39. Skin rash and eruptions Flashcards
History taking rash
HoPC: distribution, how the rash has changed, itch, associated symptoms
MHx: recent infections,
DHx: new medications, immunosuppressant medications, allergies
SHx: close contacts unwell? Contact with children? Travel history, Sexual history, occupation,
Examination steps rash
General inspection (number, distribution and size)
Configuration (shape/outline)
Colour and blanching
Morphology (form and structure)
Palpation
ddx erythematous rash
Staphylococcal scalded skin
Toxic shock syndrome
TEN and SJS
Erythema nodosum
Erythroderma and erythrodermic psoriasis
Acute generalised exanthematous pustulosis (AGEP)
(Still’s disease)
ddx maculopapualr rash
Drug reaction with eosinophilia and systemic symptoms (DRESS)
Erythema multiforme
Lyme disease
Syphilis
Childhood exanthems: measles, scarlet fever, rubella, parvovirus, roseola infantum
Pityriasis rosea
Rheumatic fever
(Kawasaki disease)
ddx vesiculobullous rash
Bullous pemphigoid
Pemphigus vulgaris
Varicella
Hand-foot-and -mouth
Eczema herpeticum
Bacterial superinfection (of chickenpox or eczema)
ddx petechial/purpuric rash
Infection (palpable)
(Meningococcal meningitis)
Disseminated gonococcal infection
(Infective endocarditis)
Immune (palpable)
(Vasculitis: HSP, polyarteritis nodosa)
Bleeding (non-palpable)
(DIC and sepsis)
(Scurvy)
(ITP)
(TTP)
(Leukaemia)
acral distribution
distal areas including the hands and feet (e.g. hand, foot and mouth disease).
extensor distribution
extensor surfaces including the elbows and knees (e.g. psoriasis).
flexural distribution
flexural surfaces including the axillae, genital region and cubital fossae (e.g. eczema).
Seborrhoeic/follicular distrubution
affecting areas with increased numbers of sebaceous glands such as the face, scalp, chest and axillae (e.g. acne). eg seborrheoic dermatitis
Dermatomal distribution
he skin lesions appear confined to one or several dermatomes and do not cross the midline (e.g. herpes zoster).
discrete vs confluent lesions
Discrete lesions: individual lesions, clearly separated from one another (e.g. normal mole).
Confluent lesions: lesions that appear to be merging together (e.g. urticaria).
linear lesions
lesions in the shape of a line (e.g. excoriations).
discoid vs target vs annular lesions
Discoid lesions: coin-shaped lesions (e.g. discoid eczema, discoid lupus).
Target lesions: concentric rings of varying colour, resembling a bullseye (e.g. erythema multiforme).
Annular lesions: ring-like lesions with a central clearing (e.g. tinea corporis).
petechiae vs purpura
Petechiae - small red lesions caused when capillaries leak blood into the skin, DO NOT blanch when pressure is applied
Purpura - petechiae that are larger than 0.5cm.
macule vs patch
Macule: a flat area of altered colour less than 1.5cm in diameter.
Patch: a flat area of altered colour greater than 1.5cm in diameter.
Papule vs nodule
Papule: a solid raised palpable lesion less than 0.5cm in diameter.
Nodule: a solid raised palpable lesion greater than 0.5cm in diameter.
plaque
Plaque: a palpable flat lesion usually greater than 1cm in diameter. Most plaques are raised, however, some may be thickened without being visibly raised.
vesicle vs bulla
Vesicle: a raised, clear fluid-filled lesion less than 0.5cm in diameter.
Bulla: a raised, clear fluid-filled lesion greater than 0.5cm in diameter.
Pustule
Pustule: a pus-containing lesion less than 0.5cm in diameter.
cyst vs boil vs abscess
Cyst: A cyst is a cavity or sac that is filled with pus or fluid semisolid material or air. Cysts can be benign or malignant and can form on any part of the body. An infected cyst = abscess.
Abscess: An abscess is an infection filled with pus, is painful, and can happen anywhere on the body.
Boil: A small skin abscess is also called a boil and can appear on any body part. A boil is also known as a furuncle.
