Transcript Common Skin Conditions as a cause for admission

Prepared by :
SIG , Dermatology Nursing
IADVL
Drug reaction(SJ/TEN syndrome)
 Blistering disorders(Pemphigus group, Bullous
pemphigoid ,CBDC, dermatitis herpatiformis)
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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)
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Most often elicited by drugs and less so idiopathic.
Common drugs –sulfur group,penicillin group,
antitubercular drugs,anti inflammatory drugs,
phenytoin, carbamazepine,allopurinol,nevirapine,etc
The 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.
Complications
Septicemia
Blindness
Acute renal failure
Gastrointestinal bleeding
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
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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.
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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.
Invesigations
Routine – Hb,TC,DC,PC,RFT,LFT
Skin biopsy
Direct and indirect IF
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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 electrolytes
Specific and supportive therapy

Systemic Steroid (DCP pulse therapy)
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Immunosuppresants (cyclophosphamide, azathioprine)
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Biologics (Rituximab)
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Antibiotics, Antifungal
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Multivitamines, Calcium
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Observation of steroid induced side effects
 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.
 Routine-Hb,TC,DC,PC,RFT,LFT
 Skin
biopsy
 Direct Immunofluorescence
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 electrolytes
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Specific and supportive therapy
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Corticosteroids,antibiotics and other antiinflammatory drugs

Immunosuppresants (cyclophosphamide,
azathioprine)
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Plasmapheresis,IVIg
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Multivitamines, Calcium
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.
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 Routine
– Hb, TC,DC,PC,LFT,RFT etc
 PS for atypical cells
 Skin biopsy
 Chest Xray
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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
 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.
 Routine
– Hb, TC,DC etc
 Skin biopsy
 Chest X-ray
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
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Topical Therapy
Emollients
Steroids
Calcipotriol
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Systemic Therapy
Methotrexate
PUVA therapy
UV-B Phototherapy
Steroids
Retinoids
Cyclosporin
 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.
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.
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•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 care
Nutritional care
•Antiviral (acyclovir,valcyclovir)
•Antibiotics,anti inflammatory drugs
 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)
 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
 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
 NSAIDs
 HCQs
 Steroid
 MDT
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.
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 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.
 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)
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 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.
 pu
 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)
 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
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)
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 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)
 Systemic
Glucocorticoids(0.5-1mg/kg of
prednisolone)
 Methyl prednisolone
 Immunosuppresants
 Sulfasalazin(1-4gm)
 Clofazimine
 Colchicine
 Infliximab