Prepared by : SIG, Dermatology Nursing IADVL. Drug reaction(SJ/TEN syndrome) Blistering...

COMMON SKIN CONDITIONS AS A CAUSE FOR ADMISSION

Prepared by :SIG , Dermatology NursingIADVL

Drug reaction(SJ/TEN syndrome) Blistering disorders(Pemphigus group, Bullous

pemphigoid ,CBDC, dermatitis herpatiformis) Erythroderma(generalised exfoliation),Pustular

Psoriasis, Reiter’s disease Lepra reactions Herpes Zoster SLE, Dermatomyositis, Scleroderma Acute Urticaria Non healing ulcers(Pyoderma

Gangrenosum,Vasculitis,Venous Ulcer)

SJ/TEN SYNDROMEMost often elicited by drugs and less so idiopathic.Common drugs –sulfur group,penicillin group, antitubercular drugs,anti inflammatory drugs, phenytoin, carbamazepine,allopurinol,nevirapine,etcThe disease is preceded by a nonspecific prodrome with fever ,myalgia ,malaise and headache.Skin lesions develops abruptly are maculopapular rash with purpuric lesions and followed by vesiculobullous lesions which rupture leaving behind erosion and ulceration.

Bullous lesions may occur in oral, conjuctival ,genital and anal mucosa.Mucocutaneous hemorrhagic crusting (eg. Lips) is the most characteristic feature.

ComplicationsSepticemiaBlindnessAcute renal failureGastrointestinal bleeding

TREATMENT Omission of causative drug(give list of drugs to

be avoided ) Supportive Therapy Maintainance of vital parameters(routine check-up for

temperature,BP,pulse and urine output chart) Daily nursing care nutritional care Maintenance of fluid and electrolytes Dressing of ulcers medical Therapy Steroids Intravenous immunoglobulin Antibiotics, Antifungal

BLISTERING DISORDERS

It includes pemphigus, bullous pemphigoid and CBDC, dermatitis herpatiformis.

Autoimmune conditions

Pemphigus vulgaris Common in 20-40 years It may start with oral lesions. Patient develops crops of vesiculobullous

lesions just like burns blisters on normal skin which rupture and produced erosions and ulcers.

These erosions continue to spread at the periphery without any tendency of healing spontaneously and often bleed with minor trauma.Erosions are being covered with dirty reddish or brownish crusts, depending on pressense of bleeding or infection or both.If more than 25% body area involved,fluid loss,electrolyte imbalance and protein loss.Erosions and ulcers may produce secondary infection which lead to septicemia.

InvesigationsRoutine – Hb,TC,DC,PC,RFT,LFT Skin biopsyDirect and indirect IF

TREATMENT Good nursing care includes daily dressing. Oral and genital mucosa may require special

nursing care. Vital data monitoring(routine check-up for

temperature,BP,pulse and urine output chart)

Nutritional care Maintenance of fluid and electrolytesSpecific and supportive therapy Systemic Steroid (DCP pulse therapy) Immunosuppresants (cyclophosphamide, azathioprine) Biologics (Rituximab) Antibiotics, Antifungal Multivitamines, Calcium Observation of steroid induced side effects

BULLOUS PEMPHIGOID Common in 40-60 years Most common sites are

flexures,proximal extremities and trunk. Mild to moderate itching is present Subepidermal large and tense bullae on

a background of erythema and edema rupture to form erosions which have a tendency to heal spontaneously.

Mucosa are not involved.

INVESTIGATIONS Routine-Hb,TC,DC,PC,RFT,LFT Skin biopsy Direct Immunofluorescence

TREATMENT

Good nursing care includes daily dressing. Vital data monitoring(routine check-up for

temperature,BP,pulse and urine output chart)

Nutritional care Maintenance of fluid and electrolytesSpecific and supportive therapy Corticosteroids,antibiotics and other anti-

inflammatory drugs Immunosuppresants (cyclophosphamide,

azathioprine) Plasmapheresis,IVIg Multivitamines, Calcium

ERYTHRODERMA(EXFOLIATIVE DERMATITS)

Inflammatory skin disease affecting more than 90% of the body surace.

Generalised erythema with exfoliation of skin. It is associated with burning,irritation,itching

or a sense of tightness. It is chronic relapsing condition with various

underlying etiology like psoriasis,eczema, lymphoma,drug induced,contact dermatits, congenital disorder like icthyosis,PRP etc.

Due to exfoliation of skin there are chances for electrolyte imbalance and hypoproteinemia.

Peripheral vasodilation leads to Congestive cardiac failure.

IX Routine – Hb, TC,DC,PC,LFT,RFT etc PS for atypical cells Skin biopsy Chest Xray

MANAGEMENT Maintainance of vital parameters(routine check-

up for temperature,BP,pulse and urine output chart)

Daily nursing care Nutritional care Maintenance of fluid and electrolytes Emollients and moisturizer application Emollient bath High protein diet Topical therapy Systemic therapy is given according to etiology In psoriasis-immunosuppresants required. In contact dermatitis and eczema-steroids

required. If drug induced-avoidance of causative drug

PUSTULAR PSORIASIS Crops of pustules based on erythema. Distributional subtypes include: Localised palmoplantar pustular

psoriasis. Generalised pustular psoriasis: • This is the life threatening variant, the

patient being febrile and toxic as waves of pustules based on tender erythema appear all over the body.

• Hypoproteinemia and hypocalcemia are common.

IX Routine – Hb, TC,DC etc Skin biopsy Chest X-ray

MANAGEMENT

Topical Therapy

Emollients Steroids Calcipotriol

Systemic Therapy Methotrexate PUVA therapy UV-B Phototherapy Steroids Retinoids Cyclosporin

Maintainance of vital parameters(routine check-up for temperature,BP,pulse and urine output chart)Daily nursing carenutritional careMaintenance of fluid and electrolytes

REITER’S SYNDROME It is chronic inflammatory disease,having

recurrent episodes of arthritis, urethritis,conjuctivitis and mucocutaneous eruptions.

It usually occurs in a genetically susceptible person,following an infection of the genitourinary tract due to chlamydiae and ureaplasma or following an attack of dysentry due to shigella, salmonella, campylobactor and yersinia.

Mucocutaneous lesions are seen in 50% cases and are prone to develop at skin,genital or oral mucosa and nails.

Skin lesions are seen in 30%cases and classical lesions are known as keratoderma blenorrhagica which commonly affects the palms,soles and toes.

Lesions start as erythematous macules which turn into vesicles, followed by formation of pustules.

When pustules are dried up, papules and plaques, covered with thick crusts are developed.

At palms and soles, lesions are covered with mollusk-like thick crust.

HERPES ZOSTER It is a viral disorder caused by reactivation

of Varicella zoster virus that is lying dormant in sensory ganglia.

Reactivation may be triggered by trauma,stress or due to old age.

It is characterised by dermatomal involvement of the skin in which pain is followed by vesicular eruption in particular dermatome.

It can be generalised or multidermatomal in immunocompromised person.

It is most common in 2nd and 3rd decade of life.

MANAGEMENT

•Require admissions in -Ophthalmic zoster -Ramsay-Hunt syndrome -Disseminated zoster•Patient may develop Post herpatic neuralgia after 3 months.

Maintainance of vital parameters(routine check-up fortemperature,BP,pulse and urine output chart)Daily nursing careNutritional care•Antiviral (acyclovir,valcyclovir)•Antibiotics,anti inflammatory drugs

LEPRA REACTION Leprosy is a slowly progressive

immunologically mediated disease,caused by M.Lepra,mainly affecting skin and peripheral nerves.

Classification Lepromatous Borderline Tuberculoid Indeterminate Borderline and lepromatous both group

develop reaction either.

Lepra reaction is the development of different sets of clinical manifestations other than existing leprosy lesions or sudden changes of existing lesions,due to hypersensitivity reactions.

Types Type I lepra reaction is caused by type IV

hypersensitivity reaction(delayed hypersensitivity reaction)

Type II lepra reaction is caused by type III hypersensitivity reaction(immune complex mediated hypersensitivity reaction)

TYPE 1 LEPRA REACTION It occurs in all form of borderline

leprosy(BT,BB and BL)1) reversal reaction Patient regains immunity following

treatment or spontaneously Existing skin lesions become tender,

erythematous, edematous and scaly. General symptoms are absent Peripheral nerves become swollen and

tender with increment of anesthesia

TYPE 2 LEPRA REACTION It occurs in BL and LL with high bacterial

index. Prominent general features-fever,

arthritis, lymphadenitis, edema of the limbs or face.

Sudden onset of crops of tender, erythematous nodules known as erythema nodosum leprosum (ENL)

Common sites-face distal upper limbs and proximal lower limbs

MANAGEMENT NSAIDs HCQs Steroid MDT

ACUTE URTICARIA

Urticaria is commonly a type I hypersensitivity reaction(IgE mediated immediate hypersensitivity) of the skin to a variety of exogenous and endogenous antigens.

Lesions begin as pruritic ill defined erythematous macules or patches which rapidly develop to form the typical lesions(‘wheals’) that are pale red edematous papules or plaques with a brighter periphery.

Rhinitis,difficulty in breathing,sensation of heaviness in chest,whezing and abdominal pain may accompany the skin lesions and are indications for urgent treatment to avoid the complication of laryngeal edema.

MANAGEMENT Should be attended to

immediately,since this is usually a manifestation of a systemic Type I hypersensitivity response and may be accompanied by laryngeal edema and bronchospasm.

IM antihistamines(inj.avil) should be given initially .

If no relief after 1-2 hours,IM or IV hydrocortisone.

If no response,IM or SC adrenaline(0.5 ml of 1:1000 solution)brings about prompt relief.

SLE,DERMATOMYOSITIS ,SCLERODERMA

All are autoimmune inflammatory connective tissue disorders.

LUPUS ERYTHEMATOSUS manifests on skin as

Discoid lesions Butterfly rash Oral ulcers Photosensitivity Alopecia Raynaud’s phenomenon Localised Scleroderma Indurated dyspigmented plaque with atrophy

DERMATOMYOSITIS Proximal muscle weakness is the most

common presenting feature. Heliotrope rash Gottrons papules Gottrons sign Shawl’s sign Confluent macular violaceous erythema Calcinosis in muscls and no terminal

resorption of tips of digits(in contrast with systemic sclerosis)

SCLERODERMA It is a common connective tissue

disorder with increased amount of dermal collagen

Skin is dry and tight Microstomia and facial disfigurement

with retraction of lips, perioral furrow and beaked nose are often present.

Telangiectasia commonly is seen at lips and palms.

Digital ulcers develop due to trauma,ischemia and fibrosis.

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NON HEALING ULCERS Ulcer is a break in the skin or mucous

membranes with associated necrosis(cell death). An ulcer heals with scarring

Common Causes: Venous Neuropathic(including due to diabetes

or leprosy) Arterial Vasculopathic(most important being

pyoderma gangrenosum)

PYODERMA GANGRENOSUM Primarily sterile inflammatory

neutrophilic dermatosis characterised by recurrent very tender cutaneous ulcerations with mucopurulent or hemorrhagic exudate,undermined bluish borders and surrounding erythema.

Variants Ulcerative Bullous Pustular Superficial granulomatous

INVESTIGATIONS Total count/DLC(Lymphocyte count)/ESR Anemia Increased lymphocyte count and raised ESR

for tuberculosis FBS/PPBS VDRL Urine for sugar Pus/discharge for culture and

sensitivity(inflammed and spreading) Mantoux test Chest Xray(tuberculous ulcers,metastatic

deposits)

Biopsy(malignancy from edge and surrounding healthy tissue)-type/invasiveness/differentiation)

X-ray of bone and joints New bone formation(gummatous ulcers

and sabre tibia) Contrast radiography-Arteriography Imaging techniques-Doppler(venous and

arterial)

MANAGEMENT Systemic Glucocorticoids(0.5-1mg/kg of

prednisolone) Methyl prednisolone Immunosuppresants Sulfasalazin(1-4gm) Clofazimine Colchicine Infliximab