Wheal
an oedematous papule or plaque caused by dermal oedema.
(urticaria)
Lichenification
Thickening of the epidermis with exaggeration of normal skin lines, typically caused by chronic rubbing or scratching of an area (e.g. chronic eczema).
Excoriation
loss of epidermis associated with trauma
crust
a rough surface consisting of dried serum, blood, bacteria and cellular debris. The serum, blood, bacteria and debris have usually exuded through an eroded epidermis.
Atrophic scarring
thinning of normal tissues underlying the scar resulting in a cratering effect.
Hypertrophic scarring
hyperproliferation of scar tissue within the wound boundary, resulting in a prominent scar.
Keloidal scarring
hyperproliferation of scar tissue beyond the wound boundary resulting in a scar that is significantly larger than the original skin insult.
ulcer
a localised defect in the skin of irregular size and shape where the epidermis and some dermis have been lost. Ulcers ultimately result in scarring when healed.
skin fissure
a sharply-defined, linear or wedge-shaped tear in the epidermis with abrupt walls, typically due to excess skin dryness.
Fissures or splits occur when there is a lack of elasticity in the skin, usually when the skin is too dry or too moist.
striae
stretch marks
why is palpation of abscess important
might be hot
red flags rashes
mucosal involvement
blistering/peeling
pain
lymphadeopathy
systemic upset (fever, abnormal lft, u&e)
4 categories of rashes
Petechial/purpuric
Erythematous
Maculopapular
Vesiculobullous
Differentiating features petechial/purpuric rash and DDX
- Fever = assume infectious
- Palpable vs non-palpable
Palpable petechiae/purpura are usually the result of perivascular inflammation or infection = inflammatory eg vasculitis or bacterial emboli
Non-palpable petechiae/purpura usually occur in low platelet states such as ITP and DIC = non-inflammatory
febrile and petechial rash, first ddx?
meningococcal disease
mechanism of DIC
DIC - bacterial endotoxin and the inflammatory response from our immune system → activate clotting cascade → micro clots → clotting factors used up –> bleeding eg petechiae
rash meningitis
The rash is initially erythematous, maculopapular and appears first on the wrist and ankles, then becomes palpable petechiae
Typical history meningitis
Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered consciousness
Seizures
Non-blanching rash
Neonates:
Hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanelle.
Therefore lumbar puncture in all children if:
Under 1 month old and presenting with fever
1-3 months with fever and unwell
Under 1 years with unexplained fever and other features of serious illness
Examination findings meningitis
Fever
Non-blanching rash
Photophobia
Kernig’s test (Kernig’s test involves lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees. This creates a slight stretch in the meninges and where there is meningitis will produce spinal pain or resistance to this movement.)
Brudzinski test (Brudzinski’s test involves lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest. A positive test is when this causes the patient to involuntarily flex their hips and knees.)
What is Meningococcal meningitis vs Meningococcal septicaemia
Meningococcal meningitis - meningococcus bacteria (neisseria meningitidis) is infecting the meninges and CSF
Meningococcal septicaemia - meningococcal bacterial infection in the bloodstream → non blanching rash due to DIC and subcutaneous haemorrhage
plan ?meningitis
Airway
Breathing
Circulation
Disability: GCS, ; focal neurological signs; seizures; papilloedema;
Initial:
if in primary care and ?meningococcal - an urgent stat injection (IM or IV) of benzylpenicillin prior to transfer to hospital as time is so important:
< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg
Once in hospital, decisions to treat empirically quickly vs LP depends on patient and senior clinician
Investigations:
Bloods:
full blood count
CRP
coagulation screen
blood culture
whole-blood PCR, this will be relied upon if lumbar puncture contraindicated
blood glucose
blood gas
Lumbar puncture
unless contraindicated eg if there is evidence of raised ICP as it can cause herniation of cerebrum. Signs of raised ICP: cushing’s reflex (raised BP, low HR), focal neurological signs, papilloedema, significant bulging of the fontanelle, disseminated intravascular coagulation (meningococcal septicaemia eg the rash), signs of cