-Strauss (Allergic Granulomatous) Angiitis
Churg-Strauss is a systemic vasculitis that shares many features with classic
PAN, but distinguished by the following features:
Frequent involvement of the lung.
Vasculitis of blood vessels of various types and sizes.
Intravascular and extravascular granuloma formation with eosinophilic
tissue infiltration.
Strong association with severe asthma and peripheral eosinophilia.
Skin lesions occur in 70% of cases but renal disease is less common or
severe as PAN.
The 5 year survival of untreated Churg-Strauss is 25%. The cause of death is
often related to cardio-pulmonary involvement as opposed to renal and
gastro-intestinal involvement of PAN. Glucocorticoid therapy alone
improves 5 year survival to 50%. Combination regimen of
cyclophosphamide and alternate day prednisolone is required for more
severe cases and may result in high rate of remission approaching that of
classic PAN.
8.2.4. Kawasaki Disease (Mucocutaneous Lymph Node Syndrome)
This is an acute vasculitis of unknown aetiology that most frequently affects
infants and children below 5 years of age. It is probably initiated by an yet
unidentified infective agent. The clinical picture is characterized by fever,
palpable cervical lymph node, bilateral conjunctivitis, red cracked lips with
strawberry tongue, and generalized erythematous desquamative rash
especially on extremities. It affects the coronary arteries in up to 30% of
cases. Overall mortality is 1-2% due to cardiovascular complications: acute
coronary thrombosis and late sequel of coronary artery aneurysm.
High dose aspirin remains the mainstay of treatment. Recent studies in Japan
and USA have shown that high dose intravenous gamma globulin is effective
in reducing coronary artery abnormalities when given early in the course of
the disease. Systemic steroids are contraindicated because they increase risk
of coronary complications.
8.3. Livedo Reticularis and Atrophie Blanche
Atrophie blanche are peculiar porcelain white scars studded with pepper-like
red macules and telangiectasia seen around the medial malleolus of both
ankles. They are frequently the result of chronic venous stasis in varicose
vein disorder, yet sometimes they represent the healed result of painful
vasculitic infarction. Livedo vasculitis associated with atrophie blanche is
considered as a distinct entity by North American Dermatologists.
Livedo reticularis describes the blotchy, mottled, net-like pattern of skin
cyanosis seen in cutaneous vasculitis as a result of reduced and sluggish
cutaneous blood flow. A similar but reversible appearance may be seen as a
physiological response to cold on the exposed lower limbs of young girls
during winter. Livedo reticularis may be secondary to cutaneous
polyarteritis, lupus vasculitis, and vasculitis associated with
antiphospholipid antibody syndrome. In the latter, livedo may occur together
with atrophie blanche.
Treatment:
The disorder is associated with a decrease in fibrinolytic activity in skin and
increase platelet adhesiveness. Phenformin and ethylestrenol in combination
are effective because of their enhancement of fibrinolytic activity.
Combination of low dose aspirin (300 mg/day) and dipyridamole (50 mg
tds) which affect platelet function are helpful. Pentoxifylline (Trental) 400
mg tds has also been used with some success.
COLLAGEN-VASCULAR DISEASES
Dr. R. SU & Dr. Y.M. TANG
CHAPTER 9
1. LUPUS ERYTHEMATOSUS
1.1. Epidemiology
In the nineteenth century, a group of diseases of erythematous and atrophic
nature was classified as lupus erythematosus (LE). It was thought the skin
appearance was due to the gnawing by a wolf (Latin: lupus). Today, the term
coins a group of autoimmune diseases that bears various characteristic
cutaneous and histological features, and protean systemic manifestations in
some. (q.v.) This group of diseases is divided into three major subsets;
namely, chronic cutaneous LE (CCLE), also called discoid LE, subacute
cutaneous LE (SCLE) and systemic LE (SLE).
CCLE affects female and male at a ratio of 2:1, from their second to eighth
decade with a mean age of 38 (37.8 in a local study). The incidence of
CCLE is not certain, it is probably under-reported as many cases are trivial
and may have escaped diagnosis. Generally speaking, females at a younger
age predominate in SLE, blacks and Chinese are more susceptible than
whites. An estimated incidence of 6.0-50.8 cases/100,000 population in the
western world is noted.
1.2. Essential Features of the Major LE Subsets
Discoid plaque is prototypic lesion in CCLE. The lesions frequently occur in
the head and neck and exposed areas with sizes varying from a few
millimetres to a few centimetres. It begins as erythematous, oedematous
scaling papules which spread centrifugally and coalesce into a plaque that
exhibits thick and adherent scales. Lifting of the scales produces a carpet-
tack appearance, revealing dilated pilosebaceous orifices occupied by horny
plugs (follicular plugging). Healing of lesion usually takes place in the
centre producing atrophy, scarring, telangiectasia and pigmentary changes
(hypopigmentation in the centre and hyperpigmentation in the active
margin). Histopathology of an established lesion shows typical histologic
changes. (q.v.) Systemic or serological abnormalities in these patients are
absent or minimal and the revised criteria of the American College of
Rheumatology (ACR) for SLE are not met.
In SCLE, skin lesions are annular or papulosquamous, and they share similar
morphology with discoid lesions but healing is not accompanied with
scarring and atrophy is minimal or absent. Photosensitivity and serological
abnormalities are more frequent than CCLE. The full gamut of LE-
associated problems can occur though mild.
SLE is a systemic disease characterised by the association of immunological
abnormalities and multiple organ involvement. The main clinical features
include fever, rashes (especially malar) and arthritis, as well as renal,
pulmonary, cardiac and neurological diseases. A diagnosis of SLE is
established if four or more of the ACR revised criteria for SLE are satisfied.
1.3. Pathogenesis of and Relationship Among Different Types of LE
The pathogenesis of LE is not definitively known. A T-cell mediated injury
is implicated in the discoid lesions. Anti-Ro (SSA) has strong implication in
the production of disease in photosensitive SCLE and neonatal LE (NLE).
Ultraviolet light induces Ro antigen expression on the keratinocytes,
targeting it for binding by anti-Ro antibody and/or sensitized T cells. In SLE,
many features are a consequence of antibody production and immune
complex formation.
It is debatable whether CCLE and SLE are distinct entities or represent
either end of a disease spectrum. They both share similar clinical,
haematological, biochemical and immunological abnormalities. Considering
that: 1) both have different age and sex distribution, 2) presence of
laboratory abnormalities in CCLE does not appear to predispose to the
development of SLE, 3) immunoglobulins and complements are present in
uninvolved skin of SLE but not in CCLE, 4) a patient with CCLE can
develop into overt SLE but is rare, and 5) evidence is available that both
have different genetics; it would appear that they share similarities but are
different diseases.
1.4. Mucocutaneous Features
Mucocutaneous lesions of LE are commonly divided into specific and non-
specific types. Table I shows the specific mucocutaneous lesions of LE.
They are characteristic of LE and help us infer which particular LE subset
the patient suffers; however, the three LE subsets are not mutually exclusive.
Table II tabulates the lesions that commonly occur during the course of LE
but are not sufficiently specific to be indicative of LE.
Table I: Specific LE Lesions
Chronic Subacute Acute
Discoid 1 Annular Malar rash 5
Hypertrophic 2 Papulosquamous Bullous SLE 6
Palmar/plantar 3 ¡@ ¡@
LE panniculitis 4 ¡@ ¡@
Discoid lesion, though is representative in CCLE, also found in 15% of SLE
and 15-30% of SCLE.

Hypertrophic lesions are thickened, nodular and warty, and reminiscent of
warts, prurigo nodularis, keratoacanthoma or squamous cell carcinoma.
Palmoplantar lesions are rare but often symptomatic and erosive, and can
impair movement.
Lupus panniculitis have a female to male ratio of 3-4:1. Lesions are
erythematous, firm, subcutaneous nodules. It is more frequently associated
with DLE, and less with SLE, and occurs in scalp, forehead, cheeks, chin,
arms, back, buttocks, thighs, breast, eyelids and chest. The overlying skin
can be normal, discoid or poikilodermatous. Ulcerations may occur.
Malar rash is characterised by erythematous, slightly oedematous patch,
with no scars or atrophy over the malar skin. The onset is usually abrupt and
lasts for hours, days or weeks. The appearance may simulate a
photosensitivity eruption, dermatomyositis, or other disorders such as
seborrhoeic dermatitis or rosacea. The lesion can affect any parts of the skin.
Bullous SLE is a rare (< 5%), acquired subepidermal blistering disease
occurring in a patient with SLE, in which immune reactants are present at
the dermoepidermal junction on either direct or indirect
immunofluorescence.
Table II: Nonspecific LE Lesions
Livedo reticularis 1
Maculopapular lesions
Mucinous infiltration
Nonscarring alopecia
Oral erosions 2
Photosensitivity 3
Vasculitis (urticarial lesions, palpable purpura, gangrene, ulcers

etc.)
Livedo reticularis describes a lace pattern of cyanotic skin discoloration. It is
due to dilatation of subpapillary venous plexuses and occlusion of small
vessels feeding the upper cutis and is accentuated by cold.
Intraoral discoid lesion is easily confused clinically and histologically with
lichen planus. They frequently become erosive, leading to further scarring
and infection.
The symptoms of photosensitivity refer to an increased redness, swelling,
itch and irritation of the pre-existing lesions upon sun exposure.
1.5. Systemic Features
About 5% of CCLE and up to half of SCLE patients will have systemic
involvement. Most SCLE patients have a relatively mild systemic illness and
neurological and renal diseases are uncommon. The features of SLE are
protean and sometimes confuse clinicians (Greenwald's hypothesis a ). A
summary of the systemic features reported in a local study involving 137 LE
cases b (> 90% of patients fulfilled four or more ACR criteria) is depicted in
Table III.
Table III: Systemic Features of SLE
Systemic features of SLE Overall incidence (% of
patients)
Arthritis/arthralgia 71
Renal 69
Haematological (thrombocytopenia,
pancytopenia, leucopenia, 38
haemolytic anaemia)
Serositis 20
Neurological 26
Others ¡@
Unexplained fever 28
Lymphadenopathy 18
Raynaud's phenomenon 15
1.6. Investigations
For every patient with skin lesions of LE irrespective of the morphology, an
initial work-up should be performed to exclude any systemic involvement. A
battery of blood tests include:
1.6.1. Blood Tests
Haematology: Haemoglobin, reticulocyte, white cell with differentials,
ESR
Biochemistry: Renal and liver functions
Urinalysis: Red cells and proteins
Serology/Immunology:
1) Anti-nuclear antibody (ANA)
2) Anti-double stranded DNA (Anti-dsDNA)
3) Anti-ENA (especially anti-Ro/La)
4) Anti-cardiolipin antibody (ACL)
5) Lupus anticoagulant
6) Immunoglobulins (Igs)
7) Complement levels
8) VDRL test for syphilis
In the absence of specific clinical symptoms and if initial investigations are
normal, a half to one yearly monitor of complete blood count, ANA, and
urinalysis is adequate. Patients with persistent abnormal test results should
be seen more frequently (e.g. 3-monthly) to identify evidence of SLE.
Compared with SLE, blood test results in cutaneous LE are usually normal
or only mildly deranged. Abnormal test results in cutaneous LE include a
low haemoglobin, thrombocytopenia, leukopenia, raised ESR, raised titres of
ANA, anti-Ro (SSA)/La (SSB), ACL and biological false positive VDRL
test for syphilis.
ANA is one of the most common tests requested. It is a group of antibodies
that react with one or several nuclear constituents. It is usually detected by
indirect immunofluorescence tests where antibodies in the patient's serum
react with a substrate (rat liver, monkey oesophagus or HEP-2 human cell
line), and after washing and incubation with fluorescein-labelled antihuman
Igs. It is then examined under the fluorescence microscope and a patterned
fluorescence in the substrate nuclei is revealed. The information on pattern
and titre can be obtained from this test. The different patterns of ANA
observed correlated with antibodies against specific nuclear antigens and
may infer different rheumatological disorders. However, pattern
differentiation needs experience, and in the case where antibodies to more
than one nuclear constituent are present, the interpretation is even more
difficult. Therefore, to identify ANAs by antigen instead of fluorescence
pattern is more rewarding. ANA titres are elevated in about 20 to 60% of
CCLE, whereas a higher incidence is noted in SLE. It should be noted that a
positive low ANA titre can occur in normal individuals and non-LE diseases
and hence its presence is not specific for LE. ANA titres fluctuate during the
course of a disease. They cannot accurately reflect disease activity and
therefore not recommended to gauge progress of LE.
Anti-Ro (SSA) antibody is present in 30-50% of SLE (this figure is higher in
Orientals b) and up to 95% of SCLE on repeated testing. Hence, absence of
these is evidence against the clinical diagnosis of SCLE. Anti-dsDNA and
anti-Sm occur in SLE, whereas anti-U1RNP suggests mixed connective
tissue diseases. The high titre of anti-Ro in SCLE is said to be related to
photosensitivity but the low titre that appears in some cases of CCLE does
not indicate the risk of photosensitivity. Lee et al b reported a 69% positive
rate for anti-dsDNA antibodies in SLE.
1.6.2. Histopathology
The early stage of acute LE rash shows non-specific features, papillary
dermal oedema and perivascular lymphocytic infiltrate can be found.
Adnexal involvement is lacking. In an established lesion, epidermal atrophy,
liquefaction degeneration, and papillary dermal fibrinoid deposition are
noted.
CCLE shows epidermal hyperkeratosis with follicular plugging, thinning
and flattening of the stratum malpighii, basal cell hydropic degeneration,
periappendageal lymphoid cell infiltration, and upper dermal oedema and
vasodilatation. SCLE shows similar histological features except that scarring
and follicular plugging are absent and epidermal atrophy is not prominent.
Lupus panniculitis is characterised by infiltration of fat cells by
lymphocytes, plasma cells, and histiocytes. Septal fibrosis, lobular
hyalinised sclerosis, and vessel wall hyalinization are evident. Lymphoid
follicles are often present.
Bullous SLE shows interface dermatitis, superficial ?/font> deep
perivascular infiltrate with neutrophil predominance. Mucin deposition in
dermis is evident. A subepidermal blister is evident in an established case.
Immunofluorescence (IMF) study is not essential for the diagnosis of LE but
is helpful when other features are not diagnostic (e.g. a biopsy from an acute
LE lesion or scalp with scarring alopecia). Direct IMF study often shows
IgG, IgM and complement deposition at the dermoepidermal junction. The
lupus band test is positive for nonlesional exposed and sometimes
unexposed skin in SLE but this is usually negative in CCLE.
1.7. Diagnostic Pitfalls

1) Discoid lesions are usually specific but at times may be confused with:
Polymorphic light eruption (PLE)
Rosacea
Seborrhoeic dermatitis and psoriasis on the face
Tinea faciei
Lichen planopilaris, pseudopelade of Brocq, and tinea tonsurans
Jessner's lymphocytic infiltration of the skin
2) Papules and plaques of SCLE:
Psoriasis
Photodrug or polymorphic eruption
Erythema centrifugum annulare and dermatophytosis
1.8. Management of Cutaneous Manifestations
General:
1) Avoidance of sun: patients should be advised on the avoidance of sun and
strong light, the use of broad brim hat and tight woven clothing should be
emphasized.
2) Sunscreens to shield out UVB and UVA are required. The sunscreen
should have sun protection factor (SPF) >15. More frequent application of
sunscreens is necessary at the time of profuse sweating and swimming.
3) Drugs that potentially aggravate LE should be avoided.
Topical:
4) Topical steroid: potent topical or intralesional steroid is helpful for
localized and mild disease. Mild steroid is sufficient for lesion of NLE. Care
should be exercised to avoid side effects induced by prolonged application,
the face is most susceptible.
Systemic:
5) Antimalarial: Hydroxychloroquine is effective for widespread cutaneous
diseases and may prevent new eruptions. It also serves as an adjunct in SLE.
The initial dose is 400 mg/day, followed by 200-400 mg/day depending on
response. Response usually occurs in four weeks. CBP, RFT and LFT should
be monitored and regular examination by ophthalmologist needed. If
response to hydroxychloroquine is poor, quinacrine can be tried but
yellowish skin discoloration is a notable side effect.
6) Dapsone: is effective for bullous SLE, vasculitis, oral ulcerations.
Haemolytic anaemia is a major side effect and should not be used in patients
who are Glucose-6-Phosphate dehydrogenase deficient.
7) Thalidomide: Alternative therapy when antimalarial fails or is
contraindicated. It is teratogenic and is contraindicated in women of child-
bearing age. Neuropathy is another important side effect, and patients should
receive periodic neurologic assessment and nerve conduction studies.
8) Etretinate: reported to be useful for hyperkeratotic lesions.
9) Prednisolone: Is very useful for cutaneous and systemic diseases. Side
effects limit its prolonged use.
10) Immunosuppressives - azathioprine is most commonly used, it is usually
given with prednisolone and hence steroid-sparing. It has been reported to be
useful for palmoplantar lesions.
1.9. Risk Factors of CCLE for Dissemination and/or Systemic
Involvement
No single data can accurately predict which patient will have progressive
skin disease or internal organ involvement. However, the following history
or test results, in different combinations at appropriate settings, should alert
the clinicians for close monitoring.
1) Clinical
Unexplained persistent fever, Raynaud's phenomenon, arthralgia/arthritis,
diffuse alopecia, progressive lower limb oedema, mucocutaneous vasculitis,
and CCLE affecting a very young patient.
2) Laboratory tests
Anaemia, thrombocytopenia, leucopenia and raised ESR.
Positive Anti-dsDNA and/or anti-Sm.
Very high ANA titre (some believed a correlation exists with dissemination
of skin lesions. It is not an useful indicator of progression to SLE).
High titre of ACL.
Biological false positive test for syphilis.
Low titres of C3, C4.
3) Lupus band test
Deposits of IgG, IgM, IgA or all three in nonlesional, non-facial,
sunprotected skin is highly suggestive of SLE.
4) Other
HLA-B8 females at the ages of 15-40.
N.B.: a) Greenwalds' hypothesis of Lupus states that anything happening to
a patient with SLE which is not immediately otherwise explicable will
automatically be blamed on the lupus, regardless of pathophysiologic
validity.
b) Modified from Lee SS. Lupus 1993;2:105-109
2. Dermatomyositis
This is characterized by skin rash, muscle weakness and tenderness. In
addition to skin and skeletal muscle involvement, there may be involvement
of muscles of gastrointestinal system (dysphagia and aspiration), heart
(cardiomyopathy, arrhythmias), and lung (pulmonary fibrosis).
2.1. Epidemiology
Dermatomyositis (DM) is an uncommon condition. Female is twice as
commonly affected as male. In young female patients it is associated with
autoimmune connective tissue diseases. There may be underlying systemic
malignancy, particularly for patients over 40 years old. DM is more often
associated with malignancy than polymyositis. Common malignancies
include breast, lung, gastrointestinal, ovarian cancer, and in our locality
nasopharyngeal carcinoma. The cancer may precede, occur simultaneously,
or follow DM. Removal of underlying malignancy may be associated with
resolution of DM, and recurrence of malignancy may lead to relapse of DM.
Presentation and clinical course may be: acute, subacute, chronic.
The severity of cutaneous involvement does not correlate particularly well
with severity of associated myositis. Muscle involvement without cutaneous
features is termed polymyositis. Cutaneous involvement may precede
muscle involvement, or occur without apparent muscle involvement.
Muscle involvement include:
Muscle pain and tenderness affecting trunk, limb girdles and proximal limbs.
Muscle weakness is symmetrical and bilateral.
Weakness is progressive, with difficulty rising from low chairs, climbing
stairs, and holding arms above shoulder during combing hair.
Facial and bulbar muscles are usually spared, but may be affected in cases
associated with malignancy or myasthenia. Dysphagia may occur due to
oesophageal involvement, arrhythmia and cardiac failure due to myocarditis.
Cutaneous features include:
Violaceus erythema and oedema of periorbital region, especially upper
eyelids. There may be diffuse redness and swelling of entire face, extending
to other sun-exposed areas.
Photosensitivity, poikiloderma (erythema, pigmentation, telangiectasia,
atrophy) of face and upper chest shoulders and arms.
Red to violaceous patches and plaques over extensor surface of elbows and
knees.
Gottron's sign refers to such patches and plaques over knuckles (dorsal
surfaces of interphalangeal joints). In LE, similar changes are
characteristically located on dorsal phalanges between the phalangeal joints
instead.
Raynauds phenomenon, periungal erythema and telangiectasia.
Lupus like and sclerodermatous skin involvement.
Calcinosis, chronic ulcers. Calcinosis universalis in juvenile DM.
Childhood form of DM is often slow and progressive, characterized by
calcinosis. The calcinosis often involve intermuscular fascial planes, but
may be subcutaneous and acral (elbow, knees, fingers) as in adults. Juvenile
DM are usually steroid responsive, but often associated with contractures
and deformity, leading to functional disability and morbidity. One variant is
characterized by vasculitis of muscles and gastrointestinal tract, rapid onset
of severe weakness, steroid unresponsiveness and death. Internal malignancy
is seldom seen in either type.
2.3. Diagnosis
This is essentially clinical, supported by investigations (q.v.).
Periorbital heliotrophic rash, especially upper eyelids.
Gottrons patches over knuckle.
Poikilodermatous rash over sun-exposed areas and extensor surfaces of
upper limbs.
Peri-ungal erythema and telangiectasia.
Proximal girdle muscle tenderness and muscle weakness.
Muscle enzymes are raised, and muscle biopsy shows typical inflammatory
changes.
Diagnosis is straightforward with classical cutaneous features and
documented muscle involvement. However diagnostic difficulty arises when
there is no apparent muscle involvement and the skin rash is relatively non-
specific. With time clinical features may become characteristic of DM, but
sometimes another diagnosis (e.g. LE) may become apparent instead. The
diagnostic implication of adult DM is to screen for underlying malignancy,
together with close monitoring and follow up.
2.4. Diagnostic Pitfalls
The following conditions may be confused with DM when the clinical
presentation is atypical. In such situations, DM needs to be considered and
differentiated from such conditions.
1) Cutaneous Features
Systemic LE, subacute lupus, mixed connective tissue disease.
Rosacea, facial eczema, photosensitive dermatitis, erythema multiforme.
Erysipelas, angioedema, lymphatic or SVC obstruction.
Radiodermatitis, mycosis fungoides, scleroderma
2) Muscle Weakness
trichinosis
myasthenia gravis
muscular dystrophy
toxoplasmosis
2.5. Investigations
1) Diagnosis
Diagnosis is essentially clinical, as cutaneous histopathological features are
non-specific. There is vacuolar interface dermatitis with sparse superficial
perivascular lympho-histiocytic infiltrate, which is consistent but not
diagnostic of DM. Immuno-flourescence studies do not show significant
immune deposits at dermo-epidermal junction. Skin biopsy may differentiate
LE from DM when clinical features are nonspecific, but this is also difficult
unless characteristic LE histopathological features are present. (q.v.)
2) Assess extent of involvement
a) Muscle enzymes CPK, AST, LDH are performed to document myositis
and assess progress during treatment. Muscle enzymes are not specific of
DM, it may be elevated in other situations or apparently normal in DM
without significant muscle involvement. Twenty four hour urine for creatine
may increase sensitivity, but is not readily available.
b) Muscle involvement is often focal, and electromyography EMG may help
to locate the affected muscles. Random muscle biopsy is subjected to
sampling errors. Magnetic resonance imaging (MRI) has recently been
investigated as a sensitive tool for locating subclinical myositis and guide
muscle biopsy, even if muscle enzymes and EMG were apparently normal.
c) ECG and echocardiography may be necessary as clinically indicated to
assess cardiac involvement. Lung function may be need to monitor
respiratory muscle involvement. Barium swallow to assess pharyngeal and
eosophageal motility, and aspiration.
3) Look for an aetiology
Routine and special investigation as directed by thorough history and careful
examination.
a) Screening for underlying malignancy
Stool for Occult Blood
CBP, ESR
Carcino-Embryonic Antigen, a -Feto Protein
IgA-EBV
Chest X Ray
Skull X Rays for NPC views
ENT examination and nasopharyngeal biopsy
Careful examinations of gastro-intestinal, breast, pelvic and gynaecological
systems, with endoscopy, mammography, and ultrasound pelvis, as
indicated.
b) Auto-immune screen
These investigations may help to differentiate DM from other auto-immune
connective tissue diseases and overlapping syndromes, in conjunction with
clinical features.
ANA is present in both LE and DM.
Anti-double stranded DNA, low C3 and C4 (systemic LE).
Anti-ENA, Anti-U1RNP (Mixed Connective Tissue Disease).
Anti-Ro, Anti-La (Subacute cutaneous lupus and Sjogrens syndrome).
Anti PM-Scl (Polymyositis scleroderma overlap syndrome).
Anti-Jo1 (histidyl tRNA synthetase) antibody, polymyositis with interstitial
lung disease, pulmonary fibrosis.
2.6. Treatment
1) Treatment of skin diseases:
Sunprotection: Avoid outdoor activity around mid-day, protective clothing,
broad spectrum UVA and UVB sunscreens with SPF>15
Topical steroids
Antimalarials: Hydroxychloroquine (below 6.5 mg/kg/day), same as for
cutaneous LE.
Systemic steroids are sometimes used but generally more effective in
controlling myositis than cutaneous manifestations Systemic steroids may
cause steroid myopathy with prolonged use, leading to paradoxical decrease
in muscle weakness following steroid dosage reduction. Twenty four hour
urine creatine levels are not elevated in steroid myopathy.
2) Treatment of muscle involvement:
This should preferably be managed in conjunction with physicians.
Bed rest during the acute phase. Physical therapy, physiotherapy especially
important in juvenile DM to prevent contractures and deformity.
Systemic steroids are the mainstay of therapy for myositis. Initial dose of
prednisolone is 1 mg/kg/day, with dose adjusted according to clinical
response and muscle enzymes.
Methotrexate, azathioprine, cyclophosphamide, cyclosporin as
immunosuppressives and steroid sparing agents.
Pulse intravenous methyl-prednisolone, plasmapheresis and intravenous
immunoglobulin infusion have been tried in acute life threatening stages for
rapid control and stabilization.
2.7. Prognosis
The prognosis of adult DM is that of the underlying malignancy. Childhood
DM usually has less mortality, but substantial morbidity including
calcification and contractures especially if not treated early. DM and
pregnancy may adversely affect each other. Facial lesions and muscle
weakness get worse, fetal loss occurs.
3. Scleroderma
Scleroderma describes the thickening and hardening of the skin due to
progressive accumulation of dermal collagen, leading to fibrosis and loss
mobility of skin. It can exist as cutaneous or systemic form. Cutaneous
forms are morphea, linear scleroderma, and generalised morphea, these are
confined to the skin as tight indurated plaques. Systemic sclerosis refers to a
similar process involving not only the skin but internal organs as well, and
may lead to organ failure or even death. Organs affected include lung, gut,
kidneys, heart and skeletal muscle. Common causes of death are aspiration
pneumonia, pulmonary fibrosis, and renal failure,
3.1. Diagnosis
Proximal diffuse (truncal) sclerosis, with skin tightness, thickening and
nonpitting induration.
Sclerodactyly, with sclerosis affecting only fingers or toes, leading to
sausage shaped digits.
Pitted scarring of finger tips due to loss of substance from digital pulp, with
tapering of fingertips.
Bilateral basal pulmonary fibrosis.
Other clinical features include: Raynauds phenomenon, telangiectasia of
posterior nail fold, calcinosis of finger tips and matted telangiectasia on face
and hands. Skin tightening may lead to mask face, beaked nose, and radial
furrows around mouth. There may be generalised hyperpigmentation with
hypopigmented patches on the skin.
3.2. Skin Biopsy
In the dermis there are thick bundles of collagen running parallel to the skin
surface, with entrapment of sweat glands and adenexal structures. The
overlying epidermis tends to be thin and atrophic.
3.3. Immunology
ANA
CREST: anti-centromere antibody positive
MCTD: associated with ENA, anti-U1RNP positivity
Systemic sclerosis: ANA, Scl 70 antibody positivity
3.4. Sclerodermatous Syndromes
Many conditions have widespread induration of the skin. It is beyond scope
here to discuss individual conditions, but they should be borne in mind in the
differential diagnosis of a sclerodermatous condition. Some conditions are
more responsive to treatment than systemic sclerosis.
Auto-immune or connective tissue diseases:
Generalised morphea
Progressive systemic sclerosis
CREST syndrome (calcinosis, Raynauds, oesophageal dysmotility,
sclerodactyly, telangiectasia)
Mixed Connective Tissue Disease (MCTD): DM, SLE, scleroderma
Eosinophilic fasciitis
Chronic graft versus host disease
Environmental agents or drugs:
Bleomycin cancer chemotherapy
Eosinophilic myalgic syndrome following L-tryptophan ingestion
Occupational vinyl chloride, epoxy resin
Metabolic or associated conditions:
Porphyrias: porphyria cutanea tarda, variegate porphyria, hereditary corpo-
porphyrias
Porphyria like conditions: pseudoporphyria, epidermolysis bullosa acquisita
Diabetic chrieopathy, scleredema
InfectiInfective, malignant, infiltrative conditions:
Papular mucinosis, scleromyxoedema
Primary systemic amyloidosis
Cutaneous T-cell lymphoma
Lepromatous leprosy
3.5. Treatment
Systemic sclerosis is an uncommon condition with a highly variable course.
Some progress relentlessly till death, others remain insidious or even
improve with time. Many agents have been tried, but to date no single agent
has predictably arrest or reverse the fibrosing process. Treatments that have
been tried include penicillammine, colchicine, ketotifen, cyclosprine, g
-interferon, plamapheresis, PUVA and extra-corporeal photochemotherapy.
Treatment is mainly symptomatic, or to prevent complications. Raynauds
phenomenon and digital ischaemia may be controlled with calcium channel
blockers such as nifedipine, supplemented with pentoxifylline,
dipyridamole, intravenous prostacyclin infusion. Cutaneous ulcers may be
managed by protective occlusive dressing. Physiotherapy with emphasis on
full range of motion of all large joints to prevent contractures and deformity,
thereby preserving function. Management of extra-cutaneous involvement
should be in conjunction with physicians. Renal hypertension is treated with
captopril. Steroids are not effective in systemic sclerosis, but useful for
myositis in MCTD and for eosinophilic fasciitis.
BL ISTER ING D ISE ASES

Dr. C.N. LOOK
CH APTE R 10
1. INT RO DU CTI ON
Blistering diseases are defined as skin disorders that primarily give rise to
vesicles (i.e. 5 mm or less in diameter) or bullae (i.e. over 5 mm in diameter).
Blisters are accumulation of fluid lying within or below the epidermis. Blistering
diseases can be classified according to the site of cleavage (see Table 1). Only
the common conditions will be discussed below.
Tab le 1 : C au ses of B li st er in g D is eases
A) Subcorneal Blisters: 1) Bullous Impetigo
2) Subcorneal Pustular dermatosis
3) Miliaria Crystallina
B) Intra-epidermal Blisters: 1) Acute Dermatitis
e.g. eczema, contact dermatitis
2) Pompholyx
3) Herpes infections
4) Fixed Drug eruptions (epidermal
type)
5) Friction Blisters
6) Erythema multiforme (epidermal
type)
7) Pemphigus Vulgaris
C) Subepidermal Blisters: 1) Bullous Pemphigoid
2) Linear IgA Diseases
3) Dermatitis Herpetiformis
4) Erythema Multiforme (dermal
type)
5) Fixed Drug Eruptions (dermal
type)
6) Epidermolysis Bullosa
The diagnosis of blistering diseases can sometimes be aided by physical
findings.
1) Morphology of blister:
Subepidermal blister occurs between the dermis and the epidermis. It contains
thick wall and may contain blood.
Intraepidermal or subcorneal blister usually has very thin roof. Intact blisters
may not be easily detected but leaving erosions only.
Palm and sole blisters usually remain intact because of the thick stratum
corneum.
Grouped vesicles along a dermatome is characteristic of herpes infection.
2) Site of blister:
Pompholyx occurs at palm and soles.
Blisters at sites of frequent trauma suggests Epidermolysis Bullosa.
3) Mucosal membrane involvement is frequently found in pemphigus, erythema
multiforme and fixed drug eruption.
2. BU LLOU S IM PETIG O
Bullous impetigo is usually caused by Staph. aureus while non-bullous type can
be caused by Staph. Aureus and occasionally by Strep. pyogenes. More common
in children and mainly affects face and hands. Bullae are flaccid and usually
contain pus. When the pustules are ruptured, they give rise to golden crusts.
Diagnosis: Swab from pustules for culture
Treatment:
1) Topical antibiotics (e.g. fusidic acid cream, mupirocin ointment,
chlortetracycline ointment) is good for localized infection.
2) Oral antibiotics (e.g. cloxacillin, erythromycin) for widespread lesions.
3. SU BC OR NEAL P USTUL AR DE RM ATOS IS

A chronic, benign, relapsing, pustular eruption with unknown aetiology. Female
is more commonly affected than male. The peak incidence occurring at the age
of 40-50. The eruption occurs mainly in the groins, axillae, submammary areas
and the flexor aspect of the limbs. The face is never affected, nor are the mucous
membranes. Lesions usually start off as intact pustules which dry up within a
few days, forming crusts or scales. Eruption tends to group together to form
clusters with advancing edge.
Differential diagnosis: 1) Pustular psoriasis
2) Impetigo
Diagnosis: Skin biopsy shows the presence of subcorneal pustules.
Treatment: 1) Dapsone: Treatment of choice (50-100 mg/day)
2) Oral Steroid: less effective as compared with dapsone
¡@
4. MIL IA RI A CR YST ALLIN A
This condition occurs in hot and humid climate when babies are wearing too
many clothes. It leads to blockage of the sweat ducts. Clinically, numerous
monomorphic clear vesicles without surrounding erythema are seen on the skin,
usually the trunk. Typically the skin remains dry. The disease is self-limiting.
Calamine lotion can be prescribed. Prevention is by avoiding prolonged hot,
humid environment and overclothing.
5. AC UTE DE RM ATITI S (A CUTE E CZEMA )

Vesicles are common sign of acute dermatitis. They are usually associated with
intense pruritus. Vesicles are easily ruptured because of self scratching and
results in multiple excoriations.
Treatment: Refer to Chapter 3.
6. PO MPH OLYX
A distinct pattern of acute dermatitis as characterized by acute onset of multiple
itchy vesicles +/- bullae at palms and soles. Vesicles seldom rupture because of
the thick stratum corneum. Usually, the cause is unknown but occasionally may
be secondary to severe tinea infection or contact dermatitis occurring in other
part of the body.
Treatment: Requires potent topical steroid (e.g. 0.025% fluocinolone). Oral
antibiotics (e.g. erythromycin) is indicated if there is evidence of secondary
bacterial infection. In very severe case, a short course of oral steroid may be
required.
7. HE RPES IN FECT IO NS (HE RPES S IMPLE X/ HER PES ZOSTE R)
Pain is the most useful symptom to differentiate blisters caused by herpes
infections from other blistering disorders. Eczema or tinea infection gives rise to
itchy rather than painful vesicles. In contrast to pemphigus or pemphigoid which
may give rise to painful lesions, the vesicles of herpes infections are more
localized.
Refer to Chapter 14 for clinical features and management.
8. FR ICT IO N BL ISTERS
It occurs at hands and feet. Diagnosis can be easily made from history e.g.
wearing ill-fitting or new shoes.
9. FI XED D RU G ER UPTI ONS

It is presented as well-circumscribed erythematous patches or bullae, frequently
occurring at hands, penis and mouth. A characteristic feature is the recurrence of
the same skin lesions at the same sites when patients are challenged by the same
offending agents again. Lesions heal with circumscribed pigmentation.
Histologically, subepidermal or epidermal blisters can occur. Basal cell
degeneration and pigmentary incontinence are often seen. The common
offending drugs include tetracycline, barbiturates, sulphonamides,
phenolphthalein, salicylate and oxyphenbutazone. The disease is self-limiting.
Avoidance of offending drug is most important.
10 . E RYT HEMA M ULTI FOR ME
10 .1 . Aet io log y a nd P at ho ge nesi s
It is a hypersensitivity reaction to infections (e.g. herpes simplex, streptococcus,
mycoplasma) or drug (e.g. penicillins, sulphonamides, barbiturates, piroxicam).
10 .2 . Clini cal Feat ures
Typically, discoid well-demarcated erythematous plaques with central blisters or
central necrosis can be found at 4 limbs (i.e. target lesions). Occasionally, bullae
with erythematous base can occur. Stevens-Johnson syndrome is a severe form
of erythema multiforme with mucosal involvement.
10 .3 . Dia gn os is
The diagnosis can be confirmed by skin biopsy. The cause can sometimes be
found by looking for primary site of infection (e.g. herpes) and by taking a
detailed drug history.
10 .4 . Treatme nt
For mild cases, giving topical steroid may be all that is needed. For frequent
recurrent attacks, one should look hard for the presence of herpes infection.
Maintenance oral acyclovir treatment can be considered in the latter. The
beneficial effect of oral prednisolone in Stevens-Johnson syndrome is
controversial.
11 . PE MPH IG US VU LGA RI S
11 .1 . Intr od uc ti on
A potentially life-threatening skin condition.
The disease occurs worldwide.
The incidence is 0.1-0.5/100,000.
The peak incidence is between 4th-6th decade.
11 .2 . Pa th og enes is
An autoimmune disease due to binding of circulating antibodies to the epidermal
intercellular substance which is desmoglein 3. The binding leads to acantholysis
i.e. loss of intercellular adhesion.
11 .3 . C/F
It presents as blisters attacking the skin including mucosae (i.e. oral mucosa,
conjunctiva). Intact blister is seldom seen because the roof of the blister is thin
and is easily ruptured. Ruptured bullae lead to the formation of erosions.
Nikolsky's sign (i.e. rubbing normal skin causes new lesion to form) is
characteristic. Eruption tends to develop on the trunk and the face with sparing
of the extremities (centripetal distribution). Involvement of the oral mucosa gives
rise to painful ulcers.
11 .4 . Inv est iga ti on
1) Skin biopsy for histology
This is done to confirm the diagnosis. In order to see the diagnostic features,
new, rather than old lesion should be chosen for biopsy. Classically, one should
find suprabasal blister with acantholysis in histology.
2) Skin biopsy for Direct Immunofluorescence (IMF)
Perilesional skin shows the presence of intercellular IgG deposition within the
epidermis.
3) Indirect Immunofluorescence (Serology)
Serum from the patient allows the titre of the circulating anti-intercellular
antibody to be measured. The titre correlates with the disease activity and is a
good parameter for monitoring the disease progress. A more than twofold
increase in titre is an indication of relapse. This test is not casually available. It
can only be done in a few hospital-based centres with special arrangement.
4) Tzanck test
A cytology method revealing the characteristic acantholytic cells. It provides an
instant diagnosis. However, it is seldom done since it requires expert cytologist
and it also carries a significant false positive as well as false negative rates.
11 .5 . Mana gement
Potentially lethal disease. Hospitalization is often required for close monitoring
of disease progress. Hospitalization is particularly indicated if any one of the
following conditions which signifies severe involvement occurs:
1) Extensive cutaneous involvement
2) Systemic upset
3) Mucosal involvement other than oral cavity
4) High indirect immunofluorescence (IMF) titre.
11 .6 . Top ica l Trea tmen t
Potent topical steroids have to be used (e.g. clobetasol propionate). Usually
given as an adjuvant therapy. Rarely, when skin lesions are very localized, then
topical treatment can be given as a single therapy. For oral lesions, one can try
triamcinolone in orabase, intralesional steroids or steroid aerosol.
11 .7 . Sys temi c Treatme nt
1) Oral Steroid
Prednisolone is the drug of choice. To control the acute attack, usually it requires
a very high dose (i.e. 60-80 mg daily) to start with. Occasionally, > 100 mg of
prednisolone has to be prescribed for very severe cases. Steroid may be
increased by 50% every 4-7 days until the disease is controlled. The dose of
prednisolone is adjusted further to consolidate the remission and is maintained
for 2-4 weeks. It can then be gradually tailed down. The control of the disease
activity is indicated by no new eruption, low titre of anti-intercellular antibody.
Watch out for complications especially silent infection during high dose oral
steroid treatment.
2) Steroid-sparing Agents
Since a relatively high dose of prednisolone is usually required to control the
disease, in order to prevent the long term side effects of oral steroid (e.g.
opportunistic infections, osteoporosis), an immunosuppressant can be added for
its steroid sparing effect. Commonly used immunosuppressants are:
a) Azathioprine (2-3 mg/kg/day)
b) Cyclophosphamide
c) Methotrexate
The major side effects of azathioprine and methotrexate are marrow suppression
and hepatotoxicity. Cyclophosphamide may give rise to haemorrhagic cystitis,
infertility as well as marrow suppression. Regular monitoring of CBP and LFT is
needed when prescribing these steroid sparing agents. Because of the delayed
onset of action of the immunosuppressants at 4-8 weeks, they are often
commenced together with the oral steroids.
11 .8 . Treatme nt o f R ecal ci tr an t Ca ses
1) Plasmaphaeresis
This in-patient treatment is only available in major hospitals. The renal team in
the hospital can be consulted for providing the treatment if it is indicated.
2) Pulse Methylprednisolone Therapy
3) Cyclosporin A
4) Dapsone
5) Tetracycline/minocycline + niacinamide
6) Gold
7) Chlorambucil
11 .9 . Ind icat io ns o f T reatme nt Res po nse
1) No new lesion develops
2) Healing of old lesions
3) Dropping circulating antibody titre (indirect IMF)
12 . B ULL OUS PE MPH IGO ID

It is about 2 times more common than pemphigus vulgaris. Usually occurs in old
age (i.e. >60). It is present worldwide and affects male to female equally.
Production of autoantibody reacting with basement membrane zone which in
turns leads to separation of epidermis from the dermis. The target sites are major
& minor bullous pemphigoid antigens which are lying in the hemidesmosomes.

Early lesions in form of urticarial plaques may precede bullae. Presents as large
intact blisters at lower abdomen, inner thighs, groin, axilla and flexures. Mucosal
lesions are less common and often less severe than Pemphigus Vulgaris.
12 .4 . Inv est iga ti on s
Fresh lesion often demonstrates subepidermal blisters with mixed dermal
infiltrates, especially eosinophils.
2) Skin biopsy for Direct Immunofluorescence (IMF)
Direct IMF of perilesional skin shows linear deposition of IgG +/- C3 at dermal-
epidermal junction (Basement membrane zone)
3) Indirect Immunofluorescence (Serology)
Circulating IgG or C3 to basement membrane zone can be detected in 75% of
patients. The serology titre does NOT correlate with disease activity. Therefore,
this test is seldom performed.
12 .5 . Mana gement
Rough indication of severity
1) Mild: < 20 lesions
2) Moderate: 20-40 lesions
3) Severe: > 40 lesions
If severe, patient needs hospitalization.
Drug Treatment:
1) Localized and mild case: Potent topical steroid (e.g. Clobetasol propionate)
alone may control the disease.
2) Generalized disease: Oral steroid
The dosage of prednisolone required for controlling the disease is usually less
than that of pemphigus vulgaris.
One can start off with 40-60 mg prednisolone daily. When the disease is under
control, gradually tails it down to maintenance dose.
Recalcitrant Cases:
Adjuvant Immunosuppressant: e.g. azathioprine, cyclophosphamide,
methotrexate, chlorambucil. Bullous pemphigoid is more commonly found in old
age. These patients are more prone to the side effects of these drugs. Long term
use of chlorambucil is not recommended because of the potential danger of
developing acute myeloid leukaemia. Regular monitoring of CBP and LFT are
needed.
Tetracycline 500 mg qid/minocycline 100 mg bd + niacinamide 500 mg tds
Pulse Methylprednisolone Therapy
Plasmaphaeresis
Cyclosporin A
Dapsone
12 .6 . Pro gn os is
The disease is often self-limiting. Spontaneous remission occurs in 3-6 years
time.
13 . L INEA R IG A D ISE ASE

A rare blistering disorder as characterized by linear IgA deposition in basement
membrane zone.

It has 2 subtypes:
1) Adult type (around 60)
2) Childhood type (average onset around age of 5)
Cutaneous Lesions:
1) Adult type: mainly affects trunk, face, perineum, hands and feet
2) Childhood type: perioral region and perineum are common sites
Blisters typically occur in clusters.
Mucosal Lesions:
Besides cutaneous lesions, half of the patients have oral or even ocular
involvement as well.
In majority of the cases, the picture resembles Dermatitis Herpetiformis.
Occasionally, some may simulate Bullous Pemphigoid histologically.
2) Direct Immunofluorescence (Direct IMF)
Characterized by linear IgA deposition in basement membrane zone (BMZ).
3) Indirect Immunofluorescence (Indirect IMF)
Test for anti-BMZ IgA Ab is not available in Hong Kong.
13 .4 . Treatme nt
1) Dapsone: It is the drug of choice. Response usually occurs within 48 hours.
One has to be careful of dose-dependent haemolytic anaemia. Before starting
dapsone, check for G-6-P-D level.
2) Prednisolone: Used as an adjuvant therapy to dapsone or when the latter is
contraindicated. Usual dosage is 5-30 mg per day.
3) Colchicine: Used in resistant cases.
4) Topical Treatment: Potent topical steroid can be prescribed e.g. fluocinolone
0.025%
1) Adult type: most patients remit within 2 years
2) Childhood type: 50% chance of remission within 3 years
14 . D ER MATIT IS HE RPETIF OR MIS

An uncommon skin condition with the peak incidence around 30-40 years of
age. Male is more common than female.
In western countries, the disease usually associates with coeliac disease (Gluten
enteropathy). In Hong Kong, since coeliac disease is extremely rare, this
association is not usually observed.
Lesions are composed of excoriated and scabbed intensely itchy papules. The
sites of predilection are extensors of 4 limbs, buttocks and face. Intact vesicles
seldom seen since they are ruptured by self scratching. Lesions heal with no
scarring.
14 .4 . Dif fe ren ti al Di ag no si s
1) Scabies: Presence of burrows, other family members are affected and sparing
of the face are features suggestive of scabies.
2) Acute eczema: Atopic eczema affects flexures more than extensors.
Skin biopsy for histology: Microabscess in dermal papillae is characteristic.
Direct Immunoflorescence: It shows granular IgA deposition in BMZ.
Screening for the presence of coeliac disease.
14 .6 . Treatme nt
1) Dapsone: It is the drug of choice. After starting the treatment, symptoms
should subside within 48 hours and rash should be cleared up within days. Side
effects are haemolytic anaemia, methaemoglobulinaemia.
2) Sulphapyridine/sulphamethoxypyridazine: They are used when dapsone is
contraindicated.
3) Gluten Free diet: It is useful only when the disease is associated with coeliac
disease. Referring to dietician if required. Dietary restriction is not easy to
follow.
Spontaneous remission rate is low.
15 . EP IDE RM OLYSI S BU LLOSA

This is a extremely rare group of hereditary blistering disorders which are
characterized by blisters and erosions resulting from trivial trauma. Blisters
occur soon after birth and mainly concentrate on bony prominence of 4 limbs.
An acquired form mimicking Bullous Pemphigoid known as epidermolysis
bullosa acquisita (EBA) occurs in adults. Bullae tend to occur at sites of trauma.
The IgG in these patients binds to the anchoring fibrils attached to the Lamina
densa. EBA may be associated with underlying systemic diseases like SLE,
inflammatory bowel disease, amyloidosis and internal malignancy.
The diagnosis can be confirmed by skin biopsy for histopathology and
electronmicroscopy. The latter is also useful in subtyping the disease. EBA can
be differentiated from bullous pemphigoid by the sodium chloride split skin test
and immunofluorescence on the skin specimen. In EBA, the blister occurs below
the split, whereas, the blister occurs on the roof of the split in bullous
pemphigoid.
15 .3 . Treatme nt
For the hereditary EB, no effective treatment is available at present. Antenatal
diagnosis and genetic counselling can be offered. Systemic steroid can be useful
in EBA.
ALOPECIA
Dr. C.N. LOOK
CHAPTER 11
1. DEFINITION
Alopecia is defined as excessive or abnormal loss of hairs.
2. PHYSIOLOGY
Natural hair loss is a physiological phenomenon. It is not a disease. Only
when the loss is excessive or when the pattern of loss is abnormal, then it is
pathological. Before one talks about the causes of alopecia, one has to
understand the physiology of hair growth (Diagram 1).
Diagram 1: Hair Cycle
2-6 years
Anagen ---------------------------------------» Catagen
| |
Hair shedding «---------------------------------Telogen
100 days
90% of our terminal hairs are at anagen phase which is the growing phase. It
lasts for 2-6 years. The scalp hair on average grows at the rate of 0.37 mm
per day.
Catagen is a transient period. Hair matrix cells stop dividing. As a result,
there is no hair growth.
Less than 10% of our hairs should be in telogen phase which lasts for 100
days (about 3 months). Since on average, each person has about 100,000
hairs. Therefore, less than 10,000 should be in telogen phase and on each
day less than 100 hairs fall off physiologically.
3. SPECIAL POINTS TO LOOK FOR

When examining patients with alopecia the following points are worth
paying attention to:
1) Pattern of alopecia
a) Diffuse alopecia is usually due to telogen effluvium, systemic disorder
(e.g. hypothyroidism, Fe deficiency, secondary syphilis), drugs.
b) Patchy alopecia is typically seen in alopecia areata, scarring alopecia.
c) Marginal alopecia affects the hair margin only. It occurs in alopecia areata
or due to hair styling.
d) Frontal and bitemporal alopecia is typical of male-type baldness.
2) Sign of scalp inflammation indicates alopecia may be secondary to
inflammatory dermatosis (e.g. tinea capitis)
3) Presence of scarring together with alopecia will switch the differential
diagnosis towards the cause of scarring alopecia (e.g. DLE, Lichen Planus).
4) Other than the scalp, see if hairs in other areas are also affected (e.g.
axillary, pubic regions, eyebrow, eyelashes etc.).
5) Detailed drug history and history of past health are important.
4. CAUSES OF DIFFUSE ALOPECIA WITH NO SIGN OF
INFLAMMATION NOR SCARRING
1) Telogen Effluvium
a) Post-Partum
b) Severe Illness
c) Major Operations
d) Malnutrition
2) Anagen Effluvium e.g. chemotherapy
3) Male Pattern Baldness
4) Female Pattern Baldness
5) Diffuse Alopecia Areata
6) Drugs e.g. heparin, antithyroid drugs, etretinate, isotretinoin
7) Systemic Disease e.g. Fe deficiency, thyroid disease, secondary syphilis,
SLE
8) Ageing: usually causes thinning of hairs
4.1. Telogen Effluvium
When a severe insult striking our bodies (severe infection, delivery, major
operation) the anagen hairs (> 90% of hair population) will all
simultaneously shift to telogen phase. As a result, about 3 months after the
insult, more than 90% of the hairs will fall off at the same time giving rise to
the condition which is called telogen effluvium.
The diagnosis can be made from a detailed history of the past health. In case
when the diagnosis is in doubt, it can be confirmed by the telogen hair count
test. It is done by plucking a bundle of hairs and counting for the percentage
of telogen hairs present. Normally, the telogen hair count should not exceed
10% of the total hair count. Unfortunately, this test is not available in most
centres.
For telogen effluvium, no specific treatment is needed since spontaneous
remission is the rule.
4.2. Anagen Effluvium

Chemotherapy attacks the rapidly dividing cells i.e. anagen hairs. As a
result, more than 90% of hairs fall off soon after chemotherapy. Usually,
there is no problem with the diagnosis since it is obvious from the history.
4.3. Male Pattern Baldness (Androgenetic Alopecia)
4.3.1. Pathogenesis
Even though the exact aetiology is unknown, there are proofs that genetic
factor, as evidenced by frequent positive family history, and androgen play
an important role in the development of the disease. Eunuchs and castrated
males never develop baldness. Under the influence of androgen in a
genetically predisposed person, the terminal hairs are gradually transforming
into vellus hairs and they eventually fall off.
4.3.2. Clinical Features
Typically, it starts off with bitemporal recession and subsequently, thinning
or complete loss of hair at the crown. Hair on the occiput and around the
sides of the scalp is seldom affected and it seems that hair in those areas are
more resistant to the effect of androgen. The diagnosis can often be made by
the characteristic pattern of hair loss and the frequently presence of a
positive family history.
4.3.3. Treatment
No good treatment is available at present.
Topical minoxidil may be useful in minority of cases but the effect
disappears soon after stopping the treatment and yet it is expensive. It is the
only FDA approved drug at presence for the treatment of androgenetic
alopecia.
Topical ether-in-spirit: the effect is no better than placebo.
Hair Transplant: based on donor dominance theory which states that hairs
from growing areas will survive and grow when transplanted to bald areas.
The operation is tedious and requires expertise.
Wigs: quite practical if it is acceptable by the patient.
4.4. Female Pattern Baldness
It is characterized by thinning of hairs at the crown or a diffuse hair loss.
Unlike male pattern baldness, there is no bitemporal and frontal recession. If
female pattern baldness occurring in a young female, especially with the
presence of menstrual disturbance, signs of hirsutism or virilization,
excessive androgen activity needs to be excluded e.g. androgen-secreting
tumour. Treatment is difficult but one may try cyproterone acetate which is
an anti-androgen.
5. CAUSES OF PATCHY ALOPECIA WITHOUT SCARRING
Alopecia areata/totalis/universalis
Trichotillomania
Traction alopecia
Tinea capitis (excluding favus)
5.1. Alopecia Areata/Totalis/Universalis
These 3 conditions all belong to a spectrum of the same disease. They only
differ in the degree of severity. When all the scalp hair is lost, it is called
alopecia totalis. If both scalp and body hair are involved, it becomes
alopecia universalis.
Alopecia areata is the commonest cause of patchy alopecia.
5.1.1. Aetiology
The exact aetiology is unknown. Genetic factor and atopy play some role as
some patients may have positive family history or history of atopy. It is
considered as a kind of autoimmune disease since it has an association with
other organ-specific autoimmune disease (e.g. Vitiligo, Hashimoto
thyroiditis). The incidence of alopecia areata is high in patients with Down's
syndrome and those who are under stress.

The disease affects male and female equally at all age. It is presented as
discrete patches of baldness with no scarring and no sign of inflammation.
Broken hairs with tapering shafts (i.e. exclamation mark hairs) are
diagnostic. Nail pitting may also be present.
5.1.3. Treatment
Local Steroid
a) Topical Steroid e.g. 0.025% fluocinolone, halometasone
b) Intralesional Steroid e.g. triamcinolone
These treatment modalities may be useful in dealing with localized disease.
Irritants or Contact Sensitizers e.g. dithranol, diphencyprone. DNCB is no
longer recommended because of its carcinogenic potential.
PUVA/UVB: May show response in some cases but need many treatment
sessions. The actual beneficial effect is controversial.
Topical minoxidil: effect is doubtful.
Oral prednisolone: it is effective in some cases but has to be reserved for
resistant or severe cases (e.g. alopecia universalis or alopecia totalis)
because of its potential side effects.
Wigs wearing: last solution.
5.1.4. Prognosis
The prognosis is usually good since 75% of patients with alopecia areata
have spontaneous remission eventually.
Signs of Poor Prognosis:
Multiple patches
Ophiasis (extensive hair loss at occipital area)
Eyebrows and eyelashes involvement
Alopecia totalis/universalis
Young age of onset
Presence of atopic disease
Frequent recurrent attacks
Nail involvement
Down's syndrome
5.2. Trichotillomania
5.2.1. Cause
The hair loss is due to self-induced twisting and pulling of hairs. It usually
occurs in children or adolescents. It may be due to a bad habit, attention
seeking or a manifestation of psychological problem.
Patches of alopecia with no sign of inflammation are seen. Unlike alopecia
areata, the margin of the lesion is less well defined and there is no
exclamation mark hairs. The hair loss is never complete. Short broken hairs
of varying length are characteristic.
5.2.3. Diagnosis
The disease can be diagnosed clinically. A detailed social and psychological
history are essential.
5.2.4. Treatment
Often, the disease is self-limiting upon reassurance. Parents have to be
interviewed so that the problem can be addressed. Sometimes, referring
patient to clinical psychologist or psychiatrist may be helpful.
5.3. Traction Alopecia
Alopecia secondary to hair styling, hot-combing to straighten kinky hair.
It is rare in Hong Kong.
5.4. Tinea Capitis
Tinea capitis must be considered as one of differential diagnosis as a cause
of patchy alopecia in children. The infected hair are brittle and are easily
broken. It is associated with inflammation i.e. redness, scaling. Even though
for most of the time, the lesion heal without scarring, in severe cases (e.g.
kerion), scarring alopecia can occur. Please refer to the chapter on skin
infection for details.
6. CAUSES OF DISCRETE PATCHY ALOPECIA WITH SCARRING
Congenital e.g. aplasia cutis, naevus sebaceus
Post-trauma e.g. burn, injury, radiotherapy
Post-infection e.g. kerion, herpes zoster
Inflammatory dermatosis e.g. DLE, lichen planus, morphoea: common cause
of scarring alopecia
Neoplasm e.g. squamous cell carcinoma of skin
Idiopathic
6.1. Aplasia Cutis
This is a very rare congenital disease and the alopecia is present since birth.
6.2. Naevus Sebaceus
It is a kind of epidermal naevus which presents at birth as a yellowish
hairless plaque on the scalp. It becomes more warty after puberty. The
diagnosis can be confirmed by skin biopsy. It has potential of undergoing
malignant change (e.g. basal cell carcinoma). For this reason, excision of the
lesion after puberty is recommended.
6.3. Inflammatory Dermatosis Causing Alopecia
DLE, lichen planus and morphoea are common causes of patchy scarring
alopecia. Sometimes, clinically, it is difficult to differentiate them one from
another. One should examine the rest of the body to look for any sign that
are related to each of these 3 diseases. Of course, skin biopsy of the lesion
on scalp is usually helpful.
6.4. Idiopathic Scarring Alopecia (Pseudopelade)
Occasionally, despite thorough examination and investigation, no cause can
be attributed to patient's scarring alopecia. If the disease is still active,
topical steroid can be tried.
NA IL DI SEASES
1. DI SEASES O F NA IL PL ATE
Pits Psoriasis, alopecia areata, hand dermatitis, nail
biting, lichen planus
Horizontal ridges Beau's lines, any inflammation affecting soft
tissues around nails
Longitudinal
ridges: Pressure effect e.g. tumour in nail fold
Single Psoriasis, lichen planus, alopecia areata,
Multiple Darier's disease
Thickening Psoriasis, onychomycosis, pachyonychia

congenita
Onycholysis Idiopathic, psoriasis, onychomycosis, trauma,

separation of nail thyroid acropachy, drug induced photo-
plate from nail onycholysis e.g. tetracyclines
bed distally)
Subungual Psoriasis, onychomycosis, trauma, ischaemia

hyperkeratosis
Koilonychia Iron deficiency, lichen planus, idiopathic
Colour changes Infection: Pseudomonas (green)

Drugs: Tetracycline (yellow)
Antimalarial (blue)
Chlorpromazine (brown)
Topical agents: Potassium permanganate
Dyes
Systemic diseases: Cirrhosis
hypoproteinaemia
(white)
Others: Cigarette smoking
(brown)
Subungual haematoma
(reddish blue)
Melanoma (black)
Leuconychia
(whiteness of
nail): Onychomycosis, trauma, congenital
True (affect nail Anaemia, hypoproteinaemia
plate)
Apparent (affect
subungual
tissues)
Pigmented Normal in pigmented skin, malignant

streaks melanoma, benign melanocytic naevi,
Addison's disease
2. DI SEASES O F NA IL F OLD
Paronychia (inflammation of
nail fold):
Acute Trauma
Chronic Trauma, wet work, drugs e.g.
etretinate
Pterygium formation (cuticle

Lichen planus, circulatory
appears to grow out over the nail
disorders, pemphigus
with loss of proximal nail fold)
Palisading of dilated nail fold Dermatomyositis, lupus

capillaries erythematosus, scleroderma
Infarcts at posterior or lateral Vasculitis, e.g. rheumatoid

folds diseases
Viral warts, myxoid cyst,

Nail fold masses periungual, fibromata,
malignant melanoma
3. DI SEASES O F NA IL B ED AN D M ATR IX
Subungual exostosis
Glomus tumour
Tumour
Naevus
Malignant melanoma
Infection Subungual wart
4. APP RO AC HES TO N AIL D ISE ASES

A thorough history is important. Occupation is clearly relevant in trauma related
nail diseases such as chronic paroncyhia. A family history of psoriasis may
explain nail changes in the absence of any other cutaneous signs. Beau's lines
may be accountable by a previous heart attack. Drug history is especially
important in looking for causes of colour changes in nails.
All finger nails and toe nails should be examined in good lighting with the digits
relaxed. If polish or lacquer is present, it should be removed prior to
examination. Particular attention should be paid to the symmetry of the changes.
Other signs of skin diseases should be looked for elsewhere in the body e.g.
psoriatic nail changes may lead to the discovery of a small patch of psoriasis at
the back.
Nail clipping for microscopy and fungal culture should be done in suspected
onychomycosis. Biopsy is sometimes indicated, e.g., suspect melanoma.
Underlying diseases should be looked for in nail diseases associated with
systemic illness, e.g., clubbing, leuconychia etc.
5. TRE ATMENT O F CO MM ON N AI L DI SEASES

5. 1. Ac ute Pa ro ny ch ia
Bacterial infection (Staph. Aureus, Strep. Pyogenes) is the commonest cause.
There is acute swelling, tenderness and collection of pus in the nail fold. A swab
should be taken if possible.
Give ampicillin 250 mg qid and cloxacillin 250 mg qid for 10 days. Analgesic
e.g. panadol should also be prescribed. Consider incision and drainage if
swelling and pain does not improve quickly.
5. 2. Ch ro nic Pa ro nyc hi a
This is a multi-factorial condition:
1) Irritant dermatosis
2) Infection: candidal; bacterial sometimes
3) Background eczema of psoriasis
All of the factors should be eliminated.
Protection: Avoid water, detergent, soap if possible. Use rubber glove with inner
cotton glove.
Emollient: frequent application of blend emollient and use as a soap substitute.
Antibiotic: A course of systemic antibiotic should be consider in the first week.
Topical treatment: A combination of topical steroid and antifungal to the nail
fold.
5. 3. Na il Di seases i n Pso ri asi s
Nail dystrophy in psoriasis is difficult to treat. Patients should be informed of the
limited effectiveness of various treatments.
General care: Avoid trauma. Keep nail short. Rubber with inner cotton gloves.
Use emollient as soap substitutes. Exclude concomitant fungal infection.
Steroid: Ultra-potent steroid to the nail fold with or without occlusion.
Intralesional steroid is an alternative but is painful.
PUVA: Nail disease may improve with systemic PUVA for the whole body.
Topical PUVA may worth trying.
Retinoids: While subungual hyperkeratosis improves, pitting and onycholysis get
worse with etretinate.
Others: Topical calciprotriol, topical 1% fluorouracil, topical cyclosporin A have
been tried with variable success.
CUTANEOUS MALIGNANCIES
Dr. H.F. HO
CHAPTER 13
Duties of dermatologists in Social Hygiene Service in the management of
cutaneous malignancy:
1) To identify the high risk patients and the suspicious lesions.
2) To confirm the diagnosis.
3) Assess and decide whether the lesion can be adequately treated in our
clinic and give the most appropriate accordingly.
4) Refer those which cannot be adequately treated in our clinics and refer
them to a multi-disciplinary clinic for further management. Prepare to give
opinion regarding choice of treatment.
5) Follow-up of the patient.
The management of basal cell carcinoma, squamous cell carcinoma,
melanoma and mycosis fungoides will be discussed in chapter.
1. BASAL CELL CARCINOMA

1.1. Introduction
Basal cell carcinoma is the most common malignant skin tumour. Three
main clinical types of BCC are identifiable:
1) Superficial BCC
2) Nodular BCC: this may appears cystic, or may evolve into a
"rodent ulcer" .
3) Infiltrative form
- Infiltrative morphoea-form BCC
- Infiltrative non-morphea-form BCC
1.2. Diagnosis
Diagnosis of skin tumour should include a careful physical examination, not
only of the target lesion but also search for the presence of other skin
tumours. A general examination paying special attention to regional lymph
nodes and organomegaly is necessary, although distant metastasis in BCC is
rare.
Skin biopsy is indicated to confirm the diagnosis.
1.3. Treatment
The treatment goals are:
1) Cure.
2) Cosmesis, when the first goal is reached.
Treatment modalities:
Common treatments: Curettage and desiccation
Surgical excision
Mohs surgery
Cryosurgery
Radiotherapy
Evolving treatments: Interferon, photodynamic therapy, oral retinoids, 5-
fluorouracil.
Systemic chemotherapy. These will not be discussed in detail.
Choosing the modality will depend on:
1) Tumour factor: BCC are considered to be high risk if:
Recurrent
Size greater than 1 to 2 cm
Long duration, fast growth
Indistinct margins
Aggressive histological pattern
High risk sites: nose eyelids, ears, medial canthus, nasolabial fold, scalp, lip,
fingers, toes, genitals.
2) Patient factors: age, medical status, psychological factors, concomitant
medications.
3) Availability of the expertise and facilities.
Surgical treatment
Excision
This is useful for both primary and recurrent lesions, and it enables
histological examination of surgical margins. In good hands, cure rates
approaches 95%. Cure rate >99% if margins histologically negative.
For lesion size more than 1.5 cm or in critical cosmetic sites, other
modalities e.g. Mohs surgery, radiotherapy, or excision by plastic surgeon
with frozen-section control are more preferrable.
Curettage and electrosurgery
Commonly used for tumour size less than 1.5 cm. Cure rate approaches 95%
in good hands. This is not the appropriate treatment for infiltrative lesion and
recurrent lesions in scar tissue.
Cryosurgery
Useful in primary tumour and sometimes in recurrent lesion, and especially
useful in patients with multiple small lesions. Curettage is done to debulk
the lesion before freezing. Local anaesthesia is not needed and there is no
bleeding and scarring may be less than it is with surgery. No tissue is
available for histological confirmation and healing takes several weeks.
Tissue needs to frozen 4-6 mm beyond the clinical border . Thermo-couples
are necessary for larger lesions and this method is not suitable for infiltrative
lesions.
Mohs surgery
The technique is recommended for recurrent, large, difficult tumour, if it is
available.
Laser surgery
Laser may used to vaporize the tumour or as a scalpel blade for excision and
for hemostasis.
Non-surgical treatment
Radiation therapy
This is useful for definitive treatment of primary and recurrent tumour and
for palliation of inoperable lesions. It is painless, without postoperative
scarring. Potentially carcinogenic, it should be reserved for the older
patients. It provides no margin control and radiation dermatitis may develop.
1.4. Follow-up
Long-term follow-up is indicated. Physical examination to search for
recurrence, new tumours (BCC, SCC, Melanomas etc.). Prevention and
education advices should be given. This will include sun avoidance,
sunscreen protection, self-examination, dietary modification to reduce
calories from fatty sources and addition of b -carotene or multivitamins.
2. CUTANEOUS SQUAMOUS CELL CARCINOMA
2.1. Introduction
Being the second most common malignant tumour of the skin, SCC
possesses a higher potential for metastasis than BCC (3%-30% in SCC and
0.3%-3% in BCC). Actinic damage is the most important factor but SCCs
may also develop in certain geno-dermatosis, immunologically
compromised chronic inflammation, UV radiation, ionizing radiation,
arsenic poisoning and other chemical agents.
2.2. Diagnosis
Histological examination is necessary to confirm the diagnosis. A detailed
history and careful examination should be done to search for regional and
distant metastasis. A CXR is basic, whereas further investigation should be
directed by clinical findings.
2.3. Risk Factors

The following factors are associated with increased aggressiveness:
Size > 1 cm
Rapid growth
Ulceration
Depth: invasion into subcutis or below
Immunocompromised
Develop from chronic inflammation or scar
Recurrence
Site: mucous membrane, ear, temple, scalp, eyelid
Histology: Undifferentiated, subcutaneous or below, perineural invasion,
lymphatic invasion.
2.4. Treatment
1) Cure
Choices of treatments:
This should depend on tumour factor (high or low risk); patient factors; and
the availability of expertise and facilities. Actinically derived SCC free of
the risk factors can be safely treated in our clinics with the following
methods of local tumour control.
Surgical treatment
Excision
This is a useful method for primary and recurrent tumours. Surgical margins
can be assessed.
Primarily for small actinically derived tumour. It is not preferrable for
recurrence and deep lesions.
Cryosurgery
Another alternative to surgery. It is useful for patients with bleeding
tendency or those refused surgery for various reasons.
For high risk lesions, the following treatments should be considered:
Mohs surgery
If available, this is one of the most effective methods for high risk lesions.
Adjuvant radiation following surgical excision:
Adjuvant radiotherapy can be used in combination with Mohs surgery or
simple excision in high risk lesions. The advantages is that the in-transit
metastasis and subclinical regional lymph node metastasis can be treated.
Radiation therapy
This can be a definitive treatment for primary or recurrent tumour and also
for palliation of inoperable tumours. It can also be used in combination with
other methods.
Evolving methods
This may include photodynamic therapy, interferon, systemic or topical
retinoids etc.
2.5. Follow-up
This is similar to BCC.
3. MALIGNANT MELANOMA
3.1. Introduction
While melanoma is relatively uncommon when compared with BCC and
SCC, it is the most frequent cause of death of tumours arising from the skin.
Advanced tumour is difficult to treat, whereas early thin lesions are potential
curable. Thus early detection and surgical removal of early lesion is the key
to improvement of survival.
3.2. Identify the High Risk Patients
1) Family or personal history of melanoma.
2) Skin type 1 or 2, easy to burn, difficult to tan.
3) Tendency to freckle.
4) History of severe sun burn.
5) Many moles or presence of atypical nevi, clinically. (Giant congenital
melanocytic naevus )
3.3. Identify the High Risk Lesions
Symptoms:
CHANGES in size, shape, height, colour of a lesion.
Bleeding, erosion, ulceration, crusting and itching.
Signs:
The "ABCDE" of malignant melanoma

Asymmetry
Border irregularity
Colour variegation
Diameter greater than 6 mm
Elevation
Physical examination should not stop at examination of the suspicious
lesion. One should examine the area around the lesion and the lymphatic
drainage area for metastases, examine for organomegaly, and ask for
symptoms of internal metastases.
The whole body surface should also be examined carefully, paying attention
to areas such as the nail fold and nail plate.
3.4. Diagnosis
Biopsy of the suspicious lesion is necessary to confirm the diagnosis and to
guide further management.
Small lesion: complete excision, elliptical or saucerization with narrow
margin with thickness to the level of subcutaneous fat should be aim arrived
at.
Large lesion: incisional biopsy, choosing the most elevated, dark or
suspected area to the level of subcutaneous fat.
3.5. Assessment and Staging
History: thorough history paying special attention to brain, chest, bone,
gastrointestinal symptoms.
Physical examination: the lymphatic drainage area, all other lymph node
area, the total skin surface, liver and spleen enlargement.
Chest X-ray: This is part and partial of the physical examination. This is the
only investigation indicated in stage I disease.
Further investigation should be guide by the physical findings and
histological examination findings.
3.6. Stage Grouping (American Joint Commission on Cancer Staging
System 1992)
Breslow Lymph Node Distant
¡@
Depth Metastasis Metastasis
Stage I ?1.5 mm no no
Stage II > 1.5 mm no no

Stage III any present no
Stage IV any any present

3.7. Treatment: The Multidisciplinary Approach
Except for stage I conditions; which can be safely treated in our clinic
setting, for all stages beyond, the joint effort with the cooperation of
surgeon, oncologist, radiologist, dermatologist and nursing specialist is most
important. Only treatment of the primary will be discussed here in detail.
Adjuvant management of early lesion without evidence of metastasis and
management of advanced diseases with metastasis is beyond the scope of
this chapter.
3.7.1. Surgical Treatment of the Primary Lesion: Wide Local Excision
The principle is to excise the lesion to the underlying muscle fascia with a
margin of normal-appearing skin. That "safety margin" is still a controversial
and continuously evolving issue, and the surgical guideline from AJCC is
quoted here:
Breslow Depth Excision Margin
< 0.75 mm 1 cm
0.76 mm - 1.49 mm 1 - 2 cm
1 - 2 cm +/-ELND +/-adjuvant
1.5 mm - 4 mm
therapy
> 4 mm 3 cm =/-adjuvant therapy

The current thought is that a 1 cm margin is appropriate for all lesions but
investigations for regional and visceral metastasis should be done for lesions
thicker than 1.5 mm and adjuvant treatment should be considered.
ELND-Elective Lymph Node Dissection:
A controversial issue again and it entails resection of lymph nodes in the
drainage region without clinical evidence of involvement. It increases
morbidity and has never been proven to improve survival. It is probably not
indicated in thin lesions (less than 1.5 mm). Morton¡¥s blue dye technique
may help to improve this procedure.
3.7.2. Mohs Micrographic Surgery
Not an established method but may be an alternative as an tissue saving
technique for lesion on the face.
3.7.3. Cryotherapy
May be considered in lentigo maligna, and lentigo maligna melanoma.
3.7.4. Therapy for Metastatic Disease
Various modalities of treatment are available for disease stage III or IV. The
more established will be listed but will not be discussed in detail. Moreover,
effectiveness of adjuvant therapy for early stages.
Surgery: for metastatic lesions.
Chemotherapy: Dacarbazine is the most effective single agent.
Isolation perfusion: for the treatment of in-transit metastasis.
Radiotherapy: for palliative treatment of metastasis.
Evolving modalities: melanoma vaccines
monoclonal antibodies
adoptive immunotherapy
gene therapy
others
3.8. Follow-Up
Life long follow-up is indicated for all patients with melanoma. Frequency
of visits should be guided by tumour stages, presence of atypical nevi etc.
The duties in the follow-up should include:
1) Examination for recurrence, new lesion, sign and symptoms of metastasis.
2) Education: sun protection, monthly self-examinations of skin and
"ABCD" of melanoma.
3) Opthalmological referral for patient with multiple primary, multiple
dysplastic nevi and family history of ocular melanoma.
4) Referral of 1st degree relative for examination for melanoma or atypical
nevi.
5) Avoidance of pregnancy for 2 years after diagnosis. This is highly
controversial, but may be considered in patient with advanced stages of
disease, multiple melanoma, or numerous atypical nevi.
4. MYCOSIS FUNGOIDES
Mycosis fungoides (MF) is the commonest cutaneous T cell lymphoma.
Three clinical stages can be identified: patch, plaque , tumour stage.

The erythrodermic stage, which is also called Sezary syndrome
(erythroderma, enlarged lymph nodes, and circulating Sezary cells) may
develop de-novo or from the earlier stages.
4.1. Diagnosis
Skin biopsy: Multiple skin biopsy on lesions of different morphology should
be taken.
Histology: One should bear in mind that the histological features is variable
and there is some correlation with the clinical features. 4 types have
described:
Epidermotrophic patches and plaques
Epidermatrophic erythroderma
Non-epidermotrophic erythroderma
Non-epidermotrophic tumours
The biopsy specimens may also send for:
Immunophenotyping: to demonstrate T cell lineage. Other markers e.g. IL2,
Ki1 are helpful in certain circumstances.
T cell recepter gene rearrangement study: by PCR, to demonstrate
monoclonality.
4.2. Evaluation
Careful history, physical examination with mapping of all lesions.
Complete blood picture with smear, Liver and renal function, Lactate
dehydrogenase level, Anti-nuclear factor.
Chest X ray.
Biopsy of enlarged lymph nodes.
CT scan of abdomen, pelvis and other sites if indicated.
4.3. Staging
Several staging schemes have been proposed and are based on cutaneous
lesions (patch, plaque, tumour, erythrodermic), presence of lymph node
involvement and visceral involvement. This will not be detailed in this
chapter.
4.4. Treatment
Choice of treatment should be determined by:
1) Clinical stages.
2) Availabilities of facilities and expertise.
3) Patient's preference.
For all stages of diseases, symptomatic relief with EMOLLIENT, TOPICAL
STEROID, ANTI-HISTAMINE are indispensable.
Choices of treatment according to stages:
Patches and plaques
PUVA, RePUVA is the first line. Topical nitrogen mustard is an alternative if
available. Total skin electron beam therapy or PUVA with a interferon are
reserved for refractory cases.
Tumours
Total skin electron beam with local booster radiation to tumours.
Extracorporeal photophoresis is an alternative (not available locally).
Erythrodermic stage and Sezary syndrome
Photophoresis, if available, is probably the best treatment, and concomitant
methotrexate may increase its effectiveness. PUVA may give symptomatic
relief but should be administered with care. Other choice of treatment may
include a interferon, systemic chemotherapy, retinoids and bone marrow tr
CUTANEOUS MALIGNANCIES
Dr. H.F. HO
CHAPTER 13
Duties of dermatologists in Social Hygiene Service in the management of
cutaneous malignancy:
1) To identify the high risk patients and the suspicious lesions.
2) To confirm the diagnosis.
3) Assess and decide whether the lesion can be adequately treated in our
clinic and give the most appropriate accordingly.
4) Refer those which cannot be adequately treated in our clinics and refer
them to a multi-disciplinary clinic for further management. Prepare to give
opinion regarding choice of treatment.
5) Follow-up of the patient.
The management of basal cell carcinoma, squamous cell carcinoma,
melanoma and mycosis fungoides will be discussed in chapter.
1. BASAL CELL CARCINOMA

1.1. Introduction
Basal cell carcinoma is the most common malignant skin tumour. Three
main clinical types of BCC are identifiable:
1) Superficial BCC
2) Nodular BCC: this may appears cystic, or may evolve into a
"rodent ulcer" .
3) Infiltrative form
- Infiltrative morphoea-form BCC
- Infiltrative non-morphea-form BCC
1.2. Diagnosis
Diagnosis of skin tumour should include a careful physical examination, not
only of the target lesion but also search for the presence of other skin
tumours. A general examination paying special attention to regional lymph
nodes and organomegaly is necessary, although distant metastasis in BCC is
rare.
Skin biopsy is indicated to confirm the diagnosis.
1.3. Treatment
1) Cure.
Treatment modalities:
Common treatments: Curettage and desiccation
Surgical excision
Mohs surgery
Cryosurgery
Radiotherapy
Evolving treatments: Interferon, photodynamic therapy, oral retinoids, 5-
fluorouracil.
Systemic chemotherapy. These will not be discussed in detail.
Choosing the modality will depend on:
1) Tumour factor: BCC are considered to be high risk if:
Recurrent
Size greater than 1 to 2 cm
Long duration, fast growth
Indistinct margins
Aggressive histological pattern
High risk sites: nose eyelids, ears, medial canthus, nasolabial fold, scalp, lip,
fingers, toes, genitals.
2) Patient factors: age, medical status, psychological factors, concomitant
medications.
3) Availability of the expertise and facilities.
Surgical treatment
Excision
This is useful for both primary and recurrent lesions, and it enables
histological examination of surgical margins. In good hands, cure rates
approaches 95%. Cure rate >99% if margins histologically negative.
For lesion size more than 1.5 cm or in critical cosmetic sites, other
modalities e.g. Mohs surgery, radiotherapy, or excision by plastic surgeon
with frozen-section control are more preferrable.
Commonly used for tumour size less than 1.5 cm. Cure rate approaches 95%
in good hands. This is not the appropriate treatment for infiltrative lesion and
recurrent lesions in scar tissue.
Cryosurgery
Useful in primary tumour and sometimes in recurrent lesion, and especially
useful in patients with multiple small lesions. Curettage is done to debulk
the lesion before freezing. Local anaesthesia is not needed and there is no
bleeding and scarring may be less than it is with surgery. No tissue is
available for histological confirmation and healing takes several weeks.
Tissue needs to frozen 4-6 mm beyond the clinical border . Thermo-couples
are necessary for larger lesions and this method is not suitable for infiltrative
lesions.
Mohs surgery
The technique is recommended for recurrent, large, difficult tumour, if it is
available.
Laser surgery
Laser may used to vaporize the tumour or as a scalpel blade for excision and
for hemostasis.
Non-surgical treatment
Radiation therapy
This is useful for definitive treatment of primary and recurrent tumour and
for palliation of inoperable lesions. It is painless, without postoperative
scarring. Potentially carcinogenic, it should be reserved for the older
patients. It provides no margin control and radiation dermatitis may develop.
1.4. Follow-up
Long-term follow-up is indicated. Physical examination to search for
recurrence, new tumours (BCC, SCC, Melanomas etc.). Prevention and
education advices should be given. This will include sun avoidance,
sunscreen protection, self-examination, dietary modification to reduce
calories from fatty sources and addition of b -carotene or multivitamins.
2. CUTANEOUS SQUAMOUS CELL CARCINOMA

2.1. Introduction
Being the second most common malignant tumour of the skin, SCC
possesses a higher potential for metastasis than BCC (3%-30% in SCC and
0.3%-3% in BCC). Actinic damage is the most important factor but SCCs
may also develop in certain geno-dermatosis, immunologically
compromised chronic inflammation, UV radiation, ionizing radiation,
arsenic poisoning and other chemical agents.
2.2. Diagnosis
Histological examination is necessary to confirm the diagnosis. A detailed
history and careful examination should be done to search for regional and
distant metastasis. A CXR is basic, whereas further investigation should be
directed by clinical findings.
2.3. Risk Factors

The following factors are associated with increased aggressiveness:
Size > 1 cm
Rapid growth
Ulceration
Depth: invasion into subcutis or below
Immunocompromised
Develop from chronic inflammation or scar
Recurrence
Site: mucous membrane, ear, temple, scalp, eyelid
Histology: Undifferentiated, subcutaneous or below, perineural invasion,
lymphatic invasion.
2.4. Treatment
1) Cure
Choices of treatments:
This should depend on tumour factor (high or low risk); patient factors; and
the availability of expertise and facilities. Actinically derived SCC free of
the risk factors can be safely treated in our clinics with the following
methods of local tumour control.
Surgical treatment
Excision
This is a useful method for primary and recurrent tumours. Surgical margins
can be assessed.
Primarily for small actinically derived tumour. It is not preferrable for
recurrence and deep lesions.
Cryosurgery
Another alternative to surgery. It is useful for patients with bleeding
tendency or those refused surgery for various reasons.
For high risk lesions, the following treatments should be considered:
Mohs surgery
If available, this is one of the most effective methods for high risk lesions.
Adjuvant radiation following surgical excision:
Adjuvant radiotherapy can be used in combination with Mohs surgery or
simple excision in high risk lesions. The advantages is that the in-transit
metastasis and subclinical regional lymph node metastasis can be treated.
Radiation therapy
This can be a definitive treatment for primary or recurrent tumour and also
for palliation of inoperable tumours. It can also be used in combination with
other methods.
Evolving methods
This may include photodynamic therapy, interferon, systemic or topical
retinoids etc.
2.5. Follow-up
This is similar to BCC.
3. MALIGNANT MELANOMA
3.1. Introduction
While melanoma is relatively uncommon when compared with BCC and
SCC, it is the most frequent cause of death of tumours arising from the skin.
Advanced tumour is difficult to treat, whereas early thin lesions are potential
curable. Thus early detection and surgical removal of early lesion is the key
to improvement of survival.
3.2. Identify the High Risk Patients
1) Family or personal history of melanoma.
2) Skin type 1 or 2, easy to burn, difficult to tan.
3) Tendency to freckle.
4) History of severe sun burn.
5) Many moles or presence of atypical nevi, clinically. (Giant congenital
melanocytic naevus )
3.3. Identify the High Risk Lesions
Symptoms:
CHANGES in size, shape, height, colour of a lesion.
Bleeding, erosion, ulceration, crusting and itching.
Signs:
The "ABCDE" of malignant melanoma

Asymmetry
Border irregularity
Colour variegation
Diameter greater than 6 mm
Elevation
Physical examination should not stop at examination of the suspicious
lesion. One should examine the area around the lesion and the lymphatic
drainage area for metastases, examine for organomegaly, and ask for
symptoms of internal metastases.
The whole body surface should also be examined carefully, paying attention
to areas such as the nail fold and nail plate.
3.4. Diagnosis
Biopsy of the suspicious lesion is necessary to confirm the diagnosis and to
guide further management.
Small lesion: complete excision, elliptical or saucerization with narrow
margin with thickness to the level of subcutaneous fat should be aim arrived
at.
Large lesion: incisional biopsy, choosing the most elevated, dark or
suspected area to the level of subcutaneous fat.
3.5. Assessment and Staging
History: thorough history paying special attention to brain, chest, bone,
gastrointestinal symptoms.
Physical examination: the lymphatic drainage area, all other lymph node
area, the total skin surface, liver and spleen enlargement.
Chest X-ray: This is part and partial of the physical examination. This is the
only investigation indicated in stage I disease.
Further investigation should be guide by the physical findings and
histological examination findings.
3.6. Stage Grouping (American Joint Commission on Cancer Staging
System 1992)
Breslow Lymph Node Distant
¡@
Depth Metastasis Metastasis
Stage I ?1.5 mm no no
Stage II > 1.5 mm no no
Stage III any present no
Stage IV any any present

3.7. Treatment: The Multidisciplinary Approach
Except for stage I conditions; which can be safely treated in our clinic
setting, for all stages beyond, the joint effort with the cooperation of
surgeon, oncologist, radiologist, dermatologist and nursing specialist is most
important. Only treatment of the primary will be discussed here in detail.
Adjuvant management of early lesion without evidence of metastasis and
management of advanced diseases with metastasis is beyond the scope of
this chapter.
3.7.1. Surgical Treatment of the Primary Lesion: Wide Local Excision
The principle is to excise the lesion to the underlying muscle fascia with a
margin of normal-appearing skin. That "safety margin" is still a controversial
and continuously evolving issue, and the surgical guideline from AJCC is
quoted here:
Breslow Depth Excision Margin
< 0.75 mm 1 cm
0.76 mm - 1.49 mm 1 - 2 cm
1 - 2 cm +/-ELND +/-adjuvant
1.5 mm - 4 mm
therapy
> 4 mm 3 cm =/-adjuvant therapy

The current thought is that a 1 cm margin is appropriate for all lesions but
investigations for regional and visceral metastasis should be done for lesions
thicker than 1.5 mm and adjuvant treatment should be considered.
ELND-Elective Lymph Node Dissection:
A controversial issue again and it entails resection of lymph nodes in the
drainage region without clinical evidence of involvement. It increases
morbidity and has never been proven to improve survival. It is probably not
indicated in thin lesions (less than 1.5 mm). Morton¡¥s blue dye technique
may help to improve this procedure.
3.7.2. Mohs Micrographic Surgery
Not an established method but may be an alternative as an tissue saving
technique for lesion on the face.
3.7.3. Cryotherapy
May be considered in lentigo maligna, and lentigo maligna melanoma.
3.7.4. Therapy for Metastatic Disease
Various modalities of treatment are available for disease stage III or IV. The
more established will be listed but will not be discussed in detail. Moreover,
effectiveness of adjuvant therapy for early stages.
Surgery: for metastatic lesions.
Chemotherapy: Dacarbazine is the most effective single agent.
Isolation perfusion: for the treatment of in-transit metastasis.
Radiotherapy: for palliative treatment of metastasis.
Evolving modalities: melanoma vaccines
monoclonal antibodies
adoptive immunotherapy
gene therapy
others
3.8. Follow-Up
Life long follow-up is indicated for all patients with melanoma. Frequency
of visits should be guided by tumour stages, presence of atypical nevi etc.
The duties in the follow-up should include:
1) Examination for recurrence, new lesion, sign and symptoms of metastasis.
2) Education: sun protection, monthly self-examinations of skin and
"ABCD" of melanoma.
3) Opthalmological referral for patient with multiple primary, multiple
dysplastic nevi and family history of ocular melanoma.
4) Referral of 1st degree relative for examination for melanoma or atypical
nevi.
5) Avoidance of pregnancy for 2 years after diagnosis. This is highly
controversial, but may be considered in patient with advanced stages of
disease, multiple melanoma, or numerous atypical nevi.
4. MYCOSIS FUNGOIDES
Mycosis fungoides (MF) is the commonest cutaneous T cell lymphoma.
Three clinical stages can be identified: patch, plaque , tumour stage.

The erythrodermic stage, which is also called Sezary syndrome
(erythroderma, enlarged lymph nodes, and circulating Sezary cells) may
develop de-novo or from the earlier stages.
4.1. Diagnosis
Skin biopsy: Multiple skin biopsy on lesions of different morphology should
be taken.
Histology: One should bear in mind that the histological features is variable
and there is some correlation with the clinical features. 4 types have
described:
Epidermotrophic patches and plaques
Epidermatrophic erythroderma
Non-epidermotrophic erythroderma
Non-epidermotrophic tumours
The biopsy specimens may also send for:
Immunophenotyping: to demonstrate T cell lineage. Other markers e.g. IL2,
Ki1 are helpful in certain circumstances.
T cell recepter gene rearrangement study: by PCR, to demonstrate
monoclonality.
4.2. Evaluation
Careful history, physical examination with mapping of all lesions.
Complete blood picture with smear, Liver and renal function, Lactate
dehydrogenase level, Anti-nuclear factor.
Chest X ray.
Biopsy of enlarged lymph nodes.
CT scan of abdomen, pelvis and other sites if indicated.
4.3. Staging
Several staging schemes have been proposed and are based on cutaneous
lesions (patch, plaque, tumour, erythrodermic), presence of lymph node
involvement and visceral involvement. This will not be detailed in this
chapter.
4.4. Treatment
Choice of treatment should be determined by:
1) Clinical stages.
2) Availabilities of facilities and expertise.
3) Patient's preference.
For all stages of diseases, symptomatic relief with EMOLLIENT, TOPICAL
STEROID, ANTI-HISTAMINE are indispensable.
Choices of treatment according to stages:
Patches and plaques
PUVA, RePUVA is the first line. Topical nitrogen mustard is an alternative if
available. Total skin electron beam therapy or PUVA with a interferon are
reserved for refractory cases.
Tumours
Total skin electron beam with local booster radiation to tumours.
Extracorporeal photophoresis is an alternative (not available locally).
Erythrodermic stage and Sezary syndrome
Photophoresis, if available, is probably the best treatment, and concomitant
methotrexate may increase its effectiveness. PUVA may give symptomatic
relief but should be administered with care. Other choice of treatment may
include a interferon, systemic chemotherapy, retinoids and bone marrow
transplant.
Histological lymph node involvement
Treatment is essential palliative: which may include local radiation to local
symtomatic disease, systemic chemotherapy, a interferon, retinoids.
Visceral involvement
Palliative treatment include systemic chemotherapy, interferons, retinoids
etc.
PUVA: Primarily indicated in patch and plaque skin diseases, this is not
effective in tumor diseases and should be used with care in erythrodermic
patients. The administration is essentially similar to PUVA in psoriasis.
Sanctuary site lesions will need addition dose or adding of other agents like
topical steroid, nitrogen mustard.
RePUVA: adding retinoids (Etretinate, isotretinoin) to PUVA gives earlier
response and longer period of remission, although the relapse rate and long
term survival is the same as PUVA alone. It should considered in patients
with poor initial response to PUVA.
Total skin electron beam therapy: The delivery of high energy electron to a
limited depth of skin and preventing systemic toxicity. While it is effective
in patch and plaque diseases, its relative poor cutaneous tolerance makes it
the treatment reserved to tumor stage or refractory extensive plaque stages.
It is relatively contraindicated in erythrodermic disease because of severe
side effects.
INFECTION: BACTERIAL, VIRAL, FUNGAL

Dr. W.K. FUNG
CHAPTER 14
1. COMMON BACTERIAL DISEASES OF SKIN
The predominant primary pathogens are the group A Streptococci or
Staphylococcus aureus. The clinical pictures vary because of the host factors
and the local anatomic infections.
1.1. Impetigo
Two clinical types of impetigo occur. The first type is due to group A
Streptococci or a mixture of Streptococci and Staph. aureus. It is a disease of
young children in which blisters appear on the skin around the mouth. The
vesicles and pustules easily rupture, forming a thick, soft, golden-yellow
"stuck on" crust, the hallmark of impetigo. The skin lesions may be
complicated with deep cellulitis or bacteraemia. Glomerulonephritis may
follow impetigo due to Streptococcus pyogenes. The second type of
impetigo is bullous impetigo, characterized by rapid progression of vesicles
to flaccid large bullae. The bullae eventually rupture, and form thin, light
brown crusts. This infection is frequently associated with Staph. aureus of
phage group II.
1.2. Ecthyma
Ecthyma initially presents as a vesicle or vesicopustule on the lower
extremities of children or neglected elderly patients, the skin lesion
gradually enlarges to form a ulcer with punched-out appearance. Post-
streptococcal glomerulonephritis is a known sequel.
1.3. Erysipelas
A spreading infection most commonly due to Group A and B Streptococci
presenting as a characteristic brawny, edematous, indurated and well
demarcated appearance. The patient may be acutely ill with high fever and
toxaemia. Predisposing factors include alcohol abuse, diabetes mellitus,
immunosuppression, venous or lymphatic obstruction.
1.4. Acute Cellulitis
This is an acute, spreading infection of subcutaneous tissue. There are two
main bacteriological forms. The acute pyogenic cellulitis is usually due to
group A Streptococci and Staph. aureus. It presents as a markedly red, hot,
infiltrated edematous skin lesion and the borders are usually ill-defined.
Lymphangitis and lymphadenitis involving local draining lymph glands are
frequently found. The second form is the Anaerobic cellulitis which is
relatively rare and is usually due to a synergistic infection with both aerobic
and anaerobic bacteria. The causal organisms include aerobes (coliforms,
Pseudomonas aeruginosa, staph. aureus) and anaerobes (bacteriodes,
anaerobic cocci). Two clinical syndromes may develop:
1) Necrotizing Fasciitis
This infection usually occurs on the lower extremities, abdominal wall,
perineum and operative wounds. The infective-ischaemic process spreads
along the fascial plane causing extensive necrosis while the external
appearance of the skin remains normal initially. So the damage is more
extensive than the extent of the overlying skin. The involved area is swollen,
red, warm and painful. Crepitus is often present. The patient is severely ill
with fever and septic shock may occur.
2) Progressive bacterial synergistic gangrene
This infection is a gangrenous ulceration of the skin due to a mixed bacteria
flora. It usually follows abdominal or thoracic infection or trauma. A small,
painful, superficial ulcer develops and gradually enlarges to form a ulcer
with a rim of gangrenous skin.
1.5. Furuncles, Boils and Carbuncles
With the exception of carbuncles, these skin infections are uncomfortable
and unsightly rather than serious. Furuncles or boils occur only in areas
where there are hair follicles. The lesion is a deep-seated inflammatory
nodule, it is tender, hard, red and fluctuate after several days. A carbuncle is
a more extensive, deeper, infiltrated lesion and usually occurs at the nape of
the neck, the back or thighs. Systemic symptoms such as fever and malaise
are often present. All these lesions are caused by infection with
Staphylococcus aureus.
1.6. Folliculitis
This is an acute, small, painful pustular eruption of hair follicles. There are
two main subtypes: superficial and deep. Bockhart's impetigo is a superficial
folliculitis. Small, dome-shaped pustule develops at the opening of a hair
follicle surrounded by erythema. It usually occurs on the limbs and the scalp.
Deep folliculitis include sycosis barbae and lupoid sycosis. Staphylococcal
or Streptococci are the commonest pathogens. Folliculitis can also be caused
by Pseudomonas aeruginosa as it is easily contracted from poorly
maintained whirlpools or jacuzzis. The clinical presentation is similar to
streptococcal or staphylococcal folliculitis. However, the patient may feel
unwell, with a low grade fever and lymphadenopathy.
Management
1) General skin care
2) Local measures
Immobilization and elevation of the involved area to reduce local trauma.
Cool, sterile saline dressing daily.
Extensive debridement and grafting may be required for the necrotic areas of
streptococcal grangrene.
Mupirocin or bacitracin ointment may be useful for its antibacterial effects
and softening of crusted lesions.
3) Specific measures
In mild cases, topical antibiotics are adequate for treatment.
In widespread and severe situation, systemic antibiotics are indicated.
Penicillin G, Penicillin V, flucloxacillin and erythromycin are good
antibiotics for both the streptococcal and staphylococcal infection.
Tetracycline should best be avoided in the treatment of known streptococcal
disease as resistant strain is not uncommon.
Special measures should be aimed at elimination of nasal and skin carriage
of Staph. aureus. This include the use of:
a) local antibiotic ointment such as fusidic acid ointment in the nasal
vestibule.
b) intranasal application of mupirocin ointment.
c) topical application of chlorhexidine or povidone iodine to eradicate Staph.
aureus harbouring in body folds before bathing.
d) oral antibiotics such as rifampicin.
1.7. Erythrasma
Erythrasma is a superficial bacterial skin infection due to Corynebacterium
minutissimum. The lesions are reddish-brown, scaly and finely wrinkled
macular patches, usually involve the intertriginuous areas. Axillary and
genitocrural areas are commonly involved. The diagnosis is supported by the
characteristic "coral-red" fluorescence under wood's light.
Treatment
1) Oral erythromycin 250 mg QID for 1 week. The lesions usually clear
within several weeks.
2) Topical therapy includes aqueous clindamycin solution, whitfield's
ointment or miconazole cream
2. COMMON VIRAL DISEASES OF SKIN

2.1. Herpes Simplex (HS)
The basic lesions are vesicles but these can take many different forms on the
mucocutaneous surface. The clinical features are divided into primary
disease and recurrent disease. Oral and facial lesions are usually due
to Herpes Simplex type 1 while anogenital lesions are mostly due to Herpes
Simplex type 2.
2.1.1. Primary Infections
Primary infection with herpes simplex occurs primarily by direct exposure
through mucocutaneous contact with another infected individual. It is
defined as the first infection with the virus in a seronegative patient. The
infection can be subclinical but below are listed the symptomatic clinical
presentations.
1) Primary gingivo-stomatitis
Primary herpetic infection (usually type 1 herpes simplex) of the mouth and
pharynx is more common in the children. Vesicles inside the mouth on the
buccal mucosa and gums coalesce to form plaques covered with a grey-
membrane. The vesicles are very painful and the infection may accompany
with high fever, tender lymphadenopathy and generalized complaints.
2) Primary genital herpes
Primary genital herpes, generally by type 2 virus, is a common sexually
transmitted disease characterized by multiple grouped, umbilicated vesicles,
oedema, fever, pain and dysuria, with regional lymphadenopathy in men and
vulvovaginitis in woman. The incubation period is from 3 to 14 days.
3) Herpetic whitlow
Herpetic whitlow refers to painful vesicles with clear serous fluid on the
fingers or hands. It is a common occupational hazard for medical and dental
personnel. The inoculation usually occurs in areas of abraded or broken skin.
The vesicles will subsequently progress to form superficial ulcers.
4) Herpetic keratoconjunctivitis
Primary herpes can involve the conjunctive and cornea. The eyelids are
usually swollen and there are vesicles and ulcers on them.
5) Aseptic meningitis, encephalitis
6) Primary herpes hepatitis
2.1.2. Recurrent Infections
The virus remains in the dorsal root ganglion, from which secondary
infections are repeatedly seeded to the skin over a period of years. Recurrent
attacks then occur and presents as grouped umbilicated vesicles on an
erythematous and somewhat edematous background.
1) Recurrent facial-oral herpes simplex (cold sores)
The cold sore usually appears at the vermilion border of the lip. The
erythematous papule becomes vesicular and then ulcerates. The open sore
heals in 8 to 9 days. Recurrent genital herpes also recur easily and these are
mainly due to type 2 virus. The number of recurrences is about 3 or 4 per
year.
2) Keratitis
Reactivation less commonly affects the eye, recurrent lesions are usually
restricted to the cornea and the conjunctiva is not involved.
3) Recurrent lumbosacral herpes simplex
Recurrent herpetic lesions appearing on the lumbal area and buttocks may
cause "sciatic pain".
4) Herpes infection in the immunocompromised patient
Reactivation of herpes is very common in patients with defective cellular
immunity from hematological malignancies, Human Immunodeficiency
Virus (HIV) infection and those receiving immunosuppressive agents or
transplant patients. Herpes infection recurs more frequently, have a more
severe and prolonged course and may present atypically e.g. in the form of
granuloma.
Common causes of recurrent infection
1) Stress
2) Pneumonia
3) Onset of menstrual cycle
4) Sun exposure
5) Mechanical trauma
6) Sexual activity (in genital herpes)
Diagnosis
1) Viral culture from scrapped tissues or fluids.
2) Immunofluorescence in scrapings from lesions to detect viral antigens.
3) Electronmicroscopy to demonstrate the virus.
4) Serology which may be useful for diagnosing primary infections is very
difficult to interpret in recurrent infections because of high levels of existing
antibody and recurrences usually do not cause a rise in titre. So serology is
not routinely performed in the Social Hygiene Clinic. Also, commercially
available serological tests cannot reliably distinguish its types 1 and 2
infection.
Treatment
1) Facial-oral herpes, Genital herpes
a) Topical antibiotic cream. e.g. aureomycin cream
b) Topical acyclovir cream
c) KMnO4 wet compress
d) Oral acyclovir therapy is only used in very severe and extensive situation.
e.g. acyclovir 200 mg 5 x daily x 5/7 with 24 hours of active new lesion.
e) Oral Famciclovir 125 mg tds x 5/7 or oral valaciclovir is an alternative
2) Herpetic Keratitis
a) Idoxuridine 0.5% eye drops.
b) Acyclovir ophthalmic ointment.
3) Treatment of herpes infections in the Immunocompromised patient
- Intravenous (IV) acyclovir
4) Recurrent infections (>6 attacks per year)
- Prophylactic oral dose acyclovir for several months has been shown to
reduce severity and frequency of relapse e.g. Acyclovir 400 mg bd.
However, the whole course of treatment is quite expensive.
2.2. Herpes Zoster (HZ)
The varicella-zoster virus causes the characteristic herpetic lesion similar to
herpes simplex. Whereas varicella represents a primary lesion, herpes zoster
(shingles) represents reactivation of the virus from the dorsal root ganglion
and results in the classic dermatomic distribution. Herpes zoster is a
common condition. There is a correlation between age and incidence of the
condition. The disease usually affects the elderly and the
immunocompromised patients. Constitutional symptoms are followed by
tingling and pain, erythema, and vesicle formation in a dermatomic
distribution .
Major complications of herpes zoster
1) Acute phase
a) Ocular involvement-Herpes ophthalmitis
b) Secondary infection
c) Cutaneous or visceral dissemination
2) Chronic phase
a) Post-herpetic neuralgia
b) Scarring
c) Motor neuropathy, post-infection encephalomyelitis, paralysis
Treatment
1) Topical agents
a) Acyclovir cream
b) Topical antibiotic cream may be useful in lesions with secondary infection
2) Systemic agents
a) Oral acyclovir 800 mg 5 times daily for 1 week
b) Oral Famciclovir 250 mg 3 times daily for 1 week
c) Oral Valaciclovir 1 gram 3 times daily for 1 week
In immunocompromised patient, IV acyclovir treatment is indicated.
Indications of systemic anti-viral treatment.
a) Patients get skin rashes within 3 days of onset, especially for the elderly
group.
b) Patients suffer from ophthalmopathy within 3 days of onset.
c) Immunocompromised patient whenever vesicles present.
2.3. Molluscum Contagiosum
It is caused by a large DNA virus of the pox group. The umbilicated pearly
lesions, often multiple, are more common in childhood and resolve
spontaneously after becoming inflamed. The lesions occur anywhere on the
body. Lesions occurring on the genitalia or lower abdomen in adults are
almost sexually transmitted. In children, the lesions can be left behind as it is
harmless and involute spontaneously. In adults, either cryotherapy or
piercing with a cocktail stick dipped in iodine can be used as treatment. In
patients with genital lesions, both the patient and the sexual partner should
be screened for other sexually transmitted diseases.
2.4. Warts
Viral warts are caused by the Human Papilloma virus (HPV). More than 50
subtypes exist. Warts are contagious and spread easily if there is local breaks
on the skin. Their morphology varies with the viral subtype and anatomical
site. Spontaneous resolution may occur.
2.4.1. Common Warts
They are mostly due to HPV type 2. The lesions are discrete, firm papules
with a rough surface . They are usually multiple.

2.4.2. Plane Warts
These are usually caused by HPV type 3. The lesions are flat-topped, flesh-
colored papules, mainly on the face, hands and limbs.
2.4.3. Plantar Warts (Verucca Plantaris)
Plantar warts are common, especially in school-children who may acquire
them from swimming-bath floors. HPV1 and HPV2 are the commonest
causative viruses. The lesions are characteristically flat with a callus on the
surface and are often very painful. They usually occur on the palm and sole.
2.4.4. Anogenital Warts
Please refer to Chapter 30 in STD Section.
2.5. Pityriasis Rosea
It usually occurs in children and young adult. A viral atiology is suspected. A
characteristic herald patch commonly precedes the later multiple lesions by
several days. The herald patch is a single erythematous oval or circular
macule of 3 to 4 cm in diameter. Subsequent lesions are similar but much
smaller and have a peripheral collarette of scale. They occur in a
symmetrical distribution and distribute along the rib lines. The lesions may
be asymptomatic or mildly itchy. They persist for 4-6 weeks. Symptomatic
treatment for pruritis is achieved by using topical steroid, oral antihistamines
or a short course of UVB. All the above measures do not modify the
eruptions and the course of the disease.
3. COMMON FUNGAL DISEASES OF SKIN

3.1. Pityriasis Versicolor
It is caused by yeasts (Pityrosporum orbiculare and P. ovale) providing
widespread fine scaly macules on the upper trunk and back. The colour of
the lesions varies. The lesions are pale in dark skin and darker in fair skin.
Recurrent attacks are common. The diagnosis is established clinically and
can be supported by the faint yellow fluorescence under Wood's light in the
affected areas.
Treatment
1) Topical treatment
a) Imidazoles cream e.g. clotrimazole, miconazole, isoconazole
b) Ketoconazole shampoo
c) 2.5% selenium sulphide shampoo
d) 3% salicylic acid in spirit
e) 20% sodium thiosulphate in spirit
2) Systemic treatment
a) Oral ketoconazole 200 mg daily for 5 days
b) Oral itraconazole 100 mg daily for 5 days
3.2. Tinea Pedis

It is a fungal infection of the toe webspaces and the soles. Trichophyton
rubrum (T. rubrum), T. Mentagrophytes Var. interdigitale and
Epidermophyton floccosum are the commonest causative organisms. There
are 3 main clinical patterns.
1) Chronic Plantar Scaling
It presents as a "Moccasin" distribution, on plantar surface and the edges of
feet. Peeling of skin and scales are common. Hyperkeratosis may develop on
weight-bearing areas.
2) Acute Vesicular Tinea Pedis
Sudden eruption of pruritic or painful vesicles develop on the soles. The
eruption is usually unilateral. This pattern may give rise to Id reaction
presenting as symmetrical, vesicular pompholyx at sites distant from the site
of active fungal infection.
3) Interdigital Tinea Pedis
Peeling, maceration and fissuring occurs frequently in the lateral toe clefts. It
is usually very itchy and is more common in people with sweaty feet or
occlusive foot-wear.
3.3. Tinea Manuum

T. rubrum is the commonest cause. There is unilateral scaling particularly in
the skin creases and the nails are usually involved.
3.4. Tinea Unguium

Infection of nail and/or the nail bed with dermatophyte fungi is usually due
to T. rubrum. It presents as distal nail edge onycholysis with subungual tan
crumbly debris, subungual hyperkeratosis and brownish discolouration from
secondary colonization by non-pathogenic fungi e.g. Aspergillus.
3.5. Tinea Cruris

Tinea cruris presents as itchy advancing red, sharply demarcated skin rashes
enlarging from inguinal folds down inner thigh or into pubic area. Central
healing followed by post-inflammatory hypopigmentation is its
characteristic. It is usually caused by Trichophyton rubrum, Epidermophyton
floccosum and T. mentagrophytes var. interdigitale.
3.6. Tinea Capitis

Scalp ringworm is uncommon in H.K. nowadays. It appears as scattered
scaly patches containing broken hairs. The lesions may be asymptomatic or
mildly itchy. In general, the pattern of involvement can be classified as
ectothrix, endothrix, kerion and favus respectively. In severe situation,
boggy mass of inflamed and purulent skin known as kerion may occur
especially by animal infections. Usually human infections produce minor
degrees of erythema and scaling while animal infections cause considerable
inflammation.
3.7. Tinea Corporis
It refers to the dermatophyte infection of smooth skin. The lesion is identical
to that of tinea cruris but occurs on the trunk and limbs. It is easily
misdiagnosed as discoid eczema or pityriasis rosea.
3.8. Tinea Faciei
It presents as an amorphous, asymptomatic reddish patch, which may be
photosensitive. The skin lesion may be mistaken for polymorphic light
eruption, lupus erythematosus and contact dermatitis. It is commonly caused
by Trichophyton rubrum, T. mentagrophytes and Microsporum species.
Outbreak of zoophilic species induced tinea faciei has been found in Hong
Kong.
Diagnosis
1) Wood's light (more useful in Tinea capitis)
2) Microscopic examination of scrapings and clippings in 10% - 30% KOH
3) Culture
Treatment of Tinea infection
Imidazole e.g. miconazole (Daktarin), clotrimazole (Canesten, Lotremin),
Tionazole (Trosyd), Ketoconazole (Nizoral), Isoconazole (Travogen),
Bifonazole (Mycospor)
Allylamine e.g. Terbinafine (Lamisil), Natifine (Exoderil)
Others e.g. Tolciclate (Tolmicen), whitfield's ointment, mycota, Castellani's
paint, Ciclo-piroxolamine (Batrafen), Tolnaftate (Tinaderm), Zinc
Undecenoate (Tineafax)
Griseofulvin, ketoconazole, Itraconazole, Terbinafine
3.9. Candidiasis
Candida infections caused by yeast-like fungi Candida albicans commonly
occur in moist, flexural sites. It is more common at the extremes of age and
during pregnancy. Predisposing factors include diabetes mellitus, pregnancy,
broad-spectrum antibiotics, obesity, Cushing disease, uraemia, malignant
disease and immunodeficiency. It can present as 10 clinical patterns,
depending on the site of involvement. They are the oral thrush, angular
cheilitis, genital candidiasis (vulvovaginitis), candida balanitis, candida
intertrigo, chronic paronychia, chronic onychia, pruritus ani, erosio
interdigitalis and candida granuloma. The diagnosis is arrived clinically and
confirmed by fungal culture.
Treatment
Nystatin, imidazole cream, amphotericin lozenges (in oral candidiasis)
Oral fluconazole, itraconazole, ketoconazole
INFESTATIONS
Dr. T.S. AU
CHAPTER 15
1. SCABIES
1.1. Morphology and Biology of the Scabies Mite
The adult female mite is 0.4 mm long while the male mite is 0.2 mm long.
Copulation occurs in a small burrow excavated by the female mite. The
fertilized female enlarges the burrow and begins egg-laying. About 50 eggs
are laid by each female mite during its life span of 4 to 6 weeks. The mite
shows a preference for certain sites to burrow. They tend to avoid area with a
high density of pilosebaceous follicles. Infested patients harbour an average
of 11 mites.
1.2. Incidence and Epidemiology
The incidence of scabies in developed countries show cyclical fluctuation. It
affects all races and social classes world-wide. The interval between the end
of one epidemic to the beginning of another is about 10-15 years. Scabies
may occur in any age but it is most common in children and young adults.
The overall sex incidence is equal. Overcrowding associated with poverty
and poor hygiene in under-developed countries encourages the spread of
scabies. Transmission is by close physical contact like sharing of a bed.
Studies have demonstrated that indirect spread by clothing and bedding is
not important. Although scabies is common in school-age children,
transmission in schools is unlikely. Outbreaks occur in hospitals, old-age
homes and other institutions. Outside the host, free adult mite and eggs can
survive 36 hours and 10 days respectively.
Symptom occurs 3 to 4 weeks after the acquire of the infection. This latency
period may not occur if an individual has had a previous infestation.
Itchiness is the most obvious symptom of scabies. It is worst at night time
when the patient is warm.
The pathognomonic sign of scabies is a burrow; it is a short, wavy, dirty-
appearing line crossing skin lines. They may occur on the wrists, the borders
of the hands, the sides of the fingers and the finger web-spaces , the
feet particularly the instep and in male the genitalia and nodules on
scrotum. Burrows are uncommon on the trunk in adult but they may be
found in elderly and infants. Pruritic papules which accompany
hypersensitivity reaction occur around axillae, peri-areolar regions, peri-
umbilical regions, buttock and thighs. The lesions do not occur above the
neck-line. Secondary change like eczematous change frequently give
confusion to the clinical picture. Inappropriate use of topical steroid may
change the clinical picture to mimic other dermatoses.
1.4. Diagnosis
Absolute confirmation can only be made by the discovery of the burrows
and microscopic examination. A burrow is gently scraped off the skin with a
blunt scalpel, and the material placed in a drop of mineral oil on a
microscopic slide. Oil mounting of the specimen sharpens the microscopic
image and does not kill the mites which may be present (as potassium
hydroxide would). Presence of mites, eggs or fragments of egg-shells
confirms the diagnosis . Other diagnostic tests include needle

extraction of mite, epidermal shave biopsy and punch biopsy.
1.5. Treatment
It is important that all members of the household and all close contacts
should be treated simultaneously. Elderly members of the family often resent
for treatment but they can be asymptomatic reservoirs of infection.
Treatment must be given on two consecutive nights but not for longer. Anti-
scabies preparations are primary irritants which will eventually cause
eczema, patients should be warned about over-use. The patient should first
take a bath, and this is followed by a brisk toweling to open the hydrated
burrows. Hot bath increases the percutaneous absorption of the drug and
may cause toxicity. Benzyl benzoate employed as a 25% emulsion should
remain on the skin for 24 hours. The emulsion is most conveniently applied
with a 2" paint brush applied to the whole body from the neck down
including the genitalia and the soles of the feet. This anointing is repeated on
the following morning. On the following evening the patient should take a
bath again and has the bed-linen and clothing changed which are then
laundered in the usual way.
After the scabicidal treatment, pruritus may persist for a further 2 weeks. A
topical antipruritic such as crotamiton cream may be applied on residual
itchy areas. Postscabetic eczema can be treated with topic steroid.
Secondary infection should be treated with a systemic antibiotic. If
eczematisation is severe, a non-irritant scabicide, preferably in an aqueous
base, should be used.
Treatment of neonates - 6.25% benzyl benzoate emulsion may be used.
Other alternatives include 10% crotamiton cream (applied nightly for 2
nights and washed off after the second application), 10% sulphur in
petrolatum (applied nightly for 3 nights and washed off 24 hours after the
last application) and 5% permethrin cream.
Other drugs used:
1) 1% gamma benzene hexachloride (Lindane) - a single application wash
off after 12-24 hours is usually recommended. It is not recommended to be
used in young children, pregnant and nursing women, and those with
neurological diseases.
2) malathion - malathion 0.5% in aqueous base has been used as scabicide. It
should be left on the skin for 24 hours. The advantage over BBE is that it is
much less stinging and acceptable.
3) permethrin - 5% dermal cream employed as a single application, wash off
8-12 hours. It is of low toxicity, and a single application which is removed in
8-10 hours is adequate. The disadvantage is that it is much more expensive
than BBE or malathion.
4) monosulfiram - 25% solution diluted with 2-3 parts of water to be applied
daily for 2 or 3 days.
5) crotamiton - 10% crotamiton cream is not highly effective and should not
be a first line treatment for scabies. It is at best an adjunctive treatment for
post-treatment pruritus and an alternative for BBE in infants and pregnant
ladies.
6) topical sulphur e.g. 10% sulphur in petrolatum.
2. CRUSTED SCABIES (NORWEGIAN SCABIES)

Crusted scabies is an infestation with Sarcoptes scabiei hominis in which
huge number of mites were present. The grossly thickened horny layer is
honeycombed with cavities which contain large number of mites, and these
are shed into the environment of the patient. Crusted scabies is highly
contagious; an undiagnosed case of crusted scabies may lead to large
outbreak of common scabies.
2.1. Aetiology and Pathogenesis
In common scabies there are few mites probably because of scratching
destroys the burrows. In some patients skin anaesthesia secondary to
neuropathy or spinal injury obviously do not perceive itch and do not scratch
crusted scabies is likely to develop.
Crusted scabies has a predilection for patients with physical debilitation,
mental retardation, sensory impairment and immunosuppression.
Masses of horny debris accumulate beneath thickened and discoloured nails.
Large warty crusts form on the hands and feet, and the palms and soles may
be irregularly thickened and fissured. Itching is often absent or slight. It may
present as exfoliative dermatitis. Differential diagnoses include
hyperkeratotic eczema, psoriasis, Darier's disease and contact dermatitis.
2.3. Treatment
There is no single treatment for crusted scabies. The general principle is that
multiple treatment is needed and sequential use of several agents may be
necessary. The following regimen is suggested with the use of 25% benzyl
benzoate emulsion (BBE), which is the most commonly used agent in public
hospitals in Hong Kong. Ivermectin, given in a single oral dose, is found to
be effective in healthy and HIV subjects in a small study.
Equipment to prepare: Soft brushes to apply the BBE, tooth brushes to rub
away the scales, nail clipper to trim the nails.
Treatment is intensive and should be given by nurses well informed and
dedicated to give the treatment.
BBE is applied from neck include behind the ear down to the toes.
Application to the face and scalp is necessary. BBE may also apply to those
area but may be too stinging. 0.5% Malathion is a good alternative which is
also effective and causing less irritation. Crotamiton is an alternative to
malathion to the area, but is much less effective.
Nails should be cut short. BBE should be scrubbed into the area under the
nail.
Scales, which are usually thick under the nail and on flexural area should be
gently rubbed away with brushes.
Repeat the above steps for 4 consecutive days at least.
Repeat examination and isolation for mite on day 5. Continue treatment until
identification is negative.
Give oral antibiotics which are effective against staphylococcus and
streptococcus unless contraindicated, for 7-10 days.
Change clothing and bed linen daily and these are treated in method
mentioned below.
Isolation can be stopped when treatment is completed (e.g. day 5 when
identification is negative).
Repeat identification procedure one week after treatment is stopped. Repeat
scrapings for identification each week as long as the patient is still in ward.
While BBE is cheap and safe, its use in crusted scabies is less reported in the
literature. It causes irritant contact dermatitis especially in areas infected or
eczematised. The local profile of resistance to BBE is not reported, but since
BBE is the most commonly used scabicide locally, resistance to the agent is
not surprising. Physician should be prepared for this possibility and ready to
use other agents if clinical response is not satisfactory. The microbiologist¡¦s
opinion is invaluable.
Management of Contacts:
Adequate treatment of contacts is as important as adequate management of
the target patient. Success of treatment depends on an all-inclusive approach:
all individuals in the ward and their family members should be treated, and
treated simultaneously, no matter whether they are symptomatic or
asymptomatic.
3. PEDICULOSIS CAPITIS
3.1. Epidemiology
The infection rate was higher in urban than in rural areas. In the early 1980s,
there was a resurgence of infection due to the emergence of the so-called
'super-louse' which was resistant to DDT powder.
Lice are more common on children than on adults, and female of all ages are
more frequently infected than males. There does not appear to be any direct
correlation between hair length and louse infection rates, and it has been
suggested that large masses of hair may, in fact, impede transmission of lice
from scalp to scalp. The vast majority of head louse infections are acquired
by direct head-to-head contact. Spread of lice is encouraged by poverty,
ignorance, poor hygiene and overcrowding. Overcrowding is perhaps the
most important factor. Transmission of head lice by sharing personal articles
such as hair brushes, combs and towels is possible.
These occur in the long hair of the scalp, but may also invade eyebrows and
eyelashes. The characteristic manifestation of head louse infection is scalp
pruritus. Secondary bacterial infection may occur as a result of scratching,
and concomitant head louse infection must always be considered in cases of
scalp impetigo. Pruritic papular lesions may occur on the nape of the neck,
and occasionally a generalized non-specific pruritic eruption develops. In
severe, neglected cases pus and exudate may produce matting of the hair.
Nits are egg-cases. They occur in greatest density on the occipital and
parietal regions. Most of the unhatched nits are within 5 mm of the scalp
surface. The eggs can be distinguished from dandruff by the fact that they
are firmly attached to the hair. Moreover, if the affected hair is cut off and
observed under microscope, the oval egg capsule can be easily identified.
Adult lice and nymphs may be seen in heavy infestation.
3.3. Treatment
Treatment of pediculosis of the scalp aims at the destruction of the lice and
the ova. Other members of the family and the whole class of school children
should be examined, otherwise re-infestation will occur.
Malathion is effective and has good ovicidal activity. It is adsorbed onto
keratin, a process which takes approximately 6 hours, and has a residual
protective effect against re-infection for about 6 weeks. Malathion should be
left on the scalp for 12 hours before washed off. The insecticide is degraded
by heat, and a hot-air dryer should not be used. Treatment should be
repeated 2 weeks later when the larvae have hatched out. Lotions are
preferable to shampoos, as the latter expose the insects to relatively low
concentrations of insecticide which will favour the development of
resistance.
Empty egg-cases are difficult to dislodge, they persist for some time until
they are gradually worn away by repeated washing. They may be removed
with a fine-tooth comb or forceps. A cream rinse containing formic acid may
facilitate the removal.
4. PEDICULOSIS CORPORIS
4.1. Incidence and Epidemiology
Pediculosis corporis is now uncommon in developed countries. It mainly
affects the poor and neglect and flourishes in overcrowded, dirty situations
where individuals seldom change their clothes. There is great variation in the
number of eggs and lice on the clothing. In most cases the number of lice is
small but in some thousand of lice may be present. Transmission is mainly
by direct close body contact or by sharing infested clothing. Lice on a
cooling dead body will look for alternate lodgings, and doctors asked to
certify death in a vagrant should be aware of this.
Intense pruritus is the chief complaint. It is due to sensitization to salivary
antigens of the lice. Excoriation with secondary bacterial infection and
hyperpigmented changes are common physical findings.
When the lice are not feeding, they stay in the clothing. Therefore, it is
important to examine the inner lining of clothing including the seams of
underpants.
Hands and feet are usually not involved and there is a predilection for the
upper back. The characteristic distribution helps to distinguish it from
scabies. The principal louse-borne diseases are epidemic typhus, trench fever
and louse borne relapsing fever.
4.3. Treatment
It is the clothing rather than the patients which require treatment.
Destruction of the lice is accomplished by laundering or boiling the clothing
and bedding. High temperature laundering of underpants and dry-cleaning of
outer clothing are also effective. Tumble-drying is the most effective means
of killing both lice and eggs.
The patient should bath thoroughly with soap and water. Theoretically, this
is sufficient. However, many dermatologists would prescribe gamma
benzene hexachloride to treat the body as well. Mass delousing of large
number of persons can be carried out successfully by simply blowing DDT
powder under the clothing with a hand dust gun.
CUTANEOUS TUBERCULOSIS AND

ATYPICAL MYCOBACTERIAL INFECTION
Dr. L.Y. CHONG
CHAPTER 16
1. INTRODUCTION
Cutaneous tuberculosis was once a relatively common chronic infection in
Hong Kong. In a study done in Social Hygiene Service in 1968, there were
totally 177 cases from January 1962 to April 1967. This represented
approximately 0.35% of all the skin cases (50,364 cases) seen in
Government Dermatological Clinics during the same period. In recent
decade, because of improved living environment, BCG vaccination and
effective antituberculous drugs, this disease now becomes uncommon in
Hong Kong. In a recent 10-year retrospective survey in Social Hygiene
Service, there were totally 179 cases of cutaneous tuberculosis from January
1983 to December 1992, representing only 0.067% of the total skin cases
(267,089 cases) seen in our clinics during that period. The relative
incidences of different clinical types of cutaneous tuberculosis are shown in
the following pie chart.
Different Types of Cutaneous Tuberculosis
Social Hygiene Service, Hong Kong (1983-1992)
Lupus vulgaris 6.3%
Tuberculosis verrucosa cutis 4.5%
Scrofuloderma 4.0%
Lichen scrofulosorum 6.3%
Erythema induratum 79.5%
Papulonecrotic tuberculid 4.0%
It can be shown from these local figures that the true cutaneous tuberculosis
is now very uncommon in Hong Kong, representing only 14.8% of all cases.
In fact, most of the reported cases are erythema induratum, which accounts
for 79.5% of the cases. Erythema induratum is one form of tuberculids and
the truth of its tuberculous aetiological origin is still open to debate.
2. AETIOLOGY
Cutaneous mycobacterial infections are chronic granulomatous lesions
affecting skin at various regions of the body. Micro-biologically they are
classified as follows:
2.1. Tuberculous, Pathogenic
M tuberculosis M bovis
M lepra M africanum
2.2. Non-tuberculous, potentially pathogenic
1) Slow growing
M marinum M ulcerans
M kansasii M avium-intracellulare
M scrofulaceum
2) Rapid growing
M fortuitum M chelonei
3. CLINICAL FEATURES
There are different clinical presentations in cutaneous tuberculous infections,
depending on the virulence and number of bacilli infected, immunological
status of the host and the route of infection. Traditionally the clinical types
are divided into two groups:
1) True cutaneous tuberculosis
Lupus vulgaris
Tuberculous verrucosa cutis
Scrofuloderma
Tuberculous chancre, gumma, cold abscess
Miliary tuberculosis
2) Tuberculids
Papulonecrotic tuberculid
Lichen scrofulosorum
Erythema induratum
3.1. True Cutaneous Tuberculosis
This group of cutaneous tuberculosis is infected through direct inoculation
from an exogenous source, contiguous or haematogenous spread from an
endogenous focus.
3.1.1. Lupus Vulgaris
This is a chronic, progressive and tissue-destructive form of cutaneous
tuberculosis in patient with moderate or high degree of immunity. It occurs
more common in females than in males. The classical lesions consist of
reddish-brown plaque with "apple-jelly" colour on diascopy. The lesions
progress by peripheral extension and central healing, atrophy and scarring.
The areas of predilection are head and neck (80%), followed by arms and
legs, then trunk. It can be associated with tuberculosis of lymph node, lung,
bone and joint. In long-standing cases, patients may have scarring,
deformity, squamous cell carcinoma, basal cell carcinoma or sarcoma. The
main differential diagnosis includes discoid lupus erythematosus,
sarcoidosis, leprosy, lupoid leishmaniasis, tertiary syphilis, deep fungal or
atypical mycobacterial infection, granulomatous rosacea and Wegener's
granulomatosis.
3.1.2. Tuberculosis Verrucosa Cutis
In the past, this condition was common in Chinese boys over the buttocks
and knees. This is mainly due to their habit of playing and squatting in the
streets with open-bottom trousers. It usually presents as an indolent, purplish
or brownish red, warty and hyperkeratotic plaque lesion. It affects patients
with moderate or high immunity through direct inoculation of the tubercle
bacilli at sites of trauma. The areas of predilection are therefore over the
buttock, knee, elbow, hand and finger. Its progression is usually very slow
and spontaneous resolution may occur. This condition must be differentiated
from lupus vulgaris, viral wart, mycobacteria marinum infection,
chromomycosis, tertiary syphilis and hypertrophic lichen planus.
3.1.3. Scrofuloderma
This results from direct extension of an underlying tuberculous focus such as
lymph node, bone or joint to the overlying skin, often associated with
pulmonary tuberculosis. It is characterized by undermined ulcers, nodules,
fistulae, sinuses and scar. The areas of predilection are neck, supraclavicular
fossae, axillae and groin. The differential diagnosis mainly includes
hydradenitis suppurativa, actinomycosis, sporotrichosis and atypical
mycobacterial infection.
3.2. Tuberculids
It has been postulated that tuberculids are the result of hypersensitivity
reaction to haematogenous dissemination of tubercle bacilli or their toxin in
patients with moderate or high degree of immunity. Usually no identifiable
focus of active tuberculosis can be detected and the tissue culture for acid-
fast bacilli is often negative. There is still much controversy about these
conditions.
3.2.1. Papulonecrotic Tuberculid
This condition usually presents with symmetrical crops of papular eruption
that proceed to central necrosis, ulceration and depressed scar. It occurs
predominantly in young adult, most commonly affecting the limbs. There
may be history or distant foci of tuberculous infection. The main differential
diagnosis includes prurigo simplex, papular eczema, folliculitis,
leukocytoclastic vasculitis, pityriasis lichenoides et varioliformis acuta and
secondary syphilis.
3.2.2. Lichen Scrofulosorum
This is a rare form of tuberculid, presenting with grouped lichenoid papules
with perifollicular pattern over the trunk. It is frequently found in children or
young adults and may be associated with tuberculosis of lymph node, bone
or joint. The lesions often involute slowly in months without scar and then
recur. This condition must be differentiated from lichenoid drug eruption,
lichen nitidus, keratosis spinulosa, sarcoidosis, lichenoid syphilis and
eruptive syringoma.
3.2.3. Erythema Induratum (Bazin)
This is a nodular tuberculid presenting with indolent inflamed deep-seated
nodule and plaque, occurring bilaterally over the calves or feet. In severe
case there may be necrosis, ulceration, depressed scar and pigmentation. It is
more common in females than males. Usually there is no evidence of other
distant tuberculous foci. The main differential diagnosis is erythema
nodosum and other forms of nodular vasculitis.
3.3. Mycobacteria Marinum Infection
(Swimming pool or fish tank granuloma)
This is a chronic granulomatous infection of the skin caused by M marinum,
acquired by inoculation through abrasions. It is more vulnerable in children
and adolescents who frequently go to swimming pools, and among
fishermen and fishmongers. The lesion commonly occurs on fingers,
knuckles, elbows, knees and feet. Clinically it presents as an inflamed
nodule, pustule, ulcer or abscess. Sporotrichoid spread may occur. The main
differential diagnosis includes lupus vulgaris, sporotrichosis and
leishmaniasis.
4. INVESTIGATIONS
4.1. Skin biopsy x histopathology (AFB stain)
x tissue culture for M tuberculosis
+ tissue culture for atypical mycobacterial and deep fungi
The histopathological diagnosis and clinical correlation are important
because there is only a small percentage of cases with positive smear or
culture. When the skin biopsy is performed, one must make sure that
adequate tissue has been taken for both histological sections and tissue
culture. Repeated skin biopsy may sometimes be necessary to make a final
diagnosis. It is also important to specify on the laboratory form if one wants
to do a culture for atypical mycobacteria. They require different temperature
for growth in culture medium, for example, M marinum requires a
temperature of 30-32 degree centigrade within 2-3 weeks.
4.2. Tuberculin Test
In Hong Kong, Mantoux test is usually done by starting with 1 unit of PPD
intradermally over the forearm. If the result is negative, then the test is
repeated with 10 units. The results are interpreted as follows:
Diameter of induration Conclusion
5-10 mm suspicious
> 10 mm positive
> 15 mm strongly positive
However this test is of limited diagnostic value locally because of the high
incidence of exposure to mycobacteria and early vaccination of BCG. A
negative result nevertheless excludes active tuberculosis, except the miliary
form and diseases in immunocompromised patients.
4.3. Screening for Extracutaneous Tuberculosis
The presence of tuberculosis elsewhere provides supportive evidence in the
diagnosis of cutaneous tuberculosis, especially in the tuberculids. Chest X-
ray is mandatory. Other tests such as sputum, pus or early morning urine for
acid-fast bacilli, lymph node biopsy or bronchoscopy should be done if
indicated.
5. TREATMENT
Combination drugs therapy should be given to all true cutaneous
tuberculosis such as lupus vulgaris, tuberculosis verrucosa cutis and
scrofuloderma. Controversy exists about whether tuberculids should receive
multiple drugs treatment. Papulonecrotic tuberculide is commonly treated
with combination therapy, whereas erythema induratum and lichen
scrofulosorum can be treated by suppressive therapy with isoniazid alone.
The regimens of antituberculous therapy used in Hong Kong are
summarized as follows:
5.1. Standard Drug Regimens (totally 6 months)
1) Initial phase (3-4 drugs daily for 2 months)
Adult Child
a) Isoniazid 300 mg 5-8 mg/kg
+
b) Rifampicin > 50 kg 600 mg 10-12 mg/kg
< 50 kg 450 mg
+
c) Pyrazinamide > 50 kg 2.0 gm 20-35 mg/kg
< 50 kg 1.5 gm
or
Ethambutol < 60 days 25 mg/kg Not recommend
> 60 days 15 mg/kg
or
Streptomycin 3/4 gm IMI 15-20 mg/kg
2) Continuation phase (2 drugs daily for 4 months)

Isoniazid + Rifampicin (same dosage)
5.2. Intermittent Regimen (totally 6 months)
1) Initial phase (3-4 drugs thrice/week for 2 months)
Adult Child
a) Isoniazid 600-800 mg 15 mg/kg
+
b) Rifampicin 600 mg 15 mg/kg
+
c) Pyrazinamide > 50 kg 2.5 gm 20-35 mg/kg
< 50 kg 2.0 gm
or
Ethambutol 30 mg/kg Not
recommend
or
Streptomycin 1 gm IMI 15-20 mg/kg
2) Continuation Phase (2 drugs thrice/week for 4 months)
Isoniazid + Rifampicin (same dosage)
All patients who have been put on antituberculous therapy should be closely
monitored. The biochemical parameters like liver function test, renal
function test and complete blood picture should be checked. Liver function
test is mandatory and should be monitored at regular interval, as a lot of
these drugs have hepatotoxic side-effects. In elderly patient or patient with
renal impairment, the dosage of streptomycin should be reduced. Almost all
the anti-tuberculous drugs may cause drug eruptions. Some of these
reactions may be serious, such as erythroderma and Stevens-Johnson
syndrome. Elderly patient or alcoholic receiving isoniazid should have
prophylactic treatment with pyridoxine. Patient who is receiving ethambutol
should have regular ophthalmological check up.
5.3. Suppressive Therapy
This is used to treat tuberculids such as erythema induratum and lichen
scrofulosorum. In the past, it had been used as prophylactic treatment in
patient who has been receiving systemic steroid or immunosuppressive
drugs for other chronic cutaneous diseases. However, it is now seldomly
given for prophylaxis.
Isoniazid 300 mg daily for 9 months to 1 year
Pyridoxine 10 mg daily as prophylactic measure or 100 mg daily as
therapeutic measure against peripheral neuropathy
5.4. Treatment for M Marinum Infection
Medical:
1) Cotrimoxazole tab 2 bd x 8-16 weeks
2) Minocycline 100 mg bd x 8-16 weeks
3) Rifampicin + Ethambutol
Surgical:
1) Electrodessication
2) Cryotherapy
3) Surgical excision
PRACTICAL GUIDELINES FOR PHOTOTHERAPY
Dr. L.Y. CHONG
CHAPTER 18
Phototherapy is now a well established treatment modality in dermatology.
Its application in cutaneous diseases has been much broadened in recent
years, though the main use is still in psoriasis. The exact mechanism of
action of ultraviolet light on various cutaneous diseases is unknown, but
probably through immunosuppressive effect or direct phototoxic effect. In
Social Hygiene Service (dermatology) of Hong Kong, it has been used for
more than one decade. Although phototherapy is relatively safe if used
properly, there is not without risks. Some essential basic knowledge in
phototherapy is important before one proceeds to use this treatment
modality.
1. ESSENTIAL INFORMATION FOR PHOTOTHERAPY

Wavelength of UVA : 320-400 nm; UVB: 290-320 nm
Dosimetry
Energy (joule) = Power (watt) x exposure time (second)
Fluence (J/cm2 = irradiance (W/cm2) x exposure time (sec)
Exposure Time (min) = Dosage / 0.06 x Irradiance
(J/cm2) (mW/cm2)
Variation of irradiance
Irradiance (power density) varies directly with power source and inversely
with surface area (therefore inversely with the square of distance from the
power source)
I1 x D12= I2 x D22 (I = irradiance; D = distance)
D12 / T1 = D22 / T2 (T = exposure time)
Grading of erythema
E0 No erythema
E1 Minimally perceptible erythema (faint pink)
E2 Marked erythema (red)
E3 Fiery red erythema with oedema
E4 Fiery red erythema with oedema and blistering
NB In pigmented patient, sometimes erythema and oedema may not be seen.
Instead of these, patient may complain of hotness and tightness of skin.
Erythema is a limiting factor in phototherapy - E1 should not be exceeded.
The onset of UVA-induced erythema has a delayed onset of 48 hours after
exposure.
MPD (Minimal phototoxic dose) = The dose of PUVA required to produce a
E1 reaction 48 hours after exposure.
MED (Minimal erythemogenic dose) = The dose of UVB required to
produce a E1 reaction 24 hours after exposure.
Skin types
I Always burn, never tan
II Always burn, but sometimes tan
III Sometimes burn, but always tan
IV Never burn, always tan
V Moderately pigmented people (Chinese, Indian)
VI Black people (West Indies, Africans)
2. PUVA (Psoralen-ultraviolet A)
2.1. Indications
1) Psoriasis
PUVA is used mainly in plaque type psoriasis. It is relatively contraindicated
for unstable, generalized pustular and erythrodermic psoriasis. Special
cautions should be exercised if PUVA is used in these situations as it may
further aggravate the disease. It is also difficult to monitor the dosage of the
ultraviolet light in erythroderma.
2) Mycosis fungoides (CTCL)
PUVA is a relatively safe and effective treatment in the patch stage and
plaque stage of mycosis fungoides.
3) Vitiligo
The response to PUVA in vitiligo is better for face than the limbs and trunk.
However, in practice only a small proportion of patients has satisfactory
response.
4) Others:
Severe atopic dermatitis, pityriasis lichenoides et varioliformis acuta
(PLEVA), pityriasis lichenoides chronica, prurigo nodularis, polymorphic
light eruption, etc.
2.2. Contraindications
PUVA is contraindicated or relatively contraindicated in the following
conditions:
1) Pregnancy
2) Children < 12-year old
3) Photosensitivity
4) Severe cardiac, hepatic or renal diseases
5) History of skin cancers
6) Aphakia or cataracts
7) Immunosuppressed patients (probably)
2.3. Factors for Consideration in Psoriasis
Age & sex
Severity (>30% involvement - arbitrary)
Previous treatment for psoriasis
Concomitant medical illness
Social & economic factors
2.4. Before Starting PUVA
Consider indications & contraindications
Thoroughly inform the patient about the nature of therapy and give the
instruction sheet of PUVA to patient
Written consent
Blood screening if indicated (LFT, RFT, ANF)
Body weight
2.5. Initiation of Treatment
Starting dose of psoralen should be calculated according to the body weight.
(0.6 mg/kg body weight)
Body Weight (Kg) Meladinine (Methoxsalen)
(10 mg/tablet)
<50 20 mg
50-65 30 mg
65-80 40 mg
80-90 50 mg
>90 60 mg
(Take medication 2 hours before treatment together with food)

Starting dose of UVA is given according to either skin type or phototesting.
Skin Type Dosage of UVA (J/cm)

I 0.5
II 1.0
III 1.5
IV 2.0
V 2.5
VI 3.0
(Phototesting: determine the Minimal phototoxic dose and use 80% of MPD
as the starting dose)
Frequency of therapy: twice per week during clearing phase
Increment of dosage at each subsequent visit:
Initial: 0.5-1.0 J/cm2 (depends on skin type and starting dose)
If no response after 10 treatments: 1.0-1.5 J/cm2
If still no response after 15 treatments: Increase dosage of methoxsalen
Defaulter
a) Miss one regularly scheduled treatment: dosage should not be increased,
use the last dosage
b) Miss more than one session: dosage should be reduced by 0.5 J/cm2per
session missed (Minimum: starting dose)
c) Default for more than two sessions: see doctor before restart the treatment
Reaction (inform doctor)
a) If trace of erythema occurs, dosage should not be increased but the patient
may be treated with previous exposure time.
b) If more than trace of erythema occur, or patient complains of hotness and
tightness, the areas affected should not be retreated until these subside.
When more than 95% clearance (flexible), the last dosage should be
maintained, and a maintenance schedule should begin.
If no significant response or still not ready for maintenance treatment after
30 treatments, patient may be designated as treatment failure.
2.6. Frequency of Assessment by Doctor
The patient should be seen by doctor two weeks after initiation of treatment,
and then every four weeks during active phase. However, patient should be
seen by doctor as soon as possible if any reaction occurs.
Doctor should specify the starting dosage, subsequent increment and
frequency of therapy on the treatment sheet.
2.7. Maintenance Therapy
1) The last clearance dose is maintained at once-weekly interval.
2) If clearing persists for 4 weeks, reduce the frequency to one exposure
every 2 weeks (most patients need this frequency for maintenance).
3) If clearing persists for another 8 weeks, reduce to one exposure every
month. If it persist for another 4 months, the treatment may be stopped.
4) If there is relapse during maintenance, treatment is increased to twice a
week and UVA dose is increased by 0.5-1.5 J/cm2 for each successive
treatment. Maintenance is then given at a higher frequency than the one
which did not work.
5) During maintenance therapy, if erythema occurs as a result of decreasing
pigmentation, the UVA dose should be decreased by 0.25 J/cm2 per
treatment until erythema is no longer present.
2.8. Sites for Special Consideration
1) Extremities, especially legs, do not respond as well as the other areas.
Additional exposure time up to one fourth of the total may be given with
shielding of the other sites.
2) Intertriginous areas, scrotum, perineum, pendulous breasts and abdomen
are more sensitive to UV light. If necessary, they may be shielded with
folded cloth for one third of the total exposure time until tanning occurs.
3) Hairy scalp does not benefit from PUVA therapy.
4) Face may be shielded with cloth after the first few exposures if it is not
affected by psoriasis.
5) Normal skin is more sensitive to UVA than psoriatic skin.
2.9. Precautions that must be taken by Nursing Staff
1) Before treatment
a) Ask whether the patient has taken psoralen
b) Check whether the patient has erythema
c) Check the correct exposure time
2) During treatment
a) Make sure that the patient is wearing the protective goggles
b) Make sure that accurate exposure time is given
c) Withhold treatment if patient complains of discomfort
3) After treatment
a) Remind the patient to wear the sunglasses (Polarised grey - or green-
tinted) for 8 hours after therapy (both indoor and outdoor), and shield from
direct sunlight with sunscreen, suitable clothing, hat or umbrella.
b) Check the next follow-up time
c) Calculate the cumulative dose given
4) Maintenance of the PUVA machine
Check the irradiance of the machine with the UVA photometer every month.
Inform the technician to change the fluorescent tubes at the recommended
interval (For Waldmann UV3001 & 8001K PUVA machine: after 1500-2000
hours; Daavlin spectra 305/350: 850 hours) or when the irradiance drops.
(new lamps of 3001: 10.5 mW/cm2 at a distance of 21 cm; change lamps if
output falls below 6 mW/cm2 or when warning message appears in control
panel of Daavlin spectra 305/350)
2.10. Complications
1) Excessive erythema
If more than E1 occurs, PUVA therapy should be withheld. Patient should
be treated as having burns.
2) Pruritus
Bland emollients and antihistamines should be given. If the pruritus is
severe and persistent, withhold the phototherapy.
3) Nausea
The following measures may help to minimize the nausea due to taking of
methoxsalen:
a) Always take methoxsalen with some food
b) Mild nausea: take half the total dose of methoxsalen two and half hours
and the remainder two hours before phototherapy
c) Severe nausea: take antiemetic half hour prior to ingestion of methoxsalen
or decrease the dose of methoxsalen by 10 mg
4) Pigmentation
Reassure the patient that it will fade as exposures become less frequent
after the clearing phase.
5) Cataract
Annual ophthalmological examination is preferred.
6) Premature ageing and potential carcinogenesis in skin
Cautions should be taken about these potential risks when the cumulative
dose of the UVA over 1500 J/cm2
3. PUVA IN VITILIGO
The treatment is essentially the same as that in psoriasis. Start the dose of
UVA as that in type I skin with 0.5 J/cm2, with each increment of 0.25 J/cm2
and a frequency of two to three treatments per week. Try PUVA for 3
months. If there is response, may continue up to one year. However if there
is no response, stop it. Patient should be fully informed about the limitation
and risk of this treatment modality to avoid overexpectation or false hope.
In Social Hygiene Service, because of the shortage of manpower and PUVA
machine, a modified regimen using Wood's lamp and topical psoralen has
been used for years in vitiligo clinic. However, it is difficult to standardize
the exposure time as different models of UV lamps are used and these lamps
wear with time. It therefore depends much on the experience of individual
therapist with that particular lamp.
3.1. Machine and Specifications
Model B-100A Blak-ray Ultraviolet Lamp:
Peak wavelength: 366 nm
Minimal intensity: 1.020 mW/cm2 at 15 inches
Radiation (measured with UVA photometer):
at 6 inches is approx 6 mw/cm2
3.2. Patient Selection
Those patients with vitiligo on the face of relatively short duration may be
offered a trial. The eyelids should be avoided from irradiation. Those with
vitiligo of long duration and with involvement on trunk and limbs usually do
not respond to the treatment.
3.3. Before starting Topical PUVA for vitiligo
1) Explanation about the procedures and possible complications
2) Written consent
3.4. Dosimetry
1) Start with 30 seconds at a distance of 6 inches
2) Frequency: twice per week
3) Increase 10 seconds each session until E1 occurs
4) Try three months' duration. Continue if there is response; stop if there is
no response.
3.5. Procedures
1) Apply topical meladinine 30 minutes before radiation. Apply a thin layer
to the site of vitiligo only. Avoid the junction between the normal skin and
vitiligo. Avoid application to eyelids. Never dispense the topical meladinine
to patient for home application.
2) Warm up the machine for 5 minutes before use.
3) Fix the required distance.
4) Treat with the required exposure time.
5) Wash away the topical meladinine after treatment.
6) Leave the lamp on until all patients are treated, do not shift on and off
frequently.
7) If the lamp is shifted off, wait for 5 minutes or more before restart.
3.6. Defaulter
1) Miss one regularly scheduled treatment: dosage should not be increased,
use the last dosage
2) Miss more than one session: dosage should be reduced by 10 seconds per
session missed (Minimum: starting dose)
3) Default for more than two sessions: see doctor before restart the treatment
1) Before treatment
a) check whether the patient has erythema
b) check the correct exposure time
2) During treatment
a) make sure that the patient is wearing the protective goggles
b) make sure that accurate exposure time is given
3) After treatment
a) Advise the patient to avoid sunlight for 2 days
Use broad-spectrum sunscreen (Coppertone 45, Sunsense, etc.) both indoor
and outdoor
b) Check the next follow-up time
4) Maintenance of the machine
Check the irradiance of the machine with the UVA photometer every month.
Inform the technician to change the bulb at the recommended interval or
when the irradiance drops (minimal: 1.020 mW/cm2 at 15 inches distance)
(same as PUVA)
3.9. Complications of Topical PUVA
1) Erythema
Local reaction with intense erythema with pain and blistering may occur
(either due to over-exposure or photoallergic contact dermatitis). For large
area of vitiligo on face, it is better to try the treatment on a small area first.
2) Photosensitivity
Photosensitivity of the skin can persist for 48-72 hours after application of
topical psoralen.
3) Hyperpigmentation
Marked hyperpigmentation may occur at the site of treatment.
4. UVB PHOTOTHERAPY
4.1. Indications
1) Psoriasis
2) PLEVA, Pityriasis lichenoides chronica, Pityriasis rosea
3) Uraemic pruritus
4.2. Regimens for Psoriasis (Chronic Plaque Type)
1) Goeckerman regimen (Tar + UVB)
2) Ingram regimen (Dithranol + UVB)
3) UVB alone
4.3. Goeckerman Regimen
- Mainly for inpatient treatment
- Average duration of treatment: 28 days
- Monitor parameters: thickness, scaling and erythema
Procedures:
1) Apply 3-10% Coal tar paste topically to the plaques (or whole body) bd.
2) Daily LPC (Liquor Pica Carbonis) bath. The coal tar paste should be
washed away with liquid paraffin one hour before the UVB irradiation.
3) After the UVB therapy in Physiotherapy Department (QMH, QEH),
reapply the coal tar.
Side-effects of coal tar:
1) Messiness and staining of the clothes
2) Irritation of uninvolved skin
3) Folliculitis especially over flexures
4.4. Ingram Regimen
- Mainly for inpatient treatment (Not used in Hong Kong now because the
dithranol in lassar paste is no longer available)
- Average duration of treatment: 21 days
Procedures:
1) Apply dithranol in Lassar paste (start with lowest concentration available:
0.25%) once daily to the plaques ONLY (Avoid the normal skin). The
applied paste is then powdered (e.g. using Talcum powder) to harden the
surface and prevent spreading to uninvolved skin. The treated areas are then
enveloped in Tubegauze and left for 24 hours. Increase the concentration of
dithranol if tolerated.
2) Daily LPC bath. The paste is removed with liquid paraffin one hour
before the UVB irradiation.
3) After the UVB therapy in Physiotherapy Department, reapply the
dithranol again.
Side-effects of dithranol:
1) Brown staining of the skin (reversible)
2) Burning, which can be severe
3) Irritation (avoid applying to flexures, face and eyes)
4.5. UVB Therapy
1) UVB machine: fluorescent bulbs with peak emission around 300 nm are
commonly used
2) Dosimetry
Unlike the relatively standardised regimen in PUVA, the empirical starting
dose and subsequent increment of UVB usually has to depend on the
recommendations of the manufacturers of different UVB machine, and on
the individual therapist's experience, taking account of the skin type of the
patient.
Another more precise approach is to determine the patient's sensitivity by
the phototesting. The aim is to achieve an erythema of E1. During the course
of therapy, patient will develop various degree of tanning, which may
require an increase of exposure dosage.
Starting dosage: 80% of the MED as determined by the phototesting or the
starting dose as recommended by the manufacturer (e.g. in Daavlin spectra
726-SP: start with 15 seconds)
Subsequent increment: 1/8 (12.5%) of the last dosage
3) Frequency
Inpatient: 5 times per week (except Saturday & Sunday)
Outpatient: 3 times per week
4) Distance
Depend on different machine used. If the distance is changed during the
treatment, the correct exposure time should be calculated accordingly.
(Waldmann UV100 and Daavlin spectra 726-SP: about 20 cm from the
lamps)
5) Maintenance
UVB phototherapy is mainly used as clearance schedules on intermittent
basis. Effect from long term maintenance is unclear, if being given, most
psoriatic patients require one to three exposures each week to maintain a
clear state.
4.6. Complications
(similar to those of PUVA)
4.7. Machines and Specifications
Clinic Model
YMT Dermatology Clinic Waldmann UV100
irradiance: approx. 1 mW/cm2
at 20 cm distance
Daavlin spectra 726-SP
irradiance: approx. 3 mW/cm2
at 20 cm distance
YFS Dermatology Clinic Hohensonne 3030
4.8. Before Starting UVB Phototherapy
1) Explanation about the procedures and possible complications
2) Written consent
3) Phototesting
4.9. Phototesting
1) A template with holes of different size (approx 2 x 2 cm2 is covered to the
back
2) Irradiate with different doses of UVB at a fixed distance
3) Read the result 24 hours later and determine the MED
4.10. Dosimetry
1) Start with 80% of MED or as recommended by the manufacturer (usually
15-30 seconds) (if phototesting has not been done) at a fixed distance
2) Frequency: three times per week
3) Increase 1/8 (12.5%) of previous dosage each session, stop the increment
if more than faint erythema (E1) occur.
4.11. Defaulter
1) Miss one regularly scheduled treatment: dosage should not be increased,
use the last dosage
2) Miss more than one session: dosage should be reduced by 1/8 (12.5%) per
session missed. (Minimum: starting dose)
3) Default for more than two sessions: see doctor before restart the treatment
1) Before treatment
a) Check whether the patient has erythema
b) Check the correct exposure time
2) During treatment
Make sure that the patient is wearing the protective goggles all the time.
Patient must be warned beforehand that the goggles should not be taken off
at any time during the treatment.
3) After treatment
Check the next follow-up time
4) Maintenance of the machine
Inform the technician to change the bulb at the recommended interval
(Waldmann UV100: should be renewed after approx. 1000 hours; Daavlin
spectra 726-SP: 450 hours).
(same as PUVA)
5. PHOTO-PATCH TEST
Photo-patch test is performed for those with photo-allergic contact
dermatitis. Most reaction can be elicited by irradiating with UVA.
5.1. Procedures
1) Patch two symmetrical strips of photoallergans on the back of patient: one
as control and the other as test strip.
2) Read the result as usual 48 hours later to see whether there is contact
dermatitis and then remove the strips.
3) Irradiate one side with 5-10 J/cm2 UVA (PUVA machine or Wood's lamp).
The control side must be covered during the irradiation. If the Wood's lamp
is used, make sure to measure the irradiance with the photometer and
calculate the correct time of irradiation.
4) Read the result again after another 48 hours.
HEALTH NURSING IN SKIN CLINICS

Ms. M. WONG, Mr. W. LEUNG, Mr. E. WAN & Subordinates
CHAPTER 19
1. INTRODUCTION TO NURSING PRACTICE IN SKIN CLINICS
Dermatology Nursing is the specialty of compassion and caring for patients
together with scientific knowledge of dermatology illness from which
patients suffer. A nurse in Skin Clinic of Social Hygiene Service is entitled
to be called as a good nurse only if he/she gets enough experience, patience,
kindness and effectiveness. To be effective, nurses and doctors must work as
a team which is a long and good tradition in the nursing profession of Social
Hygiene Service. The essential elements for nursing activities in Social
Hygiene Clinics must be maintained here with emphasis on providing our
clients with clear and concise explanations and instructions before and after
each nursing procedure, and sound advice on the proper use of the
prescribed medications. A wrong concept of skin diseases as being mostly
contagious must be clarified. Education on the general care of one's skin can
be given to our patients and the public by means of individual interviews or
group talks. Skin conditions which are generalized, weeping, acute or
involving the exposed areas, especially the face, is always very traumatizing
psychologically and usually causes the patient to panic. This, however, can
be easily overcome by the presentation of empathic, friendly and high
knowledgeable attitude of the health personnel who handles the case.
2. INVESTIGATIVE PROCEDURES
2.1. Venepuncture
This issue has been discussed in Section 2A of this chapter but the following
points are worth mentioning:
1) As skin diseases often co-exist with internal medical conditions, a variety
of serological tests may be needed. Nurses should ensure that the correct
specimen bottles and laboratory request forms are used for the tests
prescribed.
2) The amount of blood, request form and specimen bottle required may
differ from individual investigation and nurses must comply with these
different requests to prevent rejection of any incompatible specimen from
diverse institutions.
2.2. Skin Patch-Test
2.2.1. Indication
To find out patient's allergen(s).
2.2.2. Application of the Test Substances
Mark identification on the top of each tape to show the order of the test
agents through out the testing procedure.
Place the tape on the desk with the chambers facing up and remove the
protective paper.
Semi-solid test agents are applied directly into the chamber, filling slightly
more than a half of the chamber volume.
For liquid test agents, place a filter paper disc in the chamber. Moisten the
disc thoroughly without surplus and place the test tape onto the skin within a
few minutes (dry paper disc may result in weak or false negative reactions).
Patient should stand or sit in a relaxed 'normal' position.
The tests are applied to healthy skin of the back, (sometimes on the lateral
aspects of the upper arms), which is free of ointment and excessive sebum
(if present, remove by non-irritant lotion before the application).
Apply the tape starting with the lower part and press the chamber from
below upwards to let air escape.
Press each chamber gently with the finger to ensure an even distribution of
the test agents.
A blue marker may be used to locate the test sites.
Additional non-irritant tape may be applied to take margin for better
adherence.
Left Right
Patient's Back
2.2.3. Instruction to Patients
Skin Patch Test is so designed to find out the patient's allergen(s).
The patient is required to come for follow-up on the third and fifth day after
the first visit for Skin Patch Test.
Rash or itchiness at a particular test site denotes he is allergic to that kind of
substance.
Do not wet or remove the plastic adhesives until removal by nursing staff or
doctor on the third day.
Avoid heavy exercise to prevent sweating.
Avoid rubbing and scratching the back.
Protect his back from direct sunlight.
Add ordinary plaster-adhesive to the original ones if it comes off
accidentally. Report this to nursing Staff or doctor on the next visit.
Come back for follow-up if any reaction occurs on his skin within three
weeks of the Test.
2.2.4. Record and Report
Patient's details are written down on a "Patch Test Form" and attached to the
case record file.
He has to come back on the third and fifth day for reading of the test.
When the patient comes back for follow-up on the third day, the tape is
removed and the Test is read after 30 minutes by nursing staff or attending
dermatologist.
2.3. Skin Scraping and Nail Clipping
The diagnosis of a superficial fungal infection is made by the observation of
fungal elements in infected keratin. This can be achieved by direct
inspection of fungal elements by means of bright field microscopy or
mycology culture.
2.3.1. Explanation to Patient
Explain the nature and procedures of the investigation to the patient,
emphasizing that the skin will be scraped and not cut.
No pain will be encountered during the whole process.
2.3.2. Procedure
Clean the desired area thoroughly and remove all local application at the
scraping site (ether solvent is best).
A blunt scalpel is used for skin scraping.
Sterilization of the scalpel by heat before and after each procedure is
essential.
Cool down the scalpel before scraping (avoid burning the patient).
Adequate specimen should be obtained from the expanding edges of a lesion
as these are the sites of most active infection.
Separate scalpels should be used to obtain specimens from different sites for
an individual patient to avoid misinterpretation.
For nail clippings, nail fragments should be taken from any discoloured,
dystrophic or brittle parts of the suspected nail. These should be cut as far
back as possible from the free edge of nail and include its full thickness.
For hair, specimen from the scalp is best obtained by scraping with a blunt
scalpel. The sample should include hair stubs, the contents of plugged
follicles and skin scales. Hair may also be plucked from the scalp with
epilation forceps.
2.3.3. Microscopy and Reporting

Scrape the skin/nail fragment onto the middle part of a glass slide, then
cover up with a cover slip.
Add a few drops of 30% potassium hydroxide (KOH) to the edges of the
cover slip (let KOH oozes towards the prepared skin fragment slowly in
order to prevent the cellular pattern being denatured). In case of pityriasis
versicolor screening, add a few drops of Parker's stain after instillation of
KOH.
Warm up the slide on top of a sterilizer till the fragment (Skin) is dissolved.
Hairs should be handled with particular care and allowed to soften without
direct heat so that the arrangement of spores will not be destroyed.
Inspect under bright field microscope. (low power 10X for screening and
40X for confirmation.)
Fill in patient's particulars, the site of inspection and result in the
microscopic record book as well as the case file record.
When examining specimens, it is important to ensure that the tissues
obtained have been softened adequately, so a single layer of cells is lined
side by side for inspection. For better microscopic viewing, the intensity of
light passing through the aperture of the microscope should not be too
strong. It is also necessary to adjust the focus while scanning the slide in
search for suspected organisms. The fungal elements will appear and
fluoresce as ¡¥green¡¦ branches among the cell layer if present.
Dermatophyte hyphae are regular in width, have septa and can show
branching. They may be divided into arthrospores.
If hairs are infected, the size and arrangement of spores, together with the
ability to fluoresce under a Wood's lamp will help in aiding identification of
the dermatophyte species involved. Slide may show ectothrix invasion of
hair by fungi, or favus hair showing hyphae and air spaces infected by fungi.
Parker's stain (equal parts of 30% KOH & Parker's blue-black ink) is
particularly useful in demonstrating the fungus (Malassezia furfur) in scales
from Pityriasis Versicolor as the organism takes up this stain immediately.
Thick-walled yeast 3-8 m in diameter and short angular hyphae can be
revealed in the bright field microscopic examination of infected skin scales
in Parker's stain.
In nail infection (onychomycosis), thick walled, spores and scanty hyphae
(spores may be in chain and Parker's stained) can be demonstrated.
Confirm the diagnosis with experienced staff or doctor if necessary.
Discard the slide into sharp box for disposal. Slides useful for teaching and
demonstration purposes are sealed with wax for storage.
Cleanse the microscope (the stage and objectives) with xylene after use as
KOH is corrosive.
2.3.4. Fungal Culture
Put sufficient quantity of skin/nail fragment in the paper wrapper.
Write down patient's particulars, site of inspection and etc. onto the paper
wrapper. (seal up properly to avoid leakage.)
Affix the specimen to the laboratory form and send to the corresponding PI.
3. MINOR OPERATIONS
Many skin conditions can be cured by means of surgical removal whereas
others may need biopsies for confirmation of diagnosis. Nurses have been
delegated to carry out most of these minor surgeries in our service. They are
trained on the job for months and are allowed to stand on their own only
when the doctor or Nursing Officer in-charge is satisfied with their
performance. Formally speaking, experienced skin unit nurses are delegated
to perform certain minor surgeries under the supervision of dermatologist.
Clear explanation to the patients before each procedure to allay their fear
and anxiety. Concise advice to them post-operatively to ensure genuine
wound healing is basic requirements in the nursing of these clients. A large
variety of minor operations are performed in our clinics but only the most
commonly encountered are discussed here.
3.1. Cauterization and Curettage
3.1.1. Electrocautery
This is the employment of a small voltage/current, through a disposable
hyfrecator Tip to heat an element with high resistance. It is used to burn the
tissue or coagulate small vessels. Examples are common skin Warts and
Pyogenic Granuloma.
3.1.2. Curettage
This is the use of a 'curette' to remove small, well-defined tumours on sites
with a firm base and minimal mobile tissues. Examples are Milia and
Molluscum Contagiosum.
3.1.3. Procedures
Explanation, consent, positioning and sterile technique should all be
observed.
Clean and anaesthetize the lesion. (Lidocaton 2%). To reduce the risk of
drug allergy, 2 c.c. of the anaesthetizer per site of lesion is the maximum
dose used.
Identify the edges of the lesion and cauterize the upper most layer (Do not
press or puncture the lesion with the disposable hyfrecator Tip while burning
as the Tips or extreme heat may damage the under-lying normal structures.)
Trim the burnt unhealthy tissues with a pair of scissors and scrape off the
residual burnt necrotic tissues with a curette.
Repeat steps 3) and 4) to an appropriate depth (the base) until fleshy, normal
tissues is reached.
Trim and scrape the rim as well.
Vigorous use of the cautery may lead to undesirable damage of the
underlying structures and unnecessary scarring.
For common warts, Unipolar 30 setting of the hyfrecator is recommended.
3.1.4. Advice to Patients
Frequent changes of dry flexible fabric dressing strips (e.g. band-aids) are
required to absorb exudate. Change dressings whenever it is soaked through.
It may take 1-3 weeks for a crust to form.
Care must be taken to protect the wound trauma and wet. It probably heals in
3-6 weeks.
Bleeding may occur within the first 3 days. Direct pressure onto the site for
5-10 minutes will stop the bleeding.
The rate of healing depends on the amount of tissue destruction and the
location of the lesion.
The risk of infection is low, but patient should complete all the antibiotics if
prescribed by the doctor.
Return to the clinic if problem arises.
3.2. Management of Molluscum Contagiosum
3.2.1. Definition
It is caused by a DNA poxvirus that infects epidermal cells. Clinically the
lesions appear as smooth, doom-shaped papules which are often
umbilicated.
3.2.2. Incidence
It is a common childhood disease. It may spread among family members but
is uncommon. (i.e. may transmit by close body contact.)
3.2.3. Treatment Methods
1) Curettage and Iodine Application
- explain the procedure of treatment and nature of the disease to client and
their parents or guardians so to obtain their co-operation.
- It is done without anaesthesia.
- A curette is used to scrape off the molluscum. Ensure the central core
composed of molluscum bodies is scraped off.
- Apply a tinge of iodine to the wounds with a dressed applicator for
disinfection.
- Apply pressure onto the wounds for haemostasis and put on dressings if
necessary.
2) Application of TCAA (Trichloroacetic Acid 33%)
- Explain the procedure and nature of TCAA to the patient and their parents
or guardians to gain co-operation and allay any anxiety.
- Well protect the vital organs, e.g. the eyes with gauze etc.
- Apply vaseline to the surrounding healthy skin for
protection.
- Apply the TCAA with a dressed applicator to the lesions.
Healing usually takes a few days.
Keep the wounds dry for a day or two, change the dressings or band-aids if
wet.
3.3. Management of Skin Tags
3.3.1. Definition
A skin tag is a benign fleshly tumour that is acquired in adult life. It usually
appears as a pedunculated flesh-coloured growth.
3.3.2. History
Most patient ignore skin tags and accept their presence as a sign of aging.
It is a benign condition and will not become malignant.
Some patients request their removal because of irritation or cosmetic
appearance.
3.3.3. Procedures
Thorough explanation is given so as to gain full co-operation during
treatment.
It is done without anaesthesia except for very large skin tags where
diathermy is indicated for haemostasis.
The easiest means of removal is by quickly snipping them off with fine
scissors (i.e. excise the root of the skin tag).
The small bleeding can be arrested by low power diathermy or manual
pressure.
Healing usually takes a few days.
Keep the wounds dry for a day or two. Change the band-aids (if any) if wet.
3.4. Cryotherapy
3.4.1. Definition
This is a deliberate destruction of diseased tissue by ¡¥Cryogen¡¦ - extreme
COLD in a controlled manner, i.e. Liquid Nitrogen (-1960 C).
-400 C is necessary to kill normal cells by freezing alone, but
-250 C is probably adequate to destroy diseased tissue
3.4.2. Rationale
A rapid rate of freezing may cause more tissue damage.
A prolonged thaw may increase tissue damage.
3.4.3. Technique
The cryojet gun is held close to the lesion. A steady spray of liquid nitrogen
is directed at the centre of the lesion.
The ice-front gradually extends to the edge of the lesion.
Timing commences once solid ice is formed over the lesion.
Freezing is continued for the required period, normally no greater than 30
seconds. The spray is adjusted to maintain an iceball of a constant size.
The lesion is allowed to thaw slowly.
If a second freeze is required, the lesion should be allowed to thaw
completely before re-freezing.
For a malignant tumour, a 5 mm rim of normal tissue should be included
around the lesion.
Note: Various brands of ¡¥Cryojet¡¦ apparatuses are available from different
agencies. When using Cryojet gun to perform procedures, the performer
must hold the instrument in an upright position. Once the Cryojet is tilt over
45 degrees, the liquid Nitrogen inside the gun will spill out suddenly and
may cause undesirable accidents.
3.4.4. Recommended Freezing Times
Lesions Approx. Freezing Time
1) Actinic keratosis 5-10 seconds
2) Seborrhoeic wart 10 seconds
3) Viral warts: Filiform 5 seconds
Common 10 seconds
Genital 5-10 seconds
Plantar 15-30 seconds
Periungual 10-15 seconds
(beware of damaging the underlying nail matrix)
4) Acquired Pigmented Naevi 20 seconds
5) Superficial basal cell Carcinomata 30 seconds
6) All other malignant tumours Double 30 seconds
freeze-thaw cycle
A thorough medical history should be obtained prior to treatment so to
minimize the risk of unwanted reactions. Any deviated abnormalities should
be reported to doctors concerned for further evaluation. (e.g. a decrease in
platelet count may denote a bleeding tendency after treatment.)
During freezing and thawing, one may encounter a burning sensation
Analgesics, e.g. Panadol/Dologesic may be taken, before spraying.
Blisters may form soon after freezing and are occasionally haemorrhagic.
A crust will usually form in 1-2 weeks and will peel off in 3-4 weeks.
Dressing may be required to absorb exudate if the blisters rupture.
The treated area may initially be erythematous, but this fades leaving a
hypopigmented macule.
Return to the clinic if tense blisters causing much discomfort are found after
treatment.
4. PHOTOTHERAPIES
Phototherapy alone or together with ingested Psoralen (Photochemotherapy)
has been proven to be effective in the management of many difficult skin
disorders. Nurses' role in this issue includes the input of detail information
on the treatment regime and advice on the outcome, to the patients.
Supervision during the whole course of therapy and patients' compliance
with the regime must also be keenly observed.
4.1. PUVA
4.1.1. Pre-treatment Preparation
A clear verbal explanation on the nature of the therapy and the procedures in
detail together with an instruction sheet on PUVA treatment must be given to
the patient prior to commencement.
Obtain written consent.
Blood screening for LFT, RFT, ANF.
Measure patient's body weight for doctor to assess the Meladinine dosage.
Clinical photographs are taken for future assessment.
Ensure the patient has taken Psoralen (Meladinine) 2 hours before
phototherapy (Psoralen enhances absorption of solar irradiation).
Wear ultraviolet-proof sunglasses, suitable clothing, hat or umbrella to
protect exposed areas of the body after ingestion of Psoralen. This will
prevent excessive exposure to sunlight especially in summer seasons.
Observe patient's skin condition before and after each treatment for progress
or changes especially any onset of erythema.
Check the correct exposure time.
4.1.2. Procedures
Tell the patient to remove all clothing and cover the genitalia. The face may
be shielded with a towel if it is not affected. For female patients, cover the
breasts if not involved.
Ensure the patient is wearing the protective goggles.
The patient is instructed to stand or lie at a designated distance away from
the light source.
To give accurate exposure time as prescribed.
A nurse is assigned to observe the entire procedure in a special designed
observation room through an observation window. Verbal communication
during the process is essential as a reassurance to the client.
Withhold treatment if patient complains of discomfort and inform the doctor
immediately.
The lower legs frequently take longer to respond to phototherapy and may
need additional exposures. All other areas should be draped during the added
treatment.
Remind the patient not to move about during the treatment.
4.1.3. After Treatment and Advice
Remind the patient to wear sunglasses (which should be prechecked to
ensure UVA opaque) for 8 hours after therapy (both indoor and outdoor), and
shield from direct sunlight with sunscreens, suitable clothing, hat or
umbrella to avoid over absorption of solar irradiation.
Apply sufficient emollient onto skin surface to minimize irritation because
skin is usually dry after treatment.
Reassure that pigmentation that may occur will fade as exposures become
less frequent after the clearing phase.
Observe and report any pricking, painful or itching skin sensation
occurrence immediately after treatment. Inform the doctor if erythema or
discomfort arises.
For female patients, advise contraception. If query of pregnancy, inform the
doctor immediately to stop the treatment.
Check and arrange the next appointment.
Calculate the cumulative dose given.
4.1.4. Defaulters
Miss one regularly scheduled treatment: dosage should not be increased, use
the last dosage.
Miss more than one session: dosage should be reduced by 0.5 J/cm per
session missed (Minimum: starting dose).
Defaulted for more than two sessions: see doctor again before restarting the
treatment.
4.1.5. Maintenance of the Machine
Check the irradiance of the machine with the photometer every month.
interval or any deviations of intensity from normal range.
4.2. UVB
4.2.1. Pre-treatment Preparations
Thoroughly inform the patient on the nature of the therapy. Give the
instruction sheet on UVB treatment to him.
Perform phototesting as stated by Doctor.
Check whether the patient has erythema.
4.2.2. Phototesting
A test kit consisting of panels and mittens is affixed to the body or limbs
according to the site being chosen for the test.
Irradiate with different doses of UVB (10, 20, 30, 40 seconds). (NB
delivered dose of UVB will vary with different model.)
Read the result 24 hours later and determine the minimal erythemogenic
dose (MED).
4.2.3. Procedures
Fix the required distance according to different models.
Select the UV switch and reflector units.
Set the required exposure time with timer switch.
Tell the patient to remove all clothing and cover the genitalia. The face may
also be shielded if it is not affected. For female patients, cover the breasts if
not involved.
Ensure that the patient is wearing the protective goggles.
Remind the patient not to move about during treatment.
A nurse is assigned to observe the entire procedure in a special designed
observation room through an observation window. Verbal communication
during the process is essential as a reassurance to the client.
After being switched off, the system must be allowed to cool down at least
for the set period before restarted.
The field size of irradiation should be considered (e.g. if the whole body is
treated, the upper and lower parts have to be treated separately).
4.2.4. After Treatment and Advice
Reassure the patient that it takes 2-3 months to notice the outcome of the
treatment.
Apply sufficient emollient onto skin surface to minimize irritation because
skin is usually dry after treatment.
Avoid direct sunlight and protect himself by sunscreen, clothing, hat and
sunglasses.
Inform the doctor if erythema or discomfort occurs.
Check and arrange the next appointment.
4.2.5. Defaulters
Miss one regularly scheduled treatment: dosage should not be increased, use
the last dosage.
Miss more than one session: dosage should be reduced by 1/8 (12.5%) per
session missed. (Minimum: starting dose.)
Defaulted for more than two sessions: see doctor again before restarting the
treatment.
Check the irradiance of the machine with the photometer every month.
interval or any deviation of intensity from normal range.
4.3. Topical PUVA for Vitiligo
4.3.1. Pre-treatment Preparations
Explain on the procedure and possible complications.
Check whether the patient has erythema.
Put the date, dose and nurse's signature on the referral and return the referral
to the patient before he leaves.
4.3.2. Procedures
Thoroughly clean and assist patient to remove all dirt, make-up, sweat or
other local applications on the sites to be irradiated. Advice on the untoward
out-comes of such treatment, e.g. redness, blistering.
A thin layer of Meladinine paint should be applied to the leukodermic patch
or bald area by means of a dressed applicator.
The paint should be applied at least 30 minutes before Ultraviolet
illumination.
Warm up the machine for 5 minutes before use.
Refrain from applying paint to delicate areas, e.g. eyelid. Make sure no paint
gets into the eyes.
Both patient and nurse should put on goggles.
Give the correct exposure.
Wash off the topical Meladinine after treatment and application of sunscreen
agent onto the sites is advisable.
The treatment can be given twice weekly with an initial dose of 30 seconds
at a distance of 15 cm. An increase of 10 seconds per subsequent treatment
is recommended until E1 occurs.
4.3.3. Frequency of Assessment
The doctor is responsible to prescribe the starting dosage, subsequent
increment and frequency of therapy for each case. He will reassess the case
two weeks after commencement of treatment, then every four week during
active phase, but, patients should be seen by the doctor if any reaction
occurs.
Inform patient of the possible response and complication e.g. redness,
blistering, rash and pain.
Avoid exposure to sunlight especially on the day and the next of UV
treatment. Advise on the use of sunscreens both indoor and outdoor.
4.3.5. Reactions and Defaulters
If reaction is mild, maintain the dose of the last treatment. This also applies
to those who has defaulted treatment once.
If defaulted for more than one session, dosage should be reduced by 10
seconds per session missed. (Minimum: starting dose.)
Defaulted for more than two sessions, or if reaction is severe, e.g. severe
blistering, excoriation or burning sensation, withhold treatment and the
patient should be reassessed by the doctor.
Check the irradiance of the machine with the UV photometer every month.
Inform the technician to change the bulb at the recommended interval or
when the irradiance drops.
5. LASER THERAPY
Laser Safety Officer (LSO): one of the nurses in the clinic will be appointed
as LSO. His/her duty is to ensure all safety measures are followed in
operating with a laser machine.
5.1. The information of Laser Therapy in our Skin Clinic is as follow:
At present, there are two types of Laser systems being used in our Service.
1) The VisErase is a free-standing mobile unit which uses a copper vapour as
lasing medium for treating a variety of vascular and benign pigmented
cutaneous lesions. The copper vapour laser emits green (511 nm) and yellow
(578 nm) Lights.
2) HGM Surgica K1 is another type of Laser unit which uses Krypton ion as
a convenient source of light for treating cutaneous and vascular pigmented
skin lesions. This Laser system emits lights of predominately two
wavelengths: 520-530 (green) and 568 (yellow) nanometers.
5.2. Indications
1) Recommended Laser Treatment: Yellow light
a) Capillary cavernous haemangioma
b) Cherry angioma
c) Hereditary haemorrhagic telangiectasia
d) Kaposi's sarcoma
e) Lymphangioma
f) Port wine haemangioma
g) Post rhinoplasty red nose
h) Rosacea
i) Spider telangiectasia
j) Telangiectasias
2) Recommended Laser Treatment: Green light
a) Naevus of Ota
b) Freckle
c) Keratosis (Actinic/Congenital/Seborrhoeic/Solar)
d) Lentigo
f) Neurofibroma
g) Naevus
h) Viral wart
5.3. Operation of Laser Machine
5.3.1. Manual Turn On of VisErase
Check that the AC power lamp is lit.
Turn the key switch to start (fully clockwise).
Wait 5 seconds - press the HIGH button - the button should flash.
After 10 minutes check that Laser Emission Lamp is lit and that no
malfunction is indicated.
Laser emission should begin approximately 30-35 minutes after the HIGH
button has been pressed and should stabilize after 40-50 minutes.
5.3.2. Manual Turn On of Surgica K1
Check that the main circuit breaker on the back of the unit must be in the
ON position.
Turn the key switch to the ON position.
After approximately 45 seconds, the Laser system can now be switched
either to the TREAT or STANDBY modes of operation by depressing the
appropriate button on the front panel.
When the laser is first turn on, it will go into the STANDBY mode
automatically after warming up. One may change to the TREAT mode
simply by depressing the green treat button.
When in the TREAT mode, the treat button lights up and generates a red
aiming beam. Pressing onto the foot switch will light up the Laser head
which will then release laser energy to the delivery device.
Note * Safety goggles must be worn by all personnel when the laser is in
use.
* Treatment should not be commenced until the Laser power has stabilized.
5.4. Preparation of Patient
Record all the particulars: name, clinic no., laser therapy no., site of
treatment and especially contact telephone no. on the treatment progress
sheet.
Obtain consent form after explaining the procedure and aftercare to the
patient by the MO i/c.
Take Clinical photo before treatment and every follow up.
5.5. Preparation for Laser Therapy
Safety goggles must be worn by all personnel when the laser is used.
Protect patient's eyes with safety goggles or eye shield.
Provide local anaesthesia (2% Lignocaine without adrenaline) as prescribed.
Sometimes a thick layer of EMLA cream (a kind of local anaesthetic agent)
with an occlusive dressing is applied to the area to be treated 1 hour before
therapy (this allows better absorption).
For lesions near to the eyes, Novesin eyedrop is instilled if eye shields are to
be used.
A technique for reducing thermal damage to surrounding tissues during laser
surgery is to precool the surgical site prior to laser energy exposure if
possible. Constant irrigation with saline solution will also carries excessive
heat away from the surgical site.
Mark the treatment time.
Assist the doctor in certain procedures, e.g. light adjustment, vacuum suction
of excessive smoke, installation of different lens pieces.
A good functioning Smoke Evacuation system should be installed. It is
especially useful to provide a germ free environment when performing
operations with pathological conditions suspected to be of viral origin.
Make sure all windows are shut. No reflection of light is allowed. The door
should be locked while the laser is being used. Turn on the warning light
whenever therapy is proceeding.
5.6. Manual Turn Off of Laser Machine
After treatment for all patients, turn the key switch of VisErase to finish. The
Laser will shut down but the cooling fan will continue to operate for about a
further 15-30 minutes. The fan will automatically turn itself off at the end of
this period. As for Surgica K1, wait 5 minutes for cool down and then turn
off the machine.
5.7. Aftercare Following Laser Treatment
Inform patient a sunburn like reaction with possible blistering with the first
24-48 hours is expected.
A crust or scab may occur after 2-3 days. Advise the patient not to remove it
and let it fall off itself.
Keep the area clean and dry until the scab/crust falls off. Wash gently with
soap and water and apply a thin layer of antibiotic ointment.
Avoid direct sunlight or sun exposure to the treated area for 3-6 months. Use
at least an SPF of 15 or greater sunscreen, or wear a hat or other protective
clothing (preferably both).
Reassure the patient that the treatment may take up to three months to
adequately judge the true response of the skin condition to the laser
treatment.
Check and arrange next follow-up time.
5.8. Maintenance of Laser Machine
Make sure the AC power lamp is always lit. Do not turn off the main switch
for Laser.
Do not move the laser while it is operating or within 30 minutes of turning it
off.
Make sure the castor brakes are locked.
The laser unit should be protected from standing in pooled liquid.
Avoid liquid to enter the laser through apertures such as air vent holes. If
liquid does enter, terminate use immediately, disconnect power and call for
service.
Do not place the fibreoptic fibre on the floor, avoid pressing across it with
hard objects.
Never press the utility mode when controlling the panel.
5.9. Precautions
Never look directly at the Laser bean emerging from the aperture on the
main assembly or from the fibre, handpiece or scanner if one is fitted.
Never operate the laser unless all personnel in the area are wearing approved
laser safety goggles.
All laser personnel should consider the laser plume to be potentially
hazardous, both in terms of particulate matter and infectivity. Operating staff
should wear masks and latex surgical gloves.
If the laser light is being used near a patient's eyes, additional eye protection
must be provided for the patient, i.e. using the eyeshield and anaesthetic eye
drops.
Always lock the door of the room during treatment.
Never look at the laser light reflected, diffused or scattered from reflective
surfaces such as glass, mirrors, metal, glossy paint, polished floors, plastic
mouldings, window frames or paper.
Do not use the laser in the presence of flammable substances, e.g. ether.
Never point the laser handpiece at any person except at the treated area.
6. ADVICE ON THE USE OF DRUGS

Topical applications have often been mistakenly regarded as less dangerous
than drugs ingested and patient tends to use them more frequently than
prescribed by the doctor. This actually is extremely hazardous because many
of the steroid preparations are of very high potency and may cause
irreversible adverse effects if applied too often or on delicate areas such as
the face. Other clients may self-treat their newly noticed skin problems with
cream or ointment stocked up from previous consultations and result in
worsening of the conditions. Therefore, nurses must educate clients on the
proper use of all drugs prescribed, with emphasis on the above misconcepts
to ensure that untoward effects would not occur.
Numerous types of drugs are used in dermatology treatment but only a few
topical preparations which require special attentions. They are listed as
follows:
6.1. 25% Benzyl Benzoate Emulsion
It is used for the treatment of Scabies.
Take a warm soapy bath in the evening. Dry the body thoroughly and use a
brush to apply the medication thinly all over the body, sparing only the neck
and head. Make sure that the application has included the hands (particularly
between the fingers), the umbilical area, the groins, the genitalia (especially
the glans for male with prepuce), the area between the buttocks, and the feet
(particularly the toe webs). The patient should trim the fingernails and
toenails short, this allows easy assess of the medication to the undersurface
of the nails. Allow the medication to dry and put on the same old clothing.
Re-apply the emulsion to hands every time after hand washing.
Next morning, repeat the application without taking a bath, allow the
emulsion to dry, no change of clothing required.
In the evening, take a warm soapy bath to remove all the medication. Put on
clean clothing afterwards.
Old clothing and bedding should be treated by boiling for 5 minutes, hot
ironing or wrap in plastic bags & put aside for a few weeks before reuse.
Relatives or friends who are in close contact with the infected person should
also be examined and treatment at the same time if necessary.
A total of two applications of the emulsion is sufficient to kill all the mites
but itching may persist for 1 to 2 weeks. Over application will only give rise
to irritation and cause Contact Dermatitis. Successful treatment depends on
the patient conscientiously following the instruction and advice.
Return to the clinic if itchiness lasts for more than 2 weeks or in case of
other skin eruptions.
6.2. 0.5% Malathion Lotion (Derbac Liquid)
This is the drug of choice for the treatment of infestations by lice such as
Pediculosis Capitis or Pediculosis Pubis.
Treatment should be carried out for all infested personnel at the same time.
6.2.1. For Treating P. Capitis
the hair should be cut very short for boys. No shampoo is required prior to
treatment. The lotion is rubbed onto the scalp, (paying special attentions to
partings, back of the neck, fringes and around the ears) at night, preferably
half an hour before going to bed.
Wrap the hair with a clean towel and leave it over night.
In the next morning, use a dense-toothed comb to comb through the hair in
order to remove all the remains of nits and lice. Followed by a thorough
ordinary shampoo.
Disinfestation of pillow cases, bedding and cosmetic articles should be
carried out after procedures by boiling for 5 minutes or hot ironing. Articles
that do not withstand heat can be immersed in 2% hypochlorite solution for
30 minutes which will yield the same result.
6.2.2. For treatment of P. Pubis
The lotion is rubbed onto the body from umbilicus to mid-thigh, front and
back with special attention to the hairy parts including the anal region. Put
on old clothing when the lotion is dry.
Followed by a bath the next morning so as to wash off all the lotion. Put on
new clothing.
The old clothing should be treated before reuse (the same procedure as for P.
Capitis).
Note: for both cases, if signs and symptoms persist for more than a week
after treatment, seek for medical advice again.
6.3. 1% Potassium Permanganate Solution
This is a commonly prescribed medication for skin problems and if used
correctly, helps soothe a lot of conditions, especially the weeping ones.
Method of dilution:
- The stock lotion, when supplied by the pharmacy is in a 1% dilution and
purplish-black in colour.
- One portion of this stock lotion is added into 79 parts of water to give a
diluted solution of 1 : 8,000 concentration. (colours light purple)
- Adding 3 teaspoons of the stock lotion into a water-filled 1.25 litre COKE
bottle will give the same dilution.
Soak the affected skin in the solution for approximately 10 minutes twice
daily.
Rinse thoroughly and dry the affected area after soaking.
Never use the solution in any higher concentration or more often than
prescribed.
CUTANEOUS DRUG ERUPTIONS

Dr. L.Y. CHONG
CHAPTER 23
Cutaneous drug eruptions may be defined as adverse cutaneous lesions as a
consequence of administration of drugs.
The exact incidence of cutaneous drug eruptions in Hong Kong is unknown.
According to the statistics of Social Hygiene Service, drug eruptions account
for 0.5% of all new skin cases seen in dermatological outpatient clinics of
the Service in 1995. This figure does not include those seen in general
outpatient clinics, private sector and hospitals. The true incidence is
definitely much higher. The main difficulties of getting a true figure are due
to lack of a central registry and loose labelling of drug reactions on the
patients. Adverse effects of drugs are often published in the literatures
according to anecdotal reports or badly designed studies.
The pathogenesis of drug eruptions may arise as a result of immunological
or non-immunological reaction. Some of these reactions are predictable
(dose-related) while some are unpredictable (idiosyncratic). Those with an
immunological basis may due to different types of hypersensitivity
reactions, for instance, allergic type of urticaria may be the result of Type I
reaction (IgE-mediated) or Type III reaction (complement dependent
immune-complex mediated). Nevertheless, the exact mechanisms of most
drug eruptions, including fixed drug eruptions, are unknown.
Clinically drug eruptions have a wide range of different morphological
presentations. (Table 1) They can be generalized or fixed eruptions and their
severity varies from minor to fatal skin reactions. Unfortunately, apart from
fixed drug eruption, there is neither pathognomonic clinical feature nor
diagnostic investigation in drug eruption. In practice, it is often difficult to
identify the culprit with certainty, especially when the patient is taking
multiple drugs simultaneously. Diagnosis is mainly based on clinical
grounds in which the history plays the most essential part. In the history, the
temporal relationship between the taking of drug and the onset of skin
eruption is most important. Experience and statistical knowledge about the
suspected drugs are also useful as certain drugs (for examples, ampicillin or
cotrimoxazole) are more likely to cause drug eruptions, especially in certain
diseases (for examples, AIDS or infectious mononucleosis).
In the history, the following information should be carefully asked:
A detail drug history including the names and dosage of the drugs taken
(Drugs should include those prescribed by doctors and any herbal or
homeopathic medicines)
The temporal relationship between the intake of drugs and the onset of skin
lesions (Allergic drug reactions usually develop within 1 to 2 weeks of
initiation of treatment)
Any previous history of drug allergy, or similar skin lesions after taking
similar drugs
Any improvement of skin lesions after the suspected drug is withdrawn (The
skin eruption is unlikely to be drug-induced if it fails to improve after
withdrawal or if it improves even without stopping the drug. However,
sometimes it may takes weeks for drug eruption to resolve even when the
drug is stopped.)
Up to the present moment, there is still no reliable and practical
investigation for confirmation of drug eruption. Rechallange test is
dangerous and should not be carried out in usual circumstances. Perhaps the
only situations for rechallange test are those with fixed drug eruptions or
those with life-threatening conditions in which that particular drug is
essential. Skin test has little practical value as it may cause fatal systemic
reaction and false positive reaction is common. Other tests such as
radioallergosorbent tests (RAST) for drug-specific IgE antibody (penicillin,
insulin), histamine release test, leucocyte and macrophage migration
inhibition tests, lymphocyte toxicity assay, basophil degranulation test,
passive haemagglutination test and lymphocyte transformation test are
mainly for research purposes.
In mild drug eruptions, withdrawal of the culprits together with symptomatic
treatments will be adequate. For patient who is taking multiple drugs which
are essential (for instance, antituberous drugs), all drugs should be
temporarily withheld. After the skin lesions has subsided, each of these
drugs can then be reintroduced one by one under strict observation, usually
start with the drug which has lowest incidence of drug reaction. In severe
drug eruptions such as Stevens-Johnson syndrome, toxic epidermal
necrolysis, erythroderma or angioedema, reintroduction of the drug is
dangerous and immoral. In these situations, other treatment alternatives
should be seeked for. Cross-sensitivity between similar drugs should be
borne in mind in choosing alternative medication. Desensitization therapy
has little practical value. After recovery, it is essential to give the patient a
warning card, labelling the offending drug in order to avoid future retaking
of the drug.
Table 1: Morphological Classification of Drug Eruptions
Acanthosis nigricans-like eruption

Corticosteroids, Hydantoin, Nicotinic Acid, Pills, Stilbestrol
Acneiform eruption
Anticonvulsant (phenytoin, phenobarbital, trimethadione), Antituberculous
(isoniazid, ethionamide, refampicin), Azathioprine, Chloral hydrate,
Corticosteroids, Corticotropin (ACTH), Cyanocobalamin, Cyclosporin,
Halogens (bromides, chlorides, iodides, halothane), Haloperidol, Lithium,
Pills, Psoralens, Quinine, Scopolamine
Acral erythema/red palms
Adriamycin (Doxorubicin), Cystosine arabinoside, 5-fluorouracil
Acrodynia
Mercury
Alopecia
Allopurinol, Bromocriptine, Carbimazole, Chlorambucil, Chloramphenicol,
Cholesterol lowering agents, Cimetadine, Colchicine, Coumarin, Cytotoxic
drugs, Diazoxide, Ethionamide, Fluconazole, Gentamicin, Gold, Heavy
metals, Heparin, Hydantoin, Levodopa, Methotrexate, Methyldopa, NSAID
(indomethacin, piroxicam), Pills, Phenindione, Propanolol, Sodium
valproate, Thiouracil, Vitamin A or Retinoids
Anaphylactic Reaction
Acetylsalicylic acid, ACTH, Aminopyrine, Meprobamate, Mercurial
Diuretics, Para-aminosalicylic Acid, Penicillin, Pituitary Extract, Procaine,
Succinylcholine, Tetracycline, Thiouracil
Angiitis, Necrotizing
Bishydroxycoumarin (Dicumarol)
Angioedema
Meprobamate, Penicillin, Stilbestrol, Sulfonamides
Argyria
Silver Salts
Arteritis
Cyclobarbital, Chlorpromazine, Iodides, Phenylbutazone, Phenytoin, Poison
Ivy Extract, Sulfonamides, Thiouracil
Black hairy tongue
Tetracycline, Penicillin
Bowen's Disease
Arsenic, Fowler's Solution
Bullous eruption
Acetylsalicylic acid, Antipyrines, Arsenic, Barbiturates, Bromide, Chloral
hydrate, Chlorpromazine, Coumarin, Dilantin, Glutethimide, Hydantoin
derivatives, Ibuprofen, Imipramine, Iodide, Phenobarbital, Phenylbutazone,
Promethazine, Methadone, Meprobamate, Nitrazepam, Sulfonamides
Candidiasis
Tetracyclines
Chilblains-like erythema
Coumarins, Phenindione, Sulindac
Cyanosis
Acetanilide
Depigmentation
Chloroquine
Eczematous reactions (other than contact eczema)
Aminophylline, Antibiotics, Antihistamine, B-blockers, Benzocaine,
Bleomycin, Carbamazepine, Chloral Hydrate, Diphenhydramine,
Disulfuram, Fluorouracil, Fucidin, Meprobamate, Methaminodiazepoxide,
Minoxidil, Neomycin, Nystatin, Phenothiazines, Procainamide, Procaine,
Quinacrine, Quinidine, Resorcin, Streptomycin (cross-reaction with
neomycin), Sulphonamide, Thiazide
Edema
Arsenic, Chlorpromazine, Penicillin, Phenytoin, Promethazine, Chloroquine
Elastosis perforans serpiginosa
Penicillamine
Erythema/exanthem
Allopurinol, Ampicillin, Antipyrines, Arsenic, Atropine, Aurothioglucose,
Barbiturates, Carbamazepine, Chloral hydrate, Chlorpropamide, Codeine,
Corticotropin, Gentamicin, Gold, Griseofulvin, INH, Interleukin-2,
Meprobamate, Methaminodiazepoxide, Morphine, Nicotinic Acid,
Nitrofurantoin, Opium, Penicillin, Phenothiazine, Phenylbutazone,
Pilocarpine, Quinacrine, Quinidine, Quinine, Streptomycin, Sulphonamides,
Sulphamethoxypyridazine, Thiazide, Thiamine Chloride, Tolbutamide
1) Maculopapular rash
Allopurinol, Chloroquine, Meprobamate, Penicillin, Promethazine,
Streptomycin, Sulfamethoxypyridazine
2) Morbilliform erythema
Acetylsalicylic acid, Ampicillin, Barbiturates, Bromides, Chlorpromazine,
Griseofulvin, Insulin, Meprobamate, Penicillin, Promethazine, Salicylates,
Streptomycin
3) Scarlatiniform erythema
Barbiturates, Mercury, Morphine, Opium, Penicillin, Phenobarbital, Pituitary
Extract, Quinine, Salicylates, Streptomycin, Sulfonamides
4) Toxic erythema
Drugs most commonly responsible (up to 5% of patients affected):
Allopurinol, Carbamazepine, Cephalosporins, Gold, Nalidixic acid,
Penicillins, Sulphonamides
Other drugs commonly responsible (1-4% of patients affected):
Isoniazid, Para-amino salicylic acid, Phenytoin, NSAIDs, Nitrofurantoin,
Streptomycin
Erythema multiforme (including Stevens-Johnson syndrome and toxic
epidermal necrolysis)
Acetylsalicylic acid, Allopurinol, Amidopyrine, Antihistaminics, Anti-
pyrines, Barbiturates, Bromides, Carbamazepine, Chloral hydrate,
Cimetadine, Corticotropin (ACTH), Furosemide, Griseofulvin, Hydantoins,
Iodides, Mercury, NSAIDs (especially piroxicam), Para-aminosalicyclic
Acid, Penicillins, Phenytoin, Phenolphthalein, Phenothiazine, Phenyl-
butazone, Procaine, Streptomycin, Sulfamethoxy-pyridazine,
Sulphonamides, Tetracycline
Erythema Nodosum
Acetylsalicylic Acid, Bromides, Gold, Iodides, Penicillin, Phenacetin, Pills,
13-cis-retinoic acid, Salicylates, Sulfathiazole, Tetracycline
Erythroderma (Exfoliative dermatitis)
Allopurinol, Aminosalicylic Acid, Arsenicals, Aurothioglucose, Barbiturates,
Bismuth, Captopril, Carbamazepine, Cefoxitin, Chlorpromazine,
Chloroquine, Cimetadine, Dapsone, Diltiazem, Gold, Griseofulvin,
Hydantoin, Iodides, Isoniazid, Lithium, Mercury, Nitrofurantoin, NSAID,
Penicillin, Phenothiazines, Phenytoin, Quinidine, Quinacrine, Sodium
Thiosulfate, Stilbestrol, Streptomycin, Sulphamethoxypyridazine,
Sulphonamides, Sulphonylurea, Tetracycline, Thiouracil, Retinoid
Erythromelalgia
Bromocriptine, Nifedipine, Pergolide, Verapamil
Fixed drug eruption
Aminopyrine, Amphetamines, Antihistaminics, Antimony Compounds,
Antipyrines, Arsenic, Barbiturates, Bismuth, Chlordiazepoxide, Chloral
Hydrate, Chloroquine, Codeine, Dapsone, Gold, Diethylstilbestrol, Digitalis,
Ephedrine, Ergot, Hydantoin, Hydralazine, Iodides, Meprobamate, Mercury,
Metronidazole, Morphine, NSAIDs, Opium, Para-aminosalcylic acid,
Paracetamol, Penicillin, Phenacetin, Phenolphthalein, Phenothiazine,
Phenylbutazone, Potassium Chlorate, Quinacrine, Quinine, Reserpine,
Salicylates, Streptomycin, Sulfonamides, Sulindac, Tetracyclines,
Tetraiodofluorescein
Gangrene
Coumarin
Gingival hyperplasia
Cyclosporin, Nifedipine, Hydantoin
Hair color changes
Carbamate, Chloroquine, Chlorpromazine
Henoch-shonlein purpura-like eruption
Diltiazem, Frusemide
Hirsutism/hypertrichosis
Acetazolamide, Anabolic agents, Bromocryptine, Chlorobenzene,
Corticosteroid, Cyclosporin, Cyproterone, Danazol, Diazoxide, Digoxin,
Diphenylhydantoin, Dyazide, Metyrapone, Minoxidil, Penicillamine,
Phenothiazine, Progestogens, Psoralens, Spironolacton, Streptomycin
Ichthyosis, acquired
Butyrophenone, Nicotinic acid, Triparanol
Jaundice
Aurothioglucose, Erythromycin lauryl sulphate, Para-aminosalicylic Acid,
Phenobarbital, Thiouracil
Keratoderma
Gold
Keratoses
Arsenic, Fowler's Solution, Gold
LE-like syndrome
Acebutolol, Allopurinol, Aminoglutethimide, Aminosalicylic acid, Captopril,
Carbamazepine, Chlorpromazine, Cimetidine, Ethosuximide, Gold,
Griseofulvin, Hydantoin, Hydralazine, Isoniazid, Labetolol, Lithium,
Mephobarbital, Methyldopa, Minocycline, Penicillin, Phenylbutazone,
Phenytoin, Pill, Practolol, Procainamide, Reserpine, Streptomycin,
Sulfamethoxypyridazine, Sulphonamide, Tetracycline HCI (degraded),
Thiazide, Thionamide, Thiouracil
Lichenoid eruption
Beta-blocker (Practolol), Bismuth, Captopril, Carbamazepine, Chloroquine,
Cholorpropamide, Gold, Hydroxyurea, Meprobamate, Mepacrine,
Methyldopa, para-amino-salicyclic acid, Penicillamine, Phenothiazine,
Quinine, Quinidine, Streptomycin, Sulphonylurea, Tetracycline, Thiazides
Linear Ig-A dermatosis
Amiodarone, Captopril, Cefamandole, Diclophenac, Lithium, Vancomycin
Livedo reticularis
Amantadine
Lymphoproliferative disease/Pseudolymphoma
ACE-inhibitor, Carbamazepine, Cyclosporin, Dantrolene, Diltiazem,
Hydantoin, Pyrazolone, Pyrimethamine
Mucosal ulcerations, oral
Foscarnet, DDC, Interferon
Nail changes
Amodiaquin (hyperpigmentation), arsenic (longitudinal white stripes),
argyria (dark blue nail bed), Chloroquine (blue-black nail bed),
Phenolphthalein (dark blue fixed eruption), tetracycline (yellow nail and
yellow fluorescence), demethylchlortetracycline (phototoxic
onychomadesis)
Ochronosis-like pigmentation
Phenol, Quinacrine, Resorcin
Onycholysis
Demethylchlortetracycline
Papular dermatitis
Acetazolamide, Acetylsalicylic acid, Arsenic, Aurothioglucose, Digitalis,
Penicillin, Thiazide
Pellagra-like eruption
Isoniazide
Pemphigoid-like eruption
1) Bullous
5-Fluorouracil (topical), Frusemide, Ibuprofen, Penicillamine, Penicillin,
Sulphasalazine, PUVA
2) Cicatrical
Anti-glaucoma agent (topical), Clonidine, Indomethacin, D-penicillamine,
Practolol, Sulphadoxine
Pemphigus-like eruption
Ampicillin, Captopril, Enalapril, Pencillamine, Penicillin, Phenylbutazone,
Pyrazolan derivative, Rifampicin, Sulphydryl groups (pyritinol, thiopronin)
Photosensitivity
Amiodarone, Chlorthiazide, Chlorpromazine, Chlorpropamide, Cytotoxic
(Dacarazine, Methotrexate, Fenofibrate, Fluorescein, 5-fluorouracil,
Furocoumarins, Griseofulvin, Nalidixic acid, NSAID (benoxaprofen,
piroxicam, naproxen), Phenothiazine, Promethazine, Psoralen (Methoxsalen,
Trimethylpsoralen), Quinidine, Quinine, Quinolones, Reserpine, Retinoids,
Sulphonamides, Sulphonylureas, Sunscreen (PABA, oxybenzone),
Tetracyclines (demeclotetracycline, doxycycline, tetracycline), Tolbutamide,
Tricyclic antidepressant (Clomipramine, Carbamazepine)
Pigmentation
Amiodarone (slatey grey pigmentation on light-exposed skin)
Antimalarials (diffuse generalized grey/brown pigmentation; mepacrine
causes generalized yellow/orange discoloration resembling jaundice
Antipyrines, Bismuth (gums)
Clofazimine
Chlorpromazine (slate-colored)
Chloroquine (bleaching of hair)
Cytotoxic drugs (busulphan, bleomycin, cyclophosphamide, fluorouracil,
hydroxyurea, may cause generalized brown pigmentation)
Gold/silver (chrysiasis) blue/grey pigmentation on light-exposed skin)
Minocycline hydrochloride (blue/grey pigmentation on light-exposed skin
and in scars)
Oral contraceptives (melasma -brownish pigmentation on face)
Phenformin (brown pigmentation on light-exposed skin)
Phenothiazines (bluish pigmentation on light-exposed skin, especially on the
face)
Phenytoin (melasma-like pigmentation on face)
Streptomycin, Tetracosactide, Tetracyclines, Thiouracil
Zidovudine (AZT) (melanonychia, diffuse cutaneous/oral mucosal
pigmentation, acral hyperpigmented macules)
Pityriaisis rosea-like eruption
Arsenicals, Bismuth, Gold, Barbiturates, Clonidine, Captopril, Isotretinoin,
Ketotifen, Methoxypromazine, Metronidazole, Pyribenzamine
Polyarteritis nodosa-like eruption
Sulfonamides, Thiouracil, Iodides
Porphyria
(Drugs provoke variegate porphyria):
Alcohol, Androgens, Barbiturates, Carbamazepine, Chlordiazepoxide,
Chloroquine, Griseofulvin, Hexachlorobenzene, Hydantoin, Meprobamate,
Nortriptyline, Pills, Oestrogens, Sodium valproate, Sulphonamides,
Sulphonylureas
(Drugs provoke porphyria cutanea tarda):
above + Busulphan, Quinidine, Quinine, Rifampicin
Pseudo-porphyria
Amiodarone, Bumetamide, Ciprofloxacin, Frusemide, Nalidixic aid,
NSAID, Ofloxacin, Tetracycline
Pruritus
Alkaloid, Antidepressive, Antimalarial, Atropine, Aurothioglucose,
Barbiturates, Belladonna, Bismuth, Cimetadine, CNS stimulant, Cocaine,
Codeine, Coumarin, Griseofulvin, Heparin, Insulin, Iodide, Niacinamide,
Opiates, Penicillin, Phenobarbital, Procaine, Quinacrine, Streptomycin,
Tetracyclines, Thiamine Chloride, Thiouracil
Pruritus ani
Chloroquine, Codeine, Liver Extract, Tetracyclines
Purpura
ACTH, Allopurinol, Barbiturates, Carbromal, Chlorpromazine,
Corticosteroids, Coumarin, Ephedrine, Griseofulvin, Iodide, Meprobamate,
Mercury, Penicillin, Quinidine, Reserpine, Sodium thiosulfate,
Sulfamethoxypyridazine, Sulfonamides, Thiazides
Purpura Fulminans
Acetylsalicylic acid, Coumarin, Iodides
Pustular Psoriasis
Acetylsalicylic Acid, Antimalarials, Poliomyelitis vaccine
Pustuloderma
Bromides, Chloral hydrate, Iodides, Penicillin, Macrolide
Seborrhoeic dermatitis
Methyldopa, Phenothiazines
Scleroderma-like eruption
Epoxy resin monomer, Organic solvent, Perchlorethylene, Trichlorethylene,
Vinyl chloride monomer
Bleomycin, Carbidopa, Penicillamine, Pentazocine, Organic solvent, Sodium
valproate, Injection of paraffin or silicone
Stevens-Johnson Syndrome
Allopurinol, Antipyrines, barbiturates, Chlormezanone, Chloroquine,
Chlorpropamide, Cotrimoxazole, Cough Mixtures, Meprobamate, NSAID,
Phenacetin, Phenobarbital, Phenytoin, Sulfonamides
Stomatitis
Aurothioglucose, Bismuth, Chlorpromazine, Dilantin (gingivitis), Fluorides,
Methotrexate, Phenobarbital, Streptomycin, Thiouracil
Striae
Corticosteroids, Isoniazid
Telangiectasia
Oral contraceptives
Toxic Epidermal Necrolysis
Acetazolamide, Allopurinol, Aminopyrine, Antihistaminics, Anti-pyrines,
Barbiturates, Brompheniramine, Dapsone, Gold Salts, Methyl-salicylate,
Nitrofurantoin, Penicillin, Phenolphthalein, Phenylbutazone, Phenytoin,
Salicylates, Polio Vaccine, Sulfonamides, Tetracyclines, Tolbutamide
Urticaria
1) Immunological mediation
Drugs most commonly responsible:
Enzymes, Penicillins, Pollen vaccines, Polypeptide hormone, Serum,
Sulphonamides
Other drugs responsible, but lower incidence:
Barbiturate, Carbimazole, Cephalosporins, Cimetidine, Griseofulvin,
Insulin, Metronidazole, Phenytoin, Quinidine, Synthetic
adrenocorticotrophin, Tetracycline
2) Non-immunological mediation
Alcohol, Aspirin and other salicylates, Atropine, Chlortetracycline, Codeine,
Dextran, Decamethonium, Morphine, NSAID, Oestrogen, Pilocarpine,
Polymyxin antibiotics, Quinine, Radiographic contrast media, Scopolamine,
Snake venoms, Thiamine, d-Tubocurare, Vancomycin
Vasculitis
Anti-influenza, vaccine, Allopurinol, Arsenic, Captopril, Chlorpromazine,
Cimetidine, Clindamycin, Corticosteroids, Ethacrynic acid, Gold,
Griseofulvin, Guanethidine, Heparin, Hydantoin, Hydralazine,
Indomethacin, Insulin, Iodide, Ketoconazole, Methylthiouracil, Penicillin,
Phenothiazine, Phenylbutazone, Phenytoin, Pill, Poison ivy extract,
Quinidine, Serum, Streptomycin, Streptokinase, Sulphonamides, Tamoxifen,
Tetracycline, Thiazide, Thiouracil, Vancomycin
CUTANEOUS DRUG ERUPTIONS

Dr. L.Y. CHONG
CHAPTER 23
Cutaneous drug eruptions may be defined as adverse cutaneous lesions as a
consequence of administration of drugs.
The exact incidence of cutaneous drug eruptions in Hong Kong is unknown.
According to the statistics of Social Hygiene Service, drug eruptions account
for 0.5% of all new skin cases seen in dermatological outpatient clinics of
the Service in 1995. This figure does not include those seen in general
outpatient clinics, private sector and hospitals. The true incidence is
definitely much higher. The main difficulties of getting a true figure are due
to lack of a central registry and loose labelling of drug reactions on the
patients. Adverse effects of drugs are often published in the literatures
according to anecdotal reports or badly designed studies.
The pathogenesis of drug eruptions may arise as a result of immunological
or non-immunological reaction. Some of these reactions are predictable
(dose-related) while some are unpredictable (idiosyncratic). Those with an
immunological basis may due to different types of hypersensitivity
reactions, for instance, allergic type of urticaria may be the result of Type I
reaction (IgE-mediated) or Type III reaction (complement dependent
immune-complex mediated). Nevertheless, the exact mechanisms of most
drug eruptions, including fixed drug eruptions, are unknown.
Clinically drug eruptions have a wide range of different morphological
presentations. (Table 1) They can be generalized or fixed eruptions and their
severity varies from minor to fatal skin reactions. Unfortunately, apart from
fixed drug eruption, there is neither pathognomonic clinical feature nor
diagnostic investigation in drug eruption. In practice, it is often difficult to
identify the culprit with certainty, especially when the patient is taking
multiple drugs simultaneously. Diagnosis is mainly based on clinical
grounds in which the history plays the most essential part. In the history, the
temporal relationship between the taking of drug and the onset of skin
eruption is most important. Experience and statistical knowledge about the
suspected drugs are also useful as certain drugs (for examples, ampicillin or
cotrimoxazole) are more likely to cause drug eruptions, especially in certain
diseases (for examples, AIDS or infectious mononucleosis).
In the history, the following information should be carefully asked:
A detail drug history including the names and dosage of the drugs taken
(Drugs should include those prescribed by doctors and any herbal or
homeopathic medicines)
The temporal relationship between the intake of drugs and the onset of skin
lesions (Allergic drug reactions usually develop within 1 to 2 weeks of
initiation of treatment)
Any previous history of drug allergy, or similar skin lesions after taking
similar drugs
Any improvement of skin lesions after the suspected drug is withdrawn (The
skin eruption is unlikely to be drug-induced if it fails to improve after
withdrawal or if it improves even without stopping the drug. However,
sometimes it may takes weeks for drug eruption to resolve even when the
drug is stopped.)
Up to the present moment, there is still no reliable and practical
investigation for confirmation of drug eruption. Rechallange test is
dangerous and should not be carried out in usual circumstances. Perhaps the
only situations for rechallange test are those with fixed drug eruptions or
those with life-threatening conditions in which that particular drug is
essential. Skin test has little practical value as it may cause fatal systemic
reaction and false positive reaction is common. Other tests such as
radioallergosorbent tests (RAST) for drug-specific IgE antibody (penicillin,
insulin), histamine release test, leucocyte and macrophage migration
inhibition tests, lymphocyte toxicity assay, basophil degranulation test,
passive haemagglutination test and lymphocyte transformation test are
mainly for research purposes.
In mild drug eruptions, withdrawal of the culprits together with symptomatic
treatments will be adequate. For patient who is taking multiple drugs which
are essential (for instance, antituberous drugs), all drugs should be
temporarily withheld. After the skin lesions has subsided, each of these
drugs can then be reintroduced one by one under strict observation, usually
start with the drug which has lowest incidence of drug reaction. In severe
drug eruptions such as Stevens-Johnson syndrome, toxic epidermal
necrolysis, erythroderma or angioedema, reintroduction of the drug is
dangerous and immoral. In these situations, other treatment alternatives
should be seeked for. Cross-sensitivity between similar drugs should be
borne in mind in choosing alternative medication. Desensitization therapy
has little practical value. After recovery, it is essential to give the patient a
warning card, labelling the offending drug in order to avoid future retaking
of the drug.
Table 1: Morphological Classification of Drug Eruptions
Acanthosis nigricans-like eruption

Corticosteroids, Hydantoin, Nicotinic Acid, Pills, Stilbestrol
Acneiform eruption
Anticonvulsant (phenytoin, phenobarbital, trimethadione), Antituberculous
(isoniazid, ethionamide, refampicin), Azathioprine, Chloral hydrate,
Corticosteroids, Corticotropin (ACTH), Cyanocobalamin, Cyclosporin,
Halogens (bromides, chlorides, iodides, halothane), Haloperidol, Lithium,
Pills, Psoralens, Quinine, Scopolamine
Acral erythema/red palms
Adriamycin (Doxorubicin), Cystosine arabinoside, 5-fluorouracil
Acrodynia
Mercury
Alopecia
Allopurinol, Bromocriptine, Carbimazole, Chlorambucil, Chloramphenicol,
Cholesterol lowering agents, Cimetadine, Colchicine, Coumarin, Cytotoxic
drugs, Diazoxide, Ethionamide, Fluconazole, Gentamicin, Gold, Heavy
metals, Heparin, Hydantoin, Levodopa, Methotrexate, Methyldopa, NSAID
(indomethacin, piroxicam), Pills, Phenindione, Propanolol, Sodium
valproate, Thiouracil, Vitamin A or Retinoids
Anaphylactic Reaction
Acetylsalicylic acid, ACTH, Aminopyrine, Meprobamate, Mercurial
Diuretics, Para-aminosalicylic Acid, Penicillin, Pituitary Extract, Procaine,
Succinylcholine, Tetracycline, Thiouracil
Angiitis, Necrotizing
Bishydroxycoumarin (Dicumarol)
Angioedema
Meprobamate, Penicillin, Stilbestrol, Sulfonamides
Argyria
Silver Salts
Arteritis
Cyclobarbital, Chlorpromazine, Iodides, Phenylbutazone, Phenytoin, Poison
Ivy Extract, Sulfonamides, Thiouracil
Black hairy tongue
Tetracycline, Penicillin
Bowen's Disease
Arsenic, Fowler's Solution
Bullous eruption
Acetylsalicylic acid, Antipyrines, Arsenic, Barbiturates, Bromide, Chloral
hydrate, Chlorpromazine, Coumarin, Dilantin, Glutethimide, Hydantoin
derivatives, Ibuprofen, Imipramine, Iodide, Phenobarbital, Phenylbutazone,
Promethazine, Methadone, Meprobamate, Nitrazepam, Sulfonamides
Candidiasis
Tetracyclines
Chilblains-like erythema
Coumarins, Phenindione, Sulindac
Cyanosis
Acetanilide
Depigmentation
Chloroquine
Eczematous reactions (other than contact eczema)
Aminophylline, Antibiotics, Antihistamine, B-blockers, Benzocaine,
Bleomycin, Carbamazepine, Chloral Hydrate, Diphenhydramine,
Disulfuram, Fluorouracil, Fucidin, Meprobamate, Methaminodiazepoxide,
Minoxidil, Neomycin, Nystatin, Phenothiazines, Procainamide, Procaine,
Quinacrine, Quinidine, Resorcin, Streptomycin (cross-reaction with
neomycin), Sulphonamide, Thiazide
Edema
Arsenic, Chlorpromazine, Penicillin, Phenytoin, Promethazine, Chloroquine
Elastosis perforans serpiginosa
Penicillamine
Erythema/exanthem
Allopurinol, Ampicillin, Antipyrines, Arsenic, Atropine, Aurothioglucose,
Barbiturates, Carbamazepine, Chloral hydrate, Chlorpropamide, Codeine,
Corticotropin, Gentamicin, Gold, Griseofulvin, INH, Interleukin-2,
Meprobamate, Methaminodiazepoxide, Morphine, Nicotinic Acid,
Nitrofurantoin, Opium, Penicillin, Phenothiazine, Phenylbutazone,
Pilocarpine, Quinacrine, Quinidine, Quinine, Streptomycin, Sulphonamides,
Sulphamethoxypyridazine, Thiazide, Thiamine Chloride, Tolbutamide
1) Maculopapular rash
Allopurinol, Chloroquine, Meprobamate, Penicillin, Promethazine,
Streptomycin, Sulfamethoxypyridazine
2) Morbilliform erythema
Acetylsalicylic acid, Ampicillin, Barbiturates, Bromides, Chlorpromazine,
Griseofulvin, Insulin, Meprobamate, Penicillin, Promethazine, Salicylates,
Streptomycin
3) Scarlatiniform erythema
Barbiturates, Mercury, Morphine, Opium, Penicillin, Phenobarbital, Pituitary
Extract, Quinine, Salicylates, Streptomycin, Sulfonamides
4) Toxic erythema
Drugs most commonly responsible (up to 5% of patients affected):
Allopurinol, Carbamazepine, Cephalosporins, Gold, Nalidixic acid,
Penicillins, Sulphonamides
Other drugs commonly responsible (1-4% of patients affected):
Isoniazid, Para-amino salicylic acid, Phenytoin, NSAIDs, Nitrofurantoin,
Streptomycin
Erythema multiforme (including Stevens-Johnson syndrome and toxic
epidermal necrolysis)
Acetylsalicylic acid, Allopurinol, Amidopyrine, Antihistaminics, Anti-
pyrines, Barbiturates, Bromides, Carbamazepine, Chloral hydrate,
Cimetadine, Corticotropin (ACTH), Furosemide, Griseofulvin, Hydantoins,
Iodides, Mercury, NSAIDs (especially piroxicam), Para-aminosalicyclic
Acid, Penicillins, Phenytoin, Phenolphthalein, Phenothiazine, Phenyl-
butazone, Procaine, Streptomycin, Sulfamethoxy-pyridazine,
Sulphonamides, Tetracycline
Erythema Nodosum
Acetylsalicylic Acid, Bromides, Gold, Iodides, Penicillin, Phenacetin, Pills,
13-cis-retinoic acid, Salicylates, Sulfathiazole, Tetracycline
Erythroderma (Exfoliative dermatitis)
Allopurinol, Aminosalicylic Acid, Arsenicals, Aurothioglucose, Barbiturates,
Bismuth, Captopril, Carbamazepine, Cefoxitin, Chlorpromazine,
Chloroquine, Cimetadine, Dapsone, Diltiazem, Gold, Griseofulvin,
Hydantoin, Iodides, Isoniazid, Lithium, Mercury, Nitrofurantoin, NSAID,
Penicillin, Phenothiazines, Phenytoin, Quinidine, Quinacrine, Sodium
Thiosulfate, Stilbestrol, Streptomycin, Sulphamethoxypyridazine,
Sulphonamides, Sulphonylurea, Tetracycline, Thiouracil, Retinoid
Erythromelalgia
Bromocriptine, Nifedipine, Pergolide, Verapamil
Fixed drug eruption
Aminopyrine, Amphetamines, Antihistaminics, Antimony Compounds,
Antipyrines, Arsenic, Barbiturates, Bismuth, Chlordiazepoxide, Chloral
Hydrate, Chloroquine, Codeine, Dapsone, Gold, Diethylstilbestrol, Digitalis,
Ephedrine, Ergot, Hydantoin, Hydralazine, Iodides, Meprobamate, Mercury,
Metronidazole, Morphine, NSAIDs, Opium, Para-aminosalcylic acid,
Paracetamol, Penicillin, Phenacetin, Phenolphthalein, Phenothiazine,
Phenylbutazone, Potassium Chlorate, Quinacrine, Quinine, Reserpine,
Salicylates, Streptomycin, Sulfonamides, Sulindac, Tetracyclines,
Tetraiodofluorescein
Gangrene
Coumarin
Gingival hyperplasia
Cyclosporin, Nifedipine, Hydantoin
Hair color changes
Carbamate, Chloroquine, Chlorpromazine
Henoch-shonlein purpura-like eruption
Diltiazem, Frusemide
Hirsutism/hypertrichosis
Acetazolamide, Anabolic agents, Bromocryptine, Chlorobenzene,
Corticosteroid, Cyclosporin, Cyproterone, Danazol, Diazoxide, Digoxin,
Diphenylhydantoin, Dyazide, Metyrapone, Minoxidil, Penicillamine,
Phenothiazine, Progestogens, Psoralens, Spironolacton, Streptomycin
Ichthyosis, acquired
Butyrophenone, Nicotinic acid, Triparanol
Jaundice
Aurothioglucose, Erythromycin lauryl sulphate, Para-aminosalicylic Acid,
Phenobarbital, Thiouracil
Keratoderma
Gold
Keratoses
Arsenic, Fowler's Solution, Gold
LE-like syndrome
Acebutolol, Allopurinol, Aminoglutethimide, Aminosalicylic acid, Captopril,
Carbamazepine, Chlorpromazine, Cimetidine, Ethosuximide, Gold,
Griseofulvin, Hydantoin, Hydralazine, Isoniazid, Labetolol, Lithium,
Mephobarbital, Methyldopa, Minocycline, Penicillin, Phenylbutazone,
Phenytoin, Pill, Practolol, Procainamide, Reserpine, Streptomycin,
Sulfamethoxypyridazine, Sulphonamide, Tetracycline HCI (degraded),
Thiazide, Thionamide, Thiouracil
Lichenoid eruption
Beta-blocker (Practolol), Bismuth, Captopril, Carbamazepine, Chloroquine,
Cholorpropamide, Gold, Hydroxyurea, Meprobamate, Mepacrine,
Methyldopa, para-amino-salicyclic acid, Penicillamine, Phenothiazine,
Quinine, Quinidine, Streptomycin, Sulphonylurea, Tetracycline, Thiazides
Linear Ig-A dermatosis
Amiodarone, Captopril, Cefamandole, Diclophenac, Lithium, Vancomycin
Livedo reticularis
Amantadine
Lymphoproliferative disease/Pseudolymphoma
ACE-inhibitor, Carbamazepine, Cyclosporin, Dantrolene, Diltiazem,
Hydantoin, Pyrazolone, Pyrimethamine
Mucosal ulcerations, oral
Foscarnet, DDC, Interferon
Nail changes
Amodiaquin (hyperpigmentation), arsenic (longitudinal white stripes),
argyria (dark blue nail bed), Chloroquine (blue-black nail bed),
Phenolphthalein (dark blue fixed eruption), tetracycline (yellow nail and
yellow fluorescence), demethylchlortetracycline (phototoxic
onychomadesis)
Ochronosis-like pigmentation
Phenol, Quinacrine, Resorcin
Onycholysis
Demethylchlortetracycline
Papular dermatitis
Acetazolamide, Acetylsalicylic acid, Arsenic, Aurothioglucose, Digitalis,
Penicillin, Thiazide
Pellagra-like eruption
Isoniazide
Pemphigoid-like eruption
1) Bullous
5-Fluorouracil (topical), Frusemide, Ibuprofen, Penicillamine, Penicillin,
Sulphasalazine, PUVA
2) Cicatrical
Anti-glaucoma agent (topical), Clonidine, Indomethacin, D-penicillamine,
Practolol, Sulphadoxine
Pemphigus-like eruption
Ampicillin, Captopril, Enalapril, Pencillamine, Penicillin, Phenylbutazone,
Pyrazolan derivative, Rifampicin, Sulphydryl groups (pyritinol, thiopronin)
Photosensitivity
Amiodarone, Chlorthiazide, Chlorpromazine, Chlorpropamide, Cytotoxic
(Dacarazine, Methotrexate, Fenofibrate, Fluorescein, 5-fluorouracil,
Furocoumarins, Griseofulvin, Nalidixic acid, NSAID (benoxaprofen,
piroxicam, naproxen), Phenothiazine, Promethazine, Psoralen (Methoxsalen,
Trimethylpsoralen), Quinidine, Quinine, Quinolones, Reserpine, Retinoids,
Sulphonamides, Sulphonylureas, Sunscreen (PABA, oxybenzone),
Tetracyclines (demeclotetracycline, doxycycline, tetracycline), Tolbutamide,
Tricyclic antidepressant (Clomipramine, Carbamazepine)
Pigmentation
Amiodarone (slatey grey pigmentation on light-exposed skin)
Antimalarials (diffuse generalized grey/brown pigmentation; mepacrine
causes generalized yellow/orange discoloration resembling jaundice
Antipyrines, Bismuth (gums)
Clofazimine
Chlorpromazine (slate-colored)
Chloroquine (bleaching of hair)
Cytotoxic drugs (busulphan, bleomycin, cyclophosphamide, fluorouracil,
hydroxyurea, may cause generalized brown pigmentation)
Gold/silver (chrysiasis) blue/grey pigmentation on light-exposed skin)
Minocycline hydrochloride (blue/grey pigmentation on light-exposed skin
and in scars)
Oral contraceptives (melasma -brownish pigmentation on face)
Phenformin (brown pigmentation on light-exposed skin)
Phenothiazines (bluish pigmentation on light-exposed skin, especially on the
face)
Phenytoin (melasma-like pigmentation on face)
Streptomycin, Tetracosactide, Tetracyclines, Thiouracil
Zidovudine (AZT) (melanonychia, diffuse cutaneous/oral mucosal
pigmentation, acral hyperpigmented macules)
Pityriaisis rosea-like eruption
Arsenicals, Bismuth, Gold, Barbiturates, Clonidine, Captopril, Isotretinoin,
Ketotifen, Methoxypromazine, Metronidazole, Pyribenzamine
Polyarteritis nodosa-like eruption
Sulfonamides, Thiouracil, Iodides
Porphyria
(Drugs provoke variegate porphyria):
Alcohol, Androgens, Barbiturates, Carbamazepine, Chlordiazepoxide,
Chloroquine, Griseofulvin, Hexachlorobenzene, Hydantoin, Meprobamate,
Nortriptyline, Pills, Oestrogens, Sodium valproate, Sulphonamides,
Sulphonylureas
(Drugs provoke porphyria cutanea tarda):
above + Busulphan, Quinidine, Quinine, Rifampicin
Pseudo-porphyria
Amiodarone, Bumetamide, Ciprofloxacin, Frusemide, Nalidixic aid,
NSAID, Ofloxacin, Tetracycline
Pruritus
Alkaloid, Antidepressive, Antimalarial, Atropine, Aurothioglucose,
Barbiturates, Belladonna, Bismuth, Cimetadine, CNS stimulant, Cocaine,
Codeine, Coumarin, Griseofulvin, Heparin, Insulin, Iodide, Niacinamide,
Opiates, Penicillin, Phenobarbital, Procaine, Quinacrine, Streptomycin,
Tetracyclines, Thiamine Chloride, Thiouracil
Pruritus ani
Chloroquine, Codeine, Liver Extract, Tetracyclines
Purpura
ACTH, Allopurinol, Barbiturates, Carbromal, Chlorpromazine,
Corticosteroids, Coumarin, Ephedrine, Griseofulvin, Iodide, Meprobamate,
Mercury, Penicillin, Quinidine, Reserpine, Sodium thiosulfate,
Sulfamethoxypyridazine, Sulfonamides, Thiazides
Purpura Fulminans
Acetylsalicylic acid, Coumarin, Iodides
Pustular Psoriasis
Acetylsalicylic Acid, Antimalarials, Poliomyelitis vaccine
Pustuloderma
Bromides, Chloral hydrate, Iodides, Penicillin, Macrolide
Seborrhoeic dermatitis
Methyldopa, Phenothiazines
Scleroderma-like eruption
Epoxy resin monomer, Organic solvent, Perchlorethylene, Trichlorethylene,
Vinyl chloride monomer
Bleomycin, Carbidopa, Penicillamine, Pentazocine, Organic solvent, Sodium
valproate, Injection of paraffin or silicone
Stevens-Johnson Syndrome
Allopurinol, Antipyrines, barbiturates, Chlormezanone, Chloroquine,
Chlorpropamide, Cotrimoxazole, Cough Mixtures, Meprobamate, NSAID,
Phenacetin, Phenobarbital, Phenytoin, Sulfonamides
Stomatitis
Aurothioglucose, Bismuth, Chlorpromazine, Dilantin (gingivitis), Fluorides,
Methotrexate, Phenobarbital, Streptomycin, Thiouracil
Striae
Corticosteroids, Isoniazid
Telangiectasia
Oral contraceptives
Toxic Epidermal Necrolysis
Acetazolamide, Allopurinol, Aminopyrine, Antihistaminics, Anti-pyrines,
Barbiturates, Brompheniramine, Dapsone, Gold Salts, Methyl-salicylate,
Nitrofurantoin, Penicillin, Phenolphthalein, Phenylbutazone, Phenytoin,
Salicylates, Polio Vaccine, Sulfonamides, Tetracyclines, Tolbutamide
Urticaria
1) Immunological mediation
Drugs most commonly responsible:
Enzymes, Penicillins, Pollen vaccines, Polypeptide hormone, Serum,
Sulphonamides
Other drugs responsible, but lower incidence:
Barbiturate, Carbimazole, Cephalosporins, Cimetidine, Griseofulvin,
Insulin, Metronidazole, Phenytoin, Quinidine, Synthetic
adrenocorticotrophin, Tetracycline
2) Non-immunological mediation
Alcohol, Aspirin and other salicylates, Atropine, Chlortetracycline, Codeine,
Dextran, Decamethonium, Morphine, NSAID, Oestrogen, Pilocarpine,
Polymyxin antibiotics, Quinine, Radiographic contrast media, Scopolamine,
Snake venoms, Thiamine, d-Tubocurare, Vancomycin
Vasculitis
Anti-influenza, vaccine, Allopurinol, Arsenic, Captopril, Chlorpromazine,
Cimetidine, Clindamycin, Corticosteroids, Ethacrynic acid, Gold,
Griseofulvin, Guanethidine, Heparin, Hydantoin, Hydralazine,
Indomethacin, Insulin, Iodide, Ketoconazole, Methylthiouracil, Penicillin,
Phenothiazine, Phenylbutazone, Phenytoin, Pill, Poison ivy extract,
Quinidine, Serum, Streptomycin, Streptokinase, Sulphonamides, Tamoxifen,
Tetracycline, Thiazide, Thiouracil, Vancomycin
CUTANEOUS MANIFESTATION OF INTERNAL DISEASE

Dr. H.H.L. CHAN & Dr. W.K. FUNG
CHAPTER 22
Dermatology and internal medicine do not have as much overlap as other
specialties such as endocrinology. Nonetheless, some dermatologists still
consider their role in internal medicine as ¡¥the last line of defense¡¦. There
are some truth in their statement, indeed from time to time we do encounter
patients that present to us with cutaneous manifestation of systemic disease.
Recognition of these cutaneous signs are therefore, of up most important. In
this chapter, various aspect of dermatology will be discussed in greater
details.
1. CUTANEOUS MARKER OF INTERNAL MALIGNANCY

Cutaneous manifestation of underlying malignancy can be classified as
follow:
Malignant involvement of the skin
Genodermatoses
Paraneoplastic dermatoses
Environmental carcinogens
1.1. Malignant Involvement of the Skin
Metastases from visceral tumour can sometimes occur as a result of direct
extension from an underlying neoplasm. Incidence of this condition is about
2% and the cause correspond to the same malignancy that were most
frequent in the population. These include carcinoma of the stomach, lung
and breast. Paget's disease of the breast, clinically present as a patch of
eczema or moist eroded area of the nipple, is often associated with an
underlying adenocarcinoma of the breast. Carcinoma en cuirass another
condition associated with breast carcinoma, manifested clinically as an area
of leathery thickening caused by fibrosis and lymphatic blockage.
Adnexal tumour is known to be associated with extramammary Paget's, a
condition that usually presented as an area of erythematous moist patches in
the groin or the perianal are.
Systemic haematological malignancy can also involve the skin. For
example, Hodgkin's lymphoma can present as pruritis and ichthyosis
whereas gingival hypertrophy is seen in monocytic leukaemia. Cutaneous
metastasis can also occur and is presented as plum-colour nodules or
plaques.
1.2. Genodermatoses
Genetic conditions can predispose at risk individuals to develop internal
malignancy. These conditions can broadly be classified into four types:
primary immunodeficiency
gastrointestinal polyposis
chromosomal instability
others
In primary immunodeficiency, patients are more susceptible to infections as
well as the development of haematological malignancy. Others associated
features may also be present, these include cerebellar ataxia, as seen in
ataxia telangiectasia, or eczema as in the case of Wiskott-Aldrich syndrome.
Other conditions in this category include severe combined
immunodeficiency and Burton's agammagloblinemia.
A group of genodermatoses have in common gastrointestinal harmartoma,
cutaneous signs and internal neoplasm. The more commonly known of these
conditions include Gardner's and Peutz-Jeghers. Gardner's syndrome is an
autosomal dominant condition may present in childhood as multiple benign
skin tumour, such as lipoma or fibroma. When these patients reach the third
to fourth decades, they develop large bowel polyps which are usually
thought to turn malignant later in life.
Peutz-Jeghers syndrome is also dominant in inheritance and patients
presented with lentigo in the perioral area as well as bowel hamartoma.
Intestinal obstruction can occur. Interesting, these patients have an increase
risk of developing non-gastrointestinal tract tumours that include bronchial
and breast carcinoma. The risk of developing gastrointestinal tract tumour is
also increase. Other syndromes that are classified into the same category as
Peutz-Jeghers include Cowden¡¦s disease, Muir-Torre syndrome, Howel-
Evans syndrome and Multiple endocrine neoplasm type III.
Certain conditions are associated with chromosomal instability as a result of
which excessive DNA damage can occur leading to an increase risk of
internal malignancy. This group of conditions include Bloom's syndrome,
Werner's syndrome, Fanconi's anaemia and Dyskeratosis congenita.
There are other genodermatoses that are less well defined but associated
with internal malignancy. These include neurofibromatosis,
haemochromatosis and Gorlin's syndrome. Neurofibromatosis is relatively
common. It is inherited as an autosommal dominant condition and is known
to be associated with malignant schwannoma, phaeochromocytoma and
carcinoid tumour. Hepatocellular carcinoma can occur in haemochromatosis
especially in elderly male with cirrhosis. Gorlin's syndrome affects young
patient with multiple basal cell carcinomas, odontogenic cysts and skeletal
abnormalities. Medulloblastoma is a known association.
1.3. Paraneoplastic Dermatoses
In this category, cutaneous signs occur as a result of circulating factor(s)
produced by the tumour. The following conditions are considered by Poole
to suit the above criteria:
Acanthosis palmaris - Acanthosis nigricans
Acquired ichthyosis - Amyloidosis
Bazex' syndrome - Carcinoid
Clubbing - Coagulopathies
Cryoglobulinaemia - Cronkhite-Canada syndrome
Cushing's - Dermatomyositis
Erythema gyratum repens - Erythroderma
Hyertrichosis lanuginosa - Leser-Trelat sign
Pemphigus - Swee''s syndrome
Necrolytic migratory erythema
Several important topics are presented.
Acanthosis nigricans can occur in obesity, hyperinsulinaemia, Cushing's
syndrome and adenocarcinoma of the stomach. Several features help to
distinguish the benign type from the malignant form. In the malignant form,
there are mucosal involvement, pachydermatoglyphy and the disease tends
to be more extensive. Besides gut tumours, others known neoplastic
associations include lung, breast, uterus, ovary and prostate. Leser-Trelat
sign is the sudden appearance of multiple seborrhoeic keratoses in
association with an underlying malignancy. Leser-Trelat and acanthosis
nigricans can occur together and they may share similiar aetiology.
Cushing's syndrome can occur either due to excessive ACTH production by
a pituitary tumour or as a result of ectopic ACTH production. Small cell
carcinoma of the bronchus, pancreatic tumour and carcinoid tumour can all
produce ectopic ACTH. Common features seen in ectopic ACTH production
includes marked muscle wasting, severe hyperpigmentation and
hypokalaemia.
Carcinoid tumours are neoplasm that derived from amine precursor uptake
and decarboxylation (APUD) cells. These cells produce a wide range of
chemical mediators that include serotonin, histamine and substance P. Gut
and lung are the main site of their origin. The main symptoms are flushing,
diarrhoea, abdominal pain and wheezing.
Dermatomyositis is most commonly associated with carcinoma of the breast
and bronchus in the western world. Interesting in our local environment,
nasopharyngeal carcinoma is more commonly associated with
dermatomyositis.
Paraneoplastic pemphigus is an recently discovered phenomenon
characterised by the development of erythema multiforme like erosion and
extensive mucosal involvement in patients with an underlying neoplasm.
Lymphoreticular malignancy were the most commonly associated neoplasm.
1.4. Environmental Carcinogens
Nicotine stain is undoubtedly the most commonly seen cutaneous sign of
carcinogen exposure. Arsenic exposure can increase the risk of internal
malignancy such as lung, bladder, kidney and prostate. Signs of previous
arsenic exposure include hyperkeratotic lesions in palms and soles, diffuse
truncal hyperpigmentation and multiple squamous cell carcinomas.
2. CONNECTIVE TISSUE DISORDER
Cutaneous abnormalities are commonly seen in connective tissue disease. In
this section, we shall concentrate on the cutaneous manifestation of these
disorders.
2.1. Lupus Erythematous
2.1.1. Cutaneous manifestation of lupus are as follow:
Discoid lupus: lesions present as urticarial patch, scaly patch (follicular
plugging), scarred patch, with pigmentary changes.
The palms can be involved with atrophy, erosion or hyperkeratosis.
During acute flare up of systemic lupus erythematous, patient often develops
transient maculopapular butterfly rash affecting both cheeks.
In subacute lupus (SCLE), the eruption can be urticarial (annular),
papulosquamous (psoriasiform).
Mucosal involvement is also commonly seen and these include ulceration or
nosebleed.
Scalp involvement is not uncommon and both diffuse or scarring alopecia
can be seen.
Vascular lesions seen in lupus include: Raynaud's phenomenon, nail fold
telangiectasia and infarct, splinter haemorrhages, chilblain LE, acquired C1
esterase deficiency, vasculitis, urticarial vasculitis, purpura,
thrombophlebitis, livedo reticularis, phospholipid syndrome, Degos
syndrome and calcinosis.
Others less common cutaneous manifestations are Bullous LE, LE
profundus, erythema multiforme (Rowell), LE/Lichen planus overlap and
anteoderma.
2.1.2. American Rheumatology Association criteria for the diagnosis of
systemic lupus
erythematous:
(4 or more are necessary for the diagnosis)
Malar rash; discoid lupus erythematous; photosensitivity; oral ulcers;
arthritis; serositis; renal disorder; central nervous systems disorders;
haematological disorders; immunological disorders; antinuclear antibody.
2.1.3. Investigations
Urine for microscopy, 24 hours urine for protein and creatinine, completed
blood picture, renal and liver function tests, ESR, C-reactive protein,
complement levels, antinuclear factor, anti-double stranded DNA, anti-ENA.
Skin biopsy for histology and immunofluorescence.
2.1.4. Significance of Serologic Testing
Antinuclear factor: in 90% of systemic lupus erythematous (SLE)
Anti-DS DNA: only in SLE cases (40%)
Anti-single-stranded DNA: in various collagen vascular diseases; in DLE
cases, suggest disease progression
Anti-Ro: subcutaneous lupus, neonatal lupus, C2 deficient lupus, late onset
lupus overlap
Anti-Sm: only in SLE cases (about 20%)
Anti-RNP: frequently associated with systemic sclerosis
Anti-histone: drug induced lupus
Anti-cardiolipin: associated with venous and arterial thrombosis, fetal
wastage and livedo with or without ulcer
2.2. Dermatomyositis
2.2.1. Diagnostic Criteria: (4 out of 5, for dermatomyositis cutaneous
changes must present)
Proximal symmetric progressive muscle weakness
Elevated muscle enzyme
Consistent electromyography (EMG)
Consistent muscle biopsy
Cutaneous disease
2.2.2. Classification
Primary dermatomyositis
Primary polyomyositis
Αssociated with underlying malignancy
Οverlaps syndrome
Childhood dermatomyositis
Amyopathic dermatomyositis
2.2.3. Cutaneous Signs
Pathognomic signs: Heliotrope rash, Gottron's papules, Dowling's line.
Others: periungual telangiectases, cuticular hypertrophy, photosensitivity,
poikiloderma.
2.2.4. Other Findings
Proxmial muscle weakness and tenderness, dysphagia, cardiac and
pulmonary disease.
2.2.5. Investigations
Elevated muscle enzymes, EMG, muscle biopsy, MRI for early muscle
changes, antibodies, ECG, pulmonary function test.
2.2.6. Significance of Serologic Findings
PM-1: polyomyositis and scleroderma overlap
Jo-1: pulmonary fibrosis
Ku: sclerodermatomyositis
Mi-2: one in four patients with dermatomyositis
2.3. Scleroderma
Scleroderma is defined as thickening or hardening of the skin
2.3.1. Classification
1) Systemic disease
Diffuse scleroderma; acrosclerosis; CREST syndrome; overlap syndrome.
2) Localised scleroderma
Morphea
Linear scleroderma: En coup de sabre; Romberg's disease (with facial
atrophy)
Generalised morphea
3) Sclerodermoid conditions
Genetic: Progeria, Werner's syndrome
Occupational: vibration, silicosis
Metabolic: congential porphyria, carcinoid
Immunologic: Chronic graft verse host
Chemical: Polyvinyl chloride, bleomycin
Malignancy: carcinoid, bronchoalvelolar
Postinfectious: Lyme
Neurologic: limb immobilization
2.3.2. Diagnostic Criteria Developed by the American Rheumatism
Association
Major criteria: Proximal scleroderma
Minor criteria: Sclerodactyly, digital pitted scars, loss of subcutaneous of the
finger pad, bibasilar pulmonary fibrosis.
(97% certain of the diagnosis if one major or two minor criteria are present)
2.3.3. Others Findings
Pulmonary, Gastrointestinal, Musculoskeletal, Cardiac, Renal.
2.3.4. Serologic Findings
Anti-RNP: mixed connective tissue disease
Anti-centromere: CREST syndrome
Anti-topoisonmerase I (anti-Scl-70) progressive systemic sclerosis
Nucleolar ANA
2.3.5. Related Conditions
Mixed connective tissue disease, eosinophilic fasciitis, tryptophan induced
disease.
3. ENDOCRINE ABNORMALITIES
Endocrine abnormalities often present with cutaneous signs. Recognition of
which can lead to earlier diagnosis and prompt treatment. In this section, we
will discuss the clinical manifestation of endocrinological disorders.
3.1. Diabetes Mellitus
1) Necrobiosis lipoidica diabetorium (NLD)
It occurs in about 0.3 percent of patient with diabetes mellitus and is more
common in young female patients. It usually presents as symmetrical, well
defined plaques on both shins and feet. Sometimes, it may appear on the
face, arms and trunk. The plaques are irregular and are brown-red on
violaceous in colour. The epidermis is atrophic and delicate vessels occur
over the surface. In chronic stage, the lesion may develop into painful ulcer.
Treatment of NLD is very unsatisfactory. The course of the lesions do not
correlate with normalization of hyperglycaemia. Intralesional steroids are
sometimes useful.
2) Diabetic dermopathy
Multiple asymptomatic discrete atrophic brown macules are common on the
shins. These are known as diabetic shin spots (or diabetic dermopathy).
3) Granuloma annulare
Well defined, annular lesions with the margin made up of multiple discrete
flat topped papules. These lesions are commonly found over the backs of the
hands, feet, ankle and limbs. Though it responds well to intralesional
steroids, it easily recurs. The generalize form has a stronger association with
glucose intolerance than the localize variant.
4) Lipoatrophy/Lipohypertrophy
Lipoatrophy refers to depression of the skin due to repeated injections of
impurified insulin preparations. It usually occurs in children and young
women. Lipohypertrophy is due to subcutaneous deposition of fat in situ of
skin having repeated injections.
5) Bullous diabeticorum
Subepidermal blisters may occur on the lower legs of diabetics but the cause
is unknown.
6) Diabetic cheiroarthropathy (sclerodactyly)
In 40% of juvenile IDDM patients, tight thickened and waxy skin develop
over the dorsum of the hands. Subsequently, it results in contracture of the
proximal interphalangeal joints.
Others:
7) Infections
8) Kryle's disease
9) Eruptive xanthoma
10) Drug eruptions
11) Acanthosis nigricans
3.2. Thyroid Diseases
1) Hyperthyroidism
The skin is warmth and moist due to hyperdynamic circulation.
The hair is fine and friable.
On the face, there may be telangiectasia and facial flushing.
On the hands, there may be palmer erythema and onycholysis of nails. In
Grave's disease, clubbing of fingers (thyroid acropachy) may occur.
Others possible associated skin manifestations include pruritis,
dermographism and urticaria.
In Grave's disease, pretibial myxoedema occurs in 5 per cent of this group of
patient. It presents as well-defined plaques or nodules with prominent
follicles and peau d' orange appearance. It commonly appears over the
anterior aspect of the shins and is usually bilateral.
2) Hypothyroidism
On the face, there may be non-pitting oedema around the eyes. The lateral
third of the eyebrow may be thinned.
The scalp and body hair is dry and brittle. Diffuse or partial alopecia may
occur.
In general, the skin is cool, dry and with a yellow tint.
The nails are brittle and there are longitudinal ridges.
Purpura and ecchymoses are not uncommon.
3.3. Adrenal Diseases
1) Adrenal Insufficiency
Diffuse hyperpigmentation is noticed but is more marked on pressure points
such as the knees, knuckles, ischial tuberosities and in intertriginous areas.
The palmar creases are darkened.
Mucous membranes including the vagina, anus and mouth are commonly
pigmented.
New scars are easily pigmented, too.
There are longitudinal pigmented lines in the nails.
2) Cushing's Syndrome
Typical features include: moon face, buffalo hump, central obesity but with
thinning of extremities.
Skin atrophy is very common and is frequently associated with ecchymoses
and purpura.
There are striae, mainly on the flanks of the abdomen, arms and thighs.
These striae are usually broader and are purplish then the striae of
pregnancy, obesity and adolescence.
Decreased vascular tone may appear as purplish mottling on the lower limbs
(cutis marmorata).
Hypertrichosis occurring on the face, upper lip, chin and lateral cheeks is
common. Hirsutism due to over-production of adrenal androgens may occur
in females.
Acne of monomorphic type is common on the face and back.
In general, patient with cushing¡¦s syndrome is more susceptible to
cutaneous infections such as pityriasis versicolour, trichophyton rubum and
candidosis.
3.4. Pituitary Diseases
1) Panhypopituitarism
The skin is dry, smooth, soft and pale.
The face may be puffy, facial fold is decreased. Fine wrinkles are commonly
found around the eyes and mouth making the patient look older.
The scalp hair is dry, fine and generally thin.
Characteristically, there is uniform loss of body hair. Axillary hair is affected
first and public hair loss takes longer to develop. Loss of beard hair may
appear, too.
Finally, the nails are fragile, thin and opaque.
2) Acromegaly
On the face, the acromegalic appearance is very typical and presents as
frontal bossing, widening of the nose, coarsening of the skin, and
enlargement of the lips.
The facial, neck and scalp creases are accentuated. Infrequently, overgrowth
of the dermis results in ridging of the skin of the scalp (cutis verticis gyrata).
Soft tissue swelling of the hands and feet are very common.
The sebaceous glands and sweat glands are enlarged.
Sessile or pedunculated fibromas are found in 20 to 30 percent of patients.
Acanthosis nigrican is found in about 10 percent of cases.
3.5. The Porphyrias
Porphyrias result from either acquired or inherited enzymatic abnormalities
in haem synthesis. Haem is synthesized from glycine and succinyl coenzyme
A in a complex series of reaction. Eight enzymes are involved in this
complicated pathway. Most of the human porphyrias are due to the deficient
activity of the corresponding enzymes. Porphyrias are of dermatologic
interest because several of them have distinct cutaneous manifestations that
may arrive the diagnosis clinically. Porphyrias are classified by the primary
site of expression of the specific enzyme defect and the abnormal porphyrin
profile of patients with these orders.
There are 2 types: the erythropoietic porphyria and the hepatic porphyria.
1) The erythropoietic porphyria (EP)
It includes the congenital erythropoietic porphyria and erythropoietic
protoporphyria.
Congenital Erythropoietic porphyria (Gunther's disease)
This is an extremely rare autosomal recessive disorder and is due to a
decreased activity of uroporphyrinogen cosynthetase. Photosensitivity is
quite significant and presents as blisters, vesicles and bullae in sun-exposed
areas. These skin lesions heal slowly with scarring, atrophy and mutilating
deformities. Hyperpigmentation and hypertrichosis are common. Bone
abnormalities such as resorption of distal phalanges and sclerodacyl may
occur. Haemolytic anaemia and splenomegaly may be present. Erythrodontia
(red-stained teeth) in both deciduous and permanent teeth is pathognomonic
of erythropoietic porphyria. The urine also fluoresces reddish. The diagnosis
is made from the early onset of severe cutaneous photosensitivity associated
with red fluorescent urine and erythrodontia. The treatment is usually
preventive. Avoidance of sunlight must be emphasized. Splenectomy may be
useful in dealing with intractable hemolytic anaemia.
Erythropoietic protoporphyria (EPP)
An autosomal dominant disorder which is characterized by cutaneous
photosensitivity, cholelithiasis and potentially severe liver disease. The acute
episodes of photosensitivity include itching, burning or pruritis in sun-
exposed areas and occur within minutes after sun-exposure. These are
followed by erythema, oedema, urticarial lesions and rarely purpura a few
hours later. Chronically damaged skin may heal with superficial pitted and
linear scars especially on the cheeks and nose. Pseudorhagades, thickened
and leathery skin over the knuckles and fingers together with the wrinkles
give an appearance of premature aging. The diagnosis is made by detecting
elevated levels of free protoporphyria in the red blood cell and/or faeces.
Photoprotection is essential. Beta-carotene has been found helpful in
preventing or minimizing the symptoms of cutaneous photosensitivity
reactions. In severe end-stage liver failure, liver transplantation will be the
last resort.
2) The Hepatic Porphyria
The hepatic porphyria includes porphyria cutanea tarda, acute intermittent
porphyria, variegate porphyria and hereditary corproporphyria.
Porphyria Cutanea Tarda (PCT)
PCT is due to the decreased activity in uroporphyrinogen decarboxylase and
is divided into two categories. Type I (symptomatic, acquired) PCT is
characterized by the deficiency of the enzyme in the liver only. Type II
(hereditary) PCT is inherited in an autosomal dominant fashion and the
uroporphyrinogen decarboxylase is decreased approximately 50 percent in
all tissues. Vesicles and bullae appear on sun-exposed areas or in areas
subjected to repeated trauma. Increased skin fragility is common and lesions
usually heal with milia formation. Hypertrichosis (non-virilizing) is a useful
diagnostic sign. Hyperpigmentation, sclerodermoid plaques and scarring
alopecia are not uncommon. Ethyl alcohol, estrogen hormones,
hexachlorobenzene, chlorinated phenols and iron have been associated with
the exacerbation of PCT. Patients with PCT excrete increased amounts of
porphyrins in the urine, which give rise to pink-red fluorescence under
wood's lamp examination. In equivocal situation, quantitative 24 hour urine
uroporphyrin and coproporphyrin determinations and stool protoporphyrin
and coproporphyrin determinations should be performed. Drugs that may
have triggered the disease must be strictly avoided. Phlebotomy is a safe,
effective and relatively simple method of therapy for PCT. In some patients
who are not suitable for phlebotomy, may respond to antimalarials. e.g.
chloroquine and hydroxychloroquine.
Variegate Porphyria (VP)
VP is an autosomal dominant disease and is quite common among the white.
The clinical manifestations of VP include those of AIP and PCT, either or
both of which may occur in the same individual. However, the skin
manifestations do not correlate with the acute attacks in most patients. The
diagnosis is made as shown by the elevated urinary ALA and PBG levels
during acute attacks of VP but characteristically fall to normal levels
between attacks. Precipitating factors and drugs should be avoided.
Photoprotection for photosensitivity is a must.
Hereditary Coproporphyria (HCP)
HCP is an autosomal dominant disorder and is due to deficiency of
coproporphogen oxidase activity in red blood cells and lecuocytes. It is an
extremely rare disease. The acute attacks are similar to those of AIP but are
milder than that of AIP. Cutaneous photosensitivity occurs in 20 percent of
cases. HCP is characterized by increased excretion of coproporphyrin III in
urine and faeces. Avoidance of drugs, glucose loading and hematin infusions
may be helpful in dealing patients with HCP.
CUTANEOUS LASER THERAPY

Dr. L.Y. CHONG & Dr. H.H.L. CHAN
CHAPTER 21
1. INTRODUCTION
1.1. Definition
The word laser is the abbreviation of Light Amplification by the
Stimulated Emission of Radiation. Laser light is characterised by
monochromaticity, spatial coherence and high intensity.
1.2. Applications in Dermatology
Different laser systems, each with its own unique properties, are now
used for a wide range of dermatological conditions. These systems
are named after the media that are used to produce the laser lights.
They include carbon-dioxide, argon, organic dyes, heavy metal
vapour, krypton, neodymium-YAG, ruby, and alexandrite lasers.
(Table 1) In practice, dermatological applications of laser technology
can be divided into three categories:
surgery (cutting, haemostasis) and vaporisation;
selective photothermolysis of superficial vascular disorders;
selective photothermolysis of pigmented lesions and tattoos.
2. LASER BIOPHYSICS
2.1. Joules, Watts, Fluence and Power Density
Radiation energy is measured in Joules (J) and is directly
proportional to the quantity of photons of the radiation. The rate of
energy exposure is measured in Watts (W) where 1W = 1J/s. The
total amount of energy exposed to a surface is known as the fluence
(energy density) and is expressed in term of Joules per metre square
(J/m2). In laser surgery, fluence determines the total volume of tissue
damage. The rate of tissue damage depends on the power density of
the laser beam. Power density or irradiance is defined as the rate of
energy delivery per unit area (W/cm2). Power density of a laser beam
is directly proportional to its output but inversely related to its spot
size and can be calculated as follow:
Power density (W/cm2) = Power output (W)/Spot size (cm2)
2.2. Properties of Laser Light
Laser light has the following characteristics:
A high degree of monochromaticity: The active medium determines
the emission wavelength which is restricted to a very narrow band.
A high degree of coherency: This is due to the fact that all light
waves are in phase. Laser light is highly directional with a low degree
of divergence.
High intensity: The amplification process allows the emission of
high-energy level laser.
2.3. Laser Beam Modalities
Laser beams can be continuous, pulsed, superpulsed, or Q-switched.
Continuous lasers (CW) produce beams with a constant output. The
beam can be interrupted by a shutter controlled by the operator,
resulting in the production of shuttered continuous wave (mechanical
pulse). Pulsed lasers emit beams 'compressed' into high intensity
pulses. Each pulse last about several hundred microseconds,
generating energy 100 times more than that of the CW lasers. Better
understanding of the concept of selective photo-thermolysis has
resulted in the development of laser systems with very short pulses
and high peak power. These are the Q-switched lasers. This refers to
the use of techniques such as an electromagnetic switch to stop laser
passing through the cavity abruptly. This blockage is then suddenly
removed allowing the production of pulses with short duration (in the
range of nsec) and high irradiance (1,000,000 W/cm2).
2.4. Laser Delivery Systems
Three systems are currently being used to deliver laser light from the
optical cavity to the tissue: articulated arms, fiber optics, and
automatic scanning devices.
1) An articulated arm involves the use of rigid tubes with reflective
mirrors at each connecting end.
2) Fibreoptics are fibres consisting mainly of quartz and are used to
transmit light.
3) Manual control of laser light delivery is subjective and can be
inaccurate even in experience hands. Micromanipulator improves the
accuracy of laser light delivery and can be connected to the fiber
optics or the articulated arm through a microscope. Automatic
scanning devices involve the use of computer-controlled
micromanipulator that deliver laser light in a controlled manner.
2.5. Skin Optics
The interaction of light radiation with skin is determined by the optical
properties of skin constituents and on the wavelength of the incident
light. In the epidermis and stratum corneum, radiation with
wavelengths below 300 nm is absorbed rather than reflected.
Different chromophores will absorb radiation of specific wavelengths.
Protein, urocanic acid, melanin and nucleic acid are the main
chromophores for radiation in the ultraviolet C and B range (< 320
nm). Melanin also absorbs radiation with wavelengths between the
range of 320-1,000 nm. Water is the dominant chromophore for
radiation of higher wavelengths (> 1,000 nm). Radiation with
wavelengths greater than 300 nm have a greater degree of
penetration and can therefore reach the dermis. In the dermis, most
of the transmitted radiation is scattered from the collagen bundles
back to the environment. Some degree of dermal absorption by
chromophores such as haemoglobin and bilirubin do occur. Radiation
such as ultraviolet A, blue, green, and yellow light are absorbed by
haemoglobin. The term "optical window" refers to the ability of
radiation to penetrate deep into skin tissue because of low absorption
and low scattering. This applies to radiation with wavelengths
between 600-1,300 nm. Melanin is the main chromophore at this
spectrum.
2.6. Skin Chromophores and Laser
Using lasers light with wavelengths that match that of the skin
chromophores, selective tissue damage can be achieved. Light
emitted by the ruby laser (694 nm) or Nd:YAG laser (1,064 nm) can
be absorbed by melanin containing cells leading to their destruction.
Argon and yellow light lasers are absorbed by haemoglobin and can
be used for the treatment of vascular lesions. The carbon dioxide
laser has a wavelength of 10,600 nm which is absorbed by water and
is therefore nn-selective.
2.7. Types of Interactions Between Laser Light and Skin
Laser, like other electromagnetic radiation, can produce
photothermal, photomechanical and photochemical reactions in skin.
Photothermal interactions, are derived directly from heat generated
by laser. If skin is heated to temperature just below 50o C, the
consequent thermal tissue damage is still reversible. At higher
degrees (50-100o C), coagulation of protein occurs leading to
irreversible thermal damage. At even higher temperature (>100o C),
vaporisation of tissue occurs. This takes place when the water
component of the affected tissue reaches its boiling point and
vaporised. The type of thermal tissue damage induced (coagulation
or vaporisation) depends on the power density, there is, high energy
pulses cause tissue to pass its boiling point and produces
vaporisation. The extent of thermal damage is directly proportional to
the amount of heat dissipated from the target site to the surrounding
tissue. Heat requires time to diffuse outward and cause thermal
damage. The extent of thermal damage, therefore, depends upon the
rate of heating which is determined by power density and exposure
time. If the exposure time is shorter than the target's thermal
relaxation time (defined as the time required for a target to cool from
the temperature achieved immediately after laser irradiation to half
that temperature), heat will not be able to diffuse out. This allows the
thermal damage to be limited to the target site. Selective tissue
damage restricted to the target site can be achieved using a laser
with a wavelength that is specifically absorbed by the target tissue,
where it is converted to heat resulting in a thermal injury. This is
referred to as Selective photothermolysis. As the thermal relaxation
time of an object is inversely related to its size, lasers with ultra-short
pulses emitting high energy have been developed. In
photomechanical interactions, high energy-level pulse laser
disperses the target tissue by rapid thermal expansion and local
vaporisation. A good example of this reaction is the use of Q-switched
ruby laser in the removal of tattoo. High energy impulses from the
laser disperses the ink particles and the dermal macrophages that
contain them. The main role of laser induced photochemistry is
photodynamic therapy for the treatment of cancer. This involves the
use of laser, in conjunction with a topical or systemic photosensitizer,
in producing the beneficial effects.
In summary, the principle of laser therapy is to emit a specific
wavelength of photon energy is to the target tissue, aiming to have
optimal absorption of energy by the target tissue, while minimizing the
destruction of the surrounding normal tissue. Three basic elements
have to be considered: Firstly, a specific wavelength that is optimally
absorbed by the target structure (depending on absorption curve of
the chromophore); secondly, an exposure duration less than the time
necessary for cooling of the target structure (using pulsed or Q-
switched mode); and thirdly, sufficient energy fluence must be
delivered to reach a destructive temperature in the target.
3. CLINICAL APPLICATION OF SPECIFIC LASER SYSTEMS

3.1. Carbon Dioxide (CO2) laser: Surgery and Vaporisation
The CO2 laser has a wavelength of 10,600 nm (i.e. within the invisible
infrared spectrum). It is used in conjunction with a coaxial helium-
neon laser beam which is visible and acts as a guide light.
Water is the main chromophone of CO2 lasers. Ninety percent of the
skin is made up of water and the effect of the CO2 laser is therefore
non-specific. CO2 lasers can be operated either as a cutting tool
["light knife"] or as an ablation tool ["laserbrasion"]. As mentioned
above, the rate of thermal damage is related to the power density
(which is inversely proportional to the spot size for any given energy.)
For CO2 lasers to act as a cutting tool, high power density leading to
instant and precise tissue vaporisation is necessary. To achieve this,
the CO2 laser is placed close to the tissue surface (generally, less
than 1 inch) so that the beam is focused (0.1-0.2 mm in diameter)
and has a high power intensity (50,000-75,000 W/cm2). As the beam
incises tissue, It will also seal blood vessels and lymphatics, allowing
control of haemostasis. This makes it useful for patients with bleeding
disorders or patients in whom adrenaline is contraindicated. It is also
useful in patients with pacemakers in whom electrosurgery is
contraindicated. Furthermore, because of its ability to seal nerve
endings, patients tend to suffer less postoperative pain. The CO2
laser sterilises at the same time and is also useful for the
debridement of infected ulcers or burns.
The CO2 laser may also be used to vaporise tissue by positioning the
laser further away from the skin surface than for cutting so that the
beam is defocused (1-2 mm in diameter) and the power density low
(150-500 W/cm2). The power density is adjusted so that it is low
enough to achieve rapid complete tissue vaporisation without
charring. Many applications for CO2 laser vaporisation have been
reported. (Table 2) However, with advances in technology, newer
laser systems have proved to be superior to the CO2 laser in some of
these conditions.
By combining the two operational modes (excision and vaporisation)
of CO2 laser, patients with rhinophyma can be effectively treated. In
these cases, excess soft tissue is initially excised in a relatively
bloodless field using the focused laser beam. Remaining tissue can
then be contoured by tissue vaporisation. The resulting char can be
removed by cotton gauze soaked in hydrogen peroxide. The process
of tissue vaporisation and cleansing by hydrogen peroxide can be
repeated until a satisfactory cosmetic result is obtained. Complete
healing by secondary intention usually takes about 2-4 weeks.
The most frequent complication of CO2 laser therapy is hypertrophic
scarring. Others include hypopigmentation, dilated pores,
postoperative haemorrhage, infection and excessive growth of
granulation tissue. Another important hazard is the laser smoke
('plume') that occurs as a consequence of tissue vaporisation, viable
human papillomavirus DNA has been isolated. An adequate smoke
evacuation unit is essential.
4. LASERS FOR TREATING VASCULAR LESIONS (Table 3)

4.1. Argon Laser
Argon lasers have been reported to be effective in the treatment of
both vascular and pigmented lesions. They emit continuous, or
shuttered continuous wave systems and use argon gas as the active
medium. These systems emit light in the blue-green spectrum of the
electromagnetic radiation. Haemoglobin and melanin are the principal
chromophores of the argon laser. Haemoglobin is only partially
sensitive to the argon laser emissions. This leads to a significant
degree of scattering of laser energy in the dermis. In addition, a
proportion of the light is absorbed by the melanocytes. This results in
unwanted epidermal damage such as burning and blistering, and a
reduction in the amount of energy reaching the dermal vessels.
Furthermore, argon lasers generate low power emissions, resulting in
non-selective thermal damage with an increased incidence of dermal
fibrosis and scarring.
Argon lasers continue to have a role in the treatment of mature,
hypertrophic port wine stains in adults. Other vascular lesions that
have been successfully treated by the argon laser include small
haemangiomas, cherry angiomas, telangiectasias, angiokeratomas
and venous lakes. Because argon laser light is absorbed by melanin,
these systems have been applied for the treatment of melanocytic
pigmented lesions such as pigmented naevus, freckles and
lentigines. Argon lasers have also been used as energy sources for
other laser systems, for example, the continuous dye laser.
4.2. 577 or 585 nm Dye Lasers
Dye lasers emit wavelengths that are selectively absorbed by
oxyhaemoglobulin rather than epidermal melanin. In these systems,
various organic dyes are used as the active medium to generate
yellow light with wavelengths of either 577 or 585 nm. Pulsed dye
lasers have been shown to be highly successful in the treatment of
port wine stains. Lesions that show a better response are those that
are located on the neck, lateral face and eyelids. Macular lesions and
lesions in children also tend to be more responsive. Age is not a
limiting factor for the use of these systems. Superficial vascular
lesions other than port wine stains also respond to the pulsed dye
laser. Telangiectasia especially those that occur after sclerotherapy
for varicose veins are particularly responsive. The dye laser is also
used for the treatment of proliferative haemangiomas that obstruct
vital structures such as the eye. Complete resolution is obtained if the
lesion is treated at an early stage. Others vascular lesions treated
include poikiloderma of Civatte, facial spider angiomas, and the
telangiectatic component of rosacea and pyogenic granuloma. Pulsed
dye laser has also been successfully employed in the treatment of
viral wart, although the precise mechanism by which this is achieved
remains speculative.
Hexascans are automated scanning devices that can be connected to
argon-pumped tunable dye lasers for the treatment of large areas of
superficial vascular malformations. In contrast to the pulsed-dye
laser, it is effective in the treatment of hypertrophic port-wine stains
and thicker haemangiomas but paler lesions tend to be less
responsive. It can also be applied to the treatment of other cutaneous
vascular lesions.
Complications following the use of the pulsed dye laser are relatively
uncommon. Purpura can be cosmetically disfiguring but will fade over
a two weeks period. Acute changes such as the level of discomfort,
scaling, vesiculation or crusting are energy dependent and can be
reduced by careful monitoring of the tested area. Local anaethesia
using EMLA may sometimes be necessary to relieve the associated
discomfort and should be applied 60 minutes preoperatively. Scarring
occurs in less than 1% and is often associated with rubbing or
scratching the lesion after the procedure. Hypopigmentation or
hyperpigmentation is not uncommon and usually resolves after a few
months. Hexascans do not cause purpura, but its other side effects
are otherwise similar.
4.3. Copper Vapour Laser
In these systems, pieces of copper metal placed in a ceramic tube
are melted to form vapour. Neon gas is added to improve the
discharge quality of the medium. The system produces yellow light
with a wavelength of 578 nm and green light at 511 nm. Yellow light is
suitable for the treatment of vascular lesion, whereas green light is
used for pigmented conditions.
Although both the dye and copper vapour systems emit radiation of
similar frequencies, there are several important differences between
them. The laser light delivered by the copper vapour system is rapidly
pulsed with a pulse duration of 20 ns. The time between each pulse is
67 us, giving a frequency of 15 KHz. In contrast to the pulsed-dye
system which generates 100 mJ of energy per pulse, the energy
output per pulse of the copper vapour laser is only 0.2 mJ.
Summation of pulses is therefore necessary to induce the desirable
degree of tissue damage. To limit the thermal damage, a mechanical
shutter with different shutter speed is used. The spot sizes of copper
vapour systems are also much smaller (100-1,000 um). These
properties of the copper vapour laser have resulted in clinical
responses quite different from that of the pulsed-dye systems.
Copper vapour lasers seem to induce vasoconstriction rather than
intravascular coagulation as seen in the pulsed-dye system. They
can, therefore, be used in combination with pulsed-dyed lasers in the
treatment of large vascular condition such as hypertrophic or
cobblestone port wine stains. The small spot sizes of the copper
vapour lasers make them ideal for the treatment of disorders of small
blood vessels such as facial telangiectasia. The green light mode of
copper vapour laser has a wavelength of 511 nm and is largely
absorbed by melanin. It can be used for the treatment of superficial
pigmentary conditions.
4.4. Krypton Laser
These systems use Krypton gas as the active medium and generate
yellow light with a wavelength of 568-575 nm as well as green light at
520-530 nm. Their clinical applications and complications are very
much similar to that of the argon laser and copper vapour laser.
5. LASERS FOR TREATING PIGMENTED LESIONS AND

TATTOOS (Table 4)
The concept of selective photothermolysis has revolutionized the role
of the laser in cutaneous surgery. This has led to the development of
laser systems which are now increasingly employed in the treatment
of pigmented lesions and tattoos. These are the Q-switched Nd-YAG
laser, the Q-switched ruby laser, the 510 nm pulsed dye laser and the
Alexandrite crystal laser. Melanin and tattoo pigment are the main
chromophores and are rapidly heated leading to fragmentation into
small particles. Some of these small particles are removed by
phagocytosis, whereas some of the epidermal pigments are removed
transepidermally. As phagocytosis is an important means of pigment
removal, an interval is of at least three weeks is necessary before
accurate evaluation can be made. Further lightening of lesions results
from a change in the optical properties of the pigment following
fragmentation
5.1. Q-switched Neodymium:Yttrium-Aluminum-Garnet (Nd-YAG)
Laser
This system uses a YAG crystal doped with 1-3% neodymium ions as
the active medium and is powered by a high intensity flashlamp. This
leads to the generation of laser with a wavelength in the invisible
infrared portion of the spectrum (1 064 nm). This light beam is poorly
absorbed by melanin, haemoglobin and water but well absorbed by
blue-black exogenous pigment. The laser can therefore penetrate up
to 1 cm into the skin with minimal epidermal damage. The non-
selectivity of continuous wave Nd-YAG laser has led to the frequent
development of adverse effects that include scarring and pigmentary
changes. By modifying the system with Q-switching, selective
photothermolysis of exogenous blue-black pigment can be achieved.
At this wavelength, a spot size of 2 mm with energy level between 5-
10 J/cm2 is often used. By using a potassium titanyl phosphate
crystal, the wavelength of Q-switched Nd-YAG laser can be halved to
532 nm (green). At this wavelength the beam is well absorbed by red,
orange and purple ink. These pigments usually respond poorly to
treatment by the Q-switched ruby laser. As melanin also absorbs light
of this wavelength, this system has been used successfully for the
treatment of benign epidermal lesions. The fluence used is usually
around 2-4 J/cm2 with a spot size of 2 mm.
Safety procedures for Nd-YAG laser are similar to those for the
carbon dioxide laser except eye protection. Nd-YAG laser penetrates
the clear goggles that are used for the eye protection for CO2 laser.
Polycarbonated safety glasses are necessary to prevent corneal and
retinal damage. The main complications seen in the use of Q-
switched Nd-YAG laser are pigmentary changes. These occur more
frequently in the use of 532 nm laser as the 1064 nm wavelength
penetrates deeper and is poorly absorbed by melanin. Sun protection
like the use of sunscreens is a helpful measure. As the response
varies between individuals, treatment of a test area is advisable.
Scarring can also rarely occur and tends to be associated with
scratching to, or trauma at the lesion postoperatively.
5.2. Q-switched Ruby Laser
Since the development of the carbon dioxide and argon laser, the role
of ruby laser in dermatology has diminished substantially. By
modifying the system with the Q-switched device, the ruby laser has
re-established itself as an important tool for the treatment of
pigmented lesions. The beam has a wavelength of 694 nm and is
actively absorbed by melanin, blue-black and green pigment. Spot
diameters of 4-8 mm and fluences that range from 4-12 J/cm2 can be
used. For amateur tattoos, 4-6 treatment sessions are needed
whereas professional tattoos may require 8-10 and occasionally even
20 treatment sessions. The Q-switched ruby laser is effective for the
removal of blue and blue-black inks. Occasionally green and brown
pigment may also respond to Q-switched ruby. Whitening of the
lesions often occurs immediately after laser treatment and lasts about
20 minutes, this represents epidermal and dermal vacuolisation
secondary to thermal induced steam formation. Gradual fading of the
lesions, over a 5-6 week period, may then follow. In general, lower
energy levels (4-7 J/cm2) and less treatment sessions (1-2 sessions)
are needed for the treatment of benign pigmented lesions. In patients
who do not respond to Q-switched ruby laser, other laser such as the
Q-switched Nd-YAG laser can be tried.
Safety guidelines are essentially the same as for carbon dioxide laser
and Q-switched Nd-YAG laser. Purpura and even punctate bleeding
can occur at the treatment site if high energy intensity is used. Other
complications are similar to those seen with the Q-switched 532 nm
Nd-YAG laser. Transient texture change is not unusual and usually
resolves after 6-8 weeks. Pigmentary change, usually
hypopigmentation, can occur in up to 50% of the patients. The
majority of these patients recover completely within 6 months of their
treatment, although permanent hypopigmentation can occur.
Darkening after cosmetic tattoo treatment may also be seen. Scarring
is rare and is associated with trauma or infection.
5.3. Alexandrite Laser
This is the third Q-switched laser system designed for the treatment
of tattoos. It has a wavelength of 755 nm and a pulse duration of 100
ns. A spot diameter of 3 mm is usually used with fluences that range
from 4-8 J/cm2. The beam is well absorbed by blue, black and green
pigment, but absorbed poorly by red ink. The wavelength of this
system enables deep penetration and allows the removal of pigments
in the dermis. Smaller, superficial and recent tattoos are likely to
respond quicker to the Alexandrite laser.
Unlike the other Q-switched laser systems, tissue splattering does not
occur with the Alexandrite laser. This is likely to be due to the
differences in power density of the three systems. Although the
fluences are similar, the wider pulse duration of the Alexandrite
system means that it has the lowest surface power density (160
mw/cm2 as compared to 400 mw/cm2 with the Q-switched ruby laser,
and 1,000 mw/cm2 with the Q-switched Nd-YAG laser). This is
important as tissue and blood splattering carry the potential risk of
disease transmission such as HIV and hepatitis B. Immediate
whitening also occurs in the use of the Alexandrite laser. The use of
higher energy levels can cause purpura and punctuate bleeding.
Others complications are similar to those seen in Q-switched ruby
laser.
5.4. 510 nm Pulsed Dye, Argon, Copper Vapour, Krypton Lasers
The low degree of penetration of these lasers result in poor efficacy
except for superficial pigmented lesions. They are mainly used in the
treatment of freckles, lentigines, seborrhoeic keratosis and
melanocytic naevi. The result in treating naevus of Ota, chloasma or
other dermal pigmented disorders are poor. The 510 nm pulsed dye
laser is however effective in the removal of tattoos containing red,
purple, yellow and orange pigment.
6. LASER THERAPY IN SOCIAL HYGIENE SERVICE

Laser therapy had been started in Social Hygiene Service since this
form of hi-tech treatment had been introduced to the field of
dermatology in Hong Kong. However, due to the constringency of
resource, there are only two laser machines available in the service,
leading to a lot of limitations in the treatment. At the moment, copper
vapour laser is available in Yung Fung Shee Dermatological Clinic
while krypton laser in Yaumatei Dermatological Clinic. (Table 5)
These two laser machines are able to emit yellow light and green
light, thus they can be used to treat a variety of vascular and
epidermal pigmented lesions. They are good in treating telangiectasia
and purplish-dark hypertrophied portwine stain in adult. However they
are not suitable to treat the portwine stain in children because of the
relatively high incidence of scarring. They are also ineffective in
treating dermal pigmented lesions, such as naevus of Ota, chloasma
and tattoo.
Both these two machines in Social Hygiene Service are mainly
manual-driven, therefore the treatment depends much on the
experience of the operators. Good judgment of treatment endpoints
are important in order to achieve good result. (Table 6) The power
and the spot size of the handpiece of these two machines are
relatively small, hence it is very time consuming in treating large area
of lesions like portwine stain.
Laser therapy has been promoted and in fact has been proven as an
effective treatment modality in a lot of dermatological conditions.
However, they are not without risks and their end results are variable
in individual patient. Before starting the treatment, the operator needs
to consider carefully about the indications and the possible risks.
(Table 7) One should be very cautious in dealing with patients who
have keloid tendency, who are prone to post-inflammatory pigmentary
changes and who are demanding persons. Cerain areas are
considered as "dangerous areas" where scarring is more likely to
occur, such as angle of jaws, mandibular area, presternal area,
shoulders and upper arms. Risks and limitations of various forms of
therapy should be fully explained to the patients, so that they will
have psychological preparation and will not have over-expectation
before the treatment.
Precautions that should be taken by the trained operators and nurses
during the laser therapy (Table 8, 9), as these are important to the
safety of both medical personnel and patients. Clinical photograph
with good quality should be taken before and after the treatments for
comparison and documentation. Finally, full explanation about the
after-care should be given to patients in detail in order to minimized
the complications. (Table 10)
Table 1: Classification of Laser Machines

Carbon dioxide 10,600 nm Infrared
Argon 488, 514 nm blue-green
Organic dye (rhodamine, 504 nm green
fluorescein, coumarin,
acridine red) (400-1,000 nm) 577, 585 nm yellow
Copper vapour, 511 nm green
copper bromide 578 nm yellow
Krypton 521, 530 nm green
568 nm yellow
Neodymium:YAG
(yttrium-aluminum-garnet) 1064 nm infrared
KTP (potassium-titanyl
-phosphate)
(double frequency YAG) 532 nm green
Ruby 694 nm red
Alexandrite 755 nm red
¡@
Table 2: Clinical Applications of the Carbon Dioxide Laser
Lesions where the CO2 laser is potentially the treatment of
choice:
Actinic cheilitis, bowenoid papulosis, cutaneous resurfacing
procedures, epidermal nevus, rhinophyma, sublingual keratosis
Lesions where the use of CO2 laser may offer better results or
facilitate the procedure:
Tumours: squamous cell carcinoma in-situ, superficial multifocal
basal cell carcinoma, neurfibromas, giant trichoepitheliomas,
seborrheic keratosis, syringomas, xanthelasma.
Infection: extensive or large condyloma acuminatum, verruca
vulgaris, recalcitrant wart, debridement of burns or infected ulcer,
cutaneous infection such as leishmaniasis.
Vascular: adenoma sebaceum, cherry angioma, lymphangioma
circumscriptum, angiokeraomas, pyogenic granulomas, granuloma
faciale.
Other: cosmetic excisional surgery, lichen planus of the penis, Hailey-
Hailey disease, chondrodermatitis nodularis helicis chronicus, oral
florid papillomatosis, xanthelasma
Lesions that better results can now be achieved using newer
lasers:
Cafe-au-lait spots, ephelides, labial lentigines, lentigines, port wine
stain, tattoos, telangiectasia
Table 3: Lasers Used in the Treatment of Vascular Lesions

Characteristics:
Pulsed
¡@ Argon Copper vapour
dye
Argon Orange Copper metal +

Active medium
gas dye neon gas
Electric
Power source Flashlamp Electric current
current
Wavelength
488, 514 577, 585 511, 578
(nm)
400-500
Pulse duration 0.2-20 s 20 ns
us
Spot size (mm) 0.2-5 2-7 0.1-1.0
Depth of
penetration at 200-300 400, 600 300-400
50% (um)
Skin Blood, Blood,

Blood, melanin
Chromophores melanin melanin
Clinical Applications:
Portwine stain , telangiectasias, cherry angioma, rosacea,

pyogenic granuloma, spider naevi, venous lake, angiofibroma,
angiokeratoma, lymphangioma
Table 4: Lasers Used in the Treatment of Pigmented Lesions and
Tattoos
Characteristics:
¡@ Q-Nd- Q-Ruby Q-Alex Pulsed
YAG dye
Wavelength (nm) 532, 694 755 510
1,064
Pulse duration (ns) 10-20 20-40 50-100 100-500
Peak power
(mW/cm2) at fluence
2 J/cm2
4 J/cm2 20
8 J/cm2
10 J/cm2
40
800 400 160

1,000 500 200
Spot diameter (mm) 2 4-8 3 3
Depth of penetration 400/1,600 1,200 1,300 300
at 50% (um)
Skin chromophores Melanin, Melanin Melanin, Melanin
blood blood
Clinical Applications:
Freckle, lentigo, melanocytic naevus, seborrhoeic keratosis, cafe-au-
lait, mucosal melanosis, naevus of Ota, melasma,
Mongolian?/FONT>s spot, tattoo
QS: Q-switched, Alex: Alexdandrite, Nd-YAG: Neodymium: Yttrium-
Aluminum-Garnet
¡@
Table 5: Laser Machines Available in SHS
Copper Vapour Dermatological Laser System in YFS
Dermatology Clinic
(Visiray-VisErase VCM-03)
Specifications:
Green (511 nm): 0.9 W (at 0.4 mm spot size)
Yellow (578 nm): 0.7 W (at 0.4 mm spot size)
Spot Size: 0.1 mm, 0.15 mm, 0.4 mm, 0.8 mm
Focused beam
Exposure Modes: Continuous, Pulse
Air cooled
Krypton Dermatological Laser System in YMT Dermatology
Clinic
(HGM-SURGICA K1)
Specifications:
Green (520-530 nm): 2.0 W (at 1.0 mm spot size)
Yellow (568-575 nm): 1.0 W (at 1.0 mm spot size)
Spot Size: 0.1 mm, 1.0 mm
Collimated beam
Exposure Modes: Continuous, Pulse
Internal water cooled
Table 6: Operating Techniques
Method:
Tracing with the handpiece (for example: telangiectasia)
Painting with the handpiece (for example: portwine stain)
Recommended starting power and spot size (use the minimal
power as possible):
VisErase VCM-03
- 0.4 W with 0.4 mm spot size (Continuous wave)
SURGICA K1
- 0.7 W, 0.20 seconds pulse duration, with 1 mm spot size (Pulsed)
Treatment endpoint:
Tissue Temperature Tissue change Clinical observation
50 degree C Protein denatured Blanching (whitening)
100 degree C Water vaporized Shrinkage (greying)
100-150 degree C Tissue carbonized Charring (Blacking)
> 175 degree C All vaporized Smoky plume,Blubbling
sound
Reduced in volume
Level reached Clinical observation
Epidermis Grey
Papillary dermis Pink (superficial dermal capillaries)
Reticular dermis White with yellow spots (sebaceous glands)
Table 7: Complications & Hazards of Laser
Possible complications of laser therapy:
1) Immediate erythema, oedema, pain, exudation, purpura
2) Secondary infection
3) Pigmentary changes: hyperpigmentation, hypopigmentation
4) Textural changes, atrophy
5) Scarring, keloid
Potential Hazards of Laser Machine:
1) Hazard to eye
Retina, especially macula: permanent visual loss
(Suitable protective eye goggles, eye-shields)
2) Hazard to skin
Severe burns & scarring
(Training & experience)
3) Electrical hazard
High voltage: life threatening
(Strictly follow the safety precautions)
4) Hazards from fumes & vaporized tissues
HPV, HIV
(Fume evacuator, good ventilation, mask)
Table 8: Precautions in Laser Therapy
1) ALWAYS wear safety goggles with recommended filters whenever
the laser is in use.
Operator's goggles:
VisErase VCM-03
- Green: Orange filter
- Yellow: Grey filter
SURGICA K1
- Green/Yellow: Green filter
Patient's goggles: Red filter
2) ALWAYS lock the door of the room during treatment.
3) NEVER look directly into the laser beam; or at scattered or
reflected laser light.
4) NEVER point the laser handpiece at any person except at the
treated area.
5) NEVER remove any covers from the cabinet of the machine and
attempt to repair.
6) NEVER use the laser in the presence of flammable anaesthetics.
7) NEVER step on or abruptly bend the fibre-optic cable.
8) NEVER move the laser machine during operation or within 30
minutes of turning off for VisErase VCM-03.
9) Do NOT turn off the machine immediately after treatment. Wait for
30 minutes for VisErase VCM-03 and 5 minutes for SURGICA K1.
10) Do NOT turn off the main electrical switch.
Table 9: Procedures that must be Taken by Nursing Staff
Before treatment:
1) Turn on the laser machine for warm up
40 minutes for VisErase VCM-03
45 seconds for SURGICA K1
2) Written consent after explanation of the procedures
3) Take clinical photograph
4) Ensure the patient having eye-protection
5) Prepare local anaesthetics if necessary
Lignocaine (without adrenaline)
Emla cream (1 hour before treatment with Tegederm occlusion)
Novesin eyedrop if eye-shields are necessary
6) Lock the door and turn on the warning lamp
During treatment:
1) Ensure that the patient has eye-protection all the time
2) Measure the treatment time
3) Plume suction if necessary
After treatment:
1) Apply antiseptic cream (silver sulphadiazine, fucidin) or emollient
(aqueous cream) for the patient
2) Arrange follow-up appointment
3) In between treatment, keep the machine at Standby mode for
SURGICA K1
4) After treatment for all patients, wait for 30 minutes for VisErase
VCM-03 and 5 minutes for SURGICA K1 before turn off the machine
Table 10: Aftercare Following Laser Treatment
1) Expect a sunburn-like reaction with possible blistering within the
first 24-48 hours. Pain is usually minimal and can be relieved with
either Panadol and/or cool soaks with a wash cloth.
2) A crust or scab may occur and should last for 7-14 days. Do not
pick off the scab!! Just let it fall off at its own pace.
3) Keep the area clean and dry until the scab/crust falls off. Wash
gently with soap and water and apply a thin layer of moisturizer or
antibiotic ointment.
4) Once the scab/crust has come off the area may look pink and even
slightly depressed or indented. Both the pinkness and depression
should improve over the next several weeks to months.
5) Avoid direct sunlight or sun exposure to the treated areas for 3-6
months. Use at least an SPF of 15 or greater sunscreen, or wear a
hat or other protective clothing (preferably both). Be aware that
unprotected sun exposure can result in an uneven repigmentation,
producing brown spots that can take months to fade away and in rare
cases may be permanent.
6) Be patient!! It may take up to three months to adequately judge the

true response of your condition to the laser treatment. DON'T
HESITATE TO CALL IF YOU HAVE ANY QUESTIONS OR
PROBLEMS!!

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HANDBOOK OF DERMATOLOGY & VENEREOLOGY

(Social Hygiene Handbook, 2nd Edition)

INTRODUCTION OF SKIN DISEASES

1. SKIN FUNCTION AND STRUCTURE OF SKIN

Protection from harmful agents of

Preservation of a balanced internal

Shock absorber Subcutaneous fat

Insulation Subcutaneous fat

Sensation Nerve endings

Lubrication Sebaceous glands

Protection & grip Nails

Calorie reserve Subcutaneous fat

Vitamin D synthesis Epidermis

Body odour Apocrine sweat glands

Psychosocial Hair & Nails

3.5. Examples of Description of Skin Rash

3.2. General Pruritus

Stage Morphology of Symptoms Examples Treatment

1.3. Table 2: Common Types of Eczema

Allergic Contact Dermatitis Seborrhoeic Dermatitis

Infective Dermatitis Pityriasis Alba

Dermatophytide Hyperkeratotic Eczema

¡@ Juvenile Plantar Dermatosis

Eczema Associated With

¡@ Eczematous Drug Eruption

Nail polish, cosmetics, contact lens solution, metal

Airborne allergens, cosmetics, sunscreen, acne

Necklaces, airborne allergens, perfumes, aftershave

Topical medicaments, sunscreens, plants, clothing,

Axilla Deodorant, clothing

Arms Watch and watchband

Hands Soaps and detergents, foods, poison ivy, industrial

Genitals Rubber condom, allergens transfers by hands

Feet Shoes, cements spilling into boots

¡@ Potassium dichromate cement

¡@ Neomycin sulphate topical medicaments

Paraphenylenediamine hair dyes, azo dyes, fur dyes,

in all almost all trades and

¡@ Benzocaine topical anaesthetics

glues, paper, clothing,

adhesive plasters, paper,

¡@ Balsam of Peru cosmetics (perfumes, flavours)

¡@ Black rubber mix rubber products

¡@ Wool alcohols lanolin, vehicles

¡@ Mercapto mix shoes, rubber products

glues, pastes, insulator,

preservatives and vehicles in

Paratertiarybutyl phenol leather, adhesive and rubber

¡@ Fragrance mix stabilizer in medical products

earrings, metal tools, clothing

the allergen in P obconica,

3.3. Common Patterns of Hand Eczema

silvery scaling can easily be generated

Nail involvement is commonly seen in all types of psoriasis which can

psoriasiform drug eruption, lichen planus , discoid lupus erythematosus,

3. IN VESTI GAT ION

4. MA NA GEMENT I N S OC IAL H YG IENE SE RV ICE

5. OTHE R TRE ATMENT

Tab le 1 : T ype o f P so ria si s in 1 99 5 ( Derma to log y C lini cs o f S ocia l

Chronic plaque 558 91.6

Generalized pustular 3 0.49

Localized pustular 2 0.33

All Psoriasis (all new skin cases) 609 (14,569) 4.18

ACNE AND OTHER