Specials Flashcards
When is usually the onset of atopic eczema? How many will resolve
First year of life, but not in the first 2 months.
Seborrhoeic dermatitis is common in first 2 months.
resolving in 50% by 12 years of age, and in 75% by 16 years
Diagnosis of eczema
Clinical diagnosis
If tested, most affected children have an elevated total plasma IgE level.
Skin-prick and radioallergosorbent (RAST) tests if history suggests a specific allergen
Exclude immune deficiency disorder if the disease is unsually severe
Clinical features of atopic eczema
Pruritus is the main symptoms at all ages.
Scratching and exacerbation of the rash.
Excoriated areas become erythematous, weeping and crusted.
prolonged scratching and rubbing of the skin may lead to lichenification
Distribution tends to change with age. Predominantly face and trunk in infant. Flexor surfaces in older children.
Complications of eczema.
Flare-ups are common:
bacterial infection (staph, strep)
Viral infection (HSV)
Contact with an irritant or allergen
Environment (heat. humidity)
Psychological stress
Treatment of eczema
Avoid irritants and precipitants Emollients Topical corticosteroids Immunomodulators Occlusive bandages Antibiotics and antiviral agents
Psychosocial support
Recognize a herpes simplex rash
(HSV) usually enters the body through the mucous membranes or skin. Site of primary infection may be associated with intense local mucosal damage.
HSV1 - lip and skin lesions (eg. cold sores)
HSV2 - genital
Asymptomatic HSV is common
Gingivostomatitis is the most common form
Eczema herpeticum (serious). if secondary bacterial infection, septicaemia may result
Describe gingivostomatitis
From 10 months to 3 years.
Vesicular lesions on the lips, gums and anterior surfaces of the tongue and hard palate. Often progress to extensive painful ulceration with bleeding.
High fever
Miserable child
May persist for 2 weeks. Eating and drinking are painful which may cause dehydration
management is symptomatic, but severe disease may necessitate intravenous fluids and aciclovir
Treatment of herpes simplex rash
First line is acyclovir
May be used in severe symptomatic skin, ophthalmic, cerebral and systemic infections
Eye disease caused by herpes simplex
Blepharitis or conjunctivitis
May extend to involve the cornea, producing dendritic ulceration. Can lead to corneal scarring and loss of vision. requires split lamp exam
Usual sites of impetigo (highly contagious, staphylococcal or streptococcal skin infection in infants an young children mostly).
Appearance?
Mostly where there is pre-existing disease such as atopic eczema.
Face
Neck
Hands
Begin as erythematous macules which may become vesicular/pustular or even bullous
Rupture of the vesicles with exudation of fluid leads to the characteristic confluent honey-coloured crusted lesions. Rapid spread because of exudate
Treatment of impetigo
Topical abx (mupirocin) are effective for MILD.
Severe needs narrow-spectrum systemic antibiotics (eg. flucloxacillin)
Although.. broad-spectrum abx such as co-amoxiclav have simpler oral administration regimens and taste better, therefore have better adherence
Affected children should NOT go to school until lesions are dry!
Nasal carriage is an important source of infection which can be eradicated with a nasal cream of mupirocin
What is staphylococcal scalded skin syndrome?
Presentation
Caused by exfoliative staphylococcal toxin
Affects infants and young children
Fever
Malaise
Purulent, crusting, localised infection around eyes, nose, and mouth.
Subsequent widespread erythema and tenderness of the skin
Areas of epidermis separate on gentle pressure (Nikolsky sign). Leaves denuded areas of skin. They subsequently dry and heal without scarring
Management of Staphylococcal Scalded skin syndrome
Iv anti-staphylococcal abx
Analgesia
Monitoring of fluid balance
What are the causes of urticaria?
Exposure to an allergen or viral infection
Triggers urticarial skin reaction
May also involve deeper tissues to produce swelling of the lips and angioedema or even anaphylaxis
Treatment of urticaria
Second-generation, non-sedating antihistamines
What is papular urticaria?
Delayed hypersensitivity reaction - most commonly on legs, following a bite from flea, bedbug or animal or bird mite
Irritation, vesicles, papules and weals appear and secondary infection due to scratching is common
May last weeks or months and may be recurrent
Recognize a varicella rash
Papules
then vesicles
then pustules
They have surrounding erythema
Finally crusts (5-6 days in)
200-500 lesions start on head and trunk and progress to peripheries.
May also just be a few lesions.
Incubation period of varicella
14 days. Highly infection 2 days before and until 6 days after the illness starts
Complications of varicella
Bacterial superinfection which may lead to toxic shock syndrome or NF
Cerebellitis
Generalised encephalitis
Aseptic meningitis
Immunocompromised
Haemorrhagic lesions
Pneumonitis
DIC
Commonest pathogens causing adeno/tonsillar hypertrophy
Group A beta-haemolytic streptococci.
Epstein Barr virus.
marked constitutional disturbance, such as headache, apathy and abdominal pain, white tonsillar exudate and cervical lymphadenopathy, is more common with bacterial infection
Management of severe adeno/tonsillitis
May require hospital admission for iv fluids and analgesia if unable to swallow fluids or liquids
Amoxicillin is best avoided! widespread rash if Epstein Barr V
Indications for tonsillectomy in children
Controversial.
Recurrent severe tonsillitis. Reduces number of episodes, but not symptoms.
Peritonsillar abscess (quinsy)
Obstructive sleep apnoea!!! - adenoids as well usually
Recurrent OME with hearing loss is an indication of tonsil+adenoidectomy
Symptoms and signs of rhinitis
Coryza
Conjunctivitis
There may be a cough due to post-nasal drip
Sleep disturbance from chronically blocked nose with impaired daytime behavior and concentration
Associations of rhinitis
Eczema
Sinusitis
Adenoidal hypertrophy
ASTHMA!
Treatment of rhinitis
Second-generation non-sedating antihistamines. Topically or systematically.
Topical corticosteroid nasal or eye preparations. (ophthalmology supervision needed for latter)
LTRA (montelukast) Nasal decongestants (no more than 10 days! risk of rebound effect)
NO systemic corticosteroids due to risk of adverse effects
Key aspects of history in OSA
Loud snoring
Witnessed pauses in breathing (apnoeas)
Restlessness
Disturbed sleep
Affected child may be obese or have growth failure
Consequences of OSA
Excessive daytime sleepiness
Learning and behavior problems
Acute life-threatening cardiorespiratory events
Pulmonary HTN
Causes of OSA in childhood
Comonly adenotonsillar hypertrophy
Predisposing factors are hypotonia, muscle weakness and anatomical problems.
(Downs, achondroplasia, CP, craniofacial abnormalities - these groups may be screened regularly)
Assessment of OSA
Overnight pusle oxymetry. At home. Quantify frequency and severity of periods of desaturation (92%)
-normal oxymetry does not exclude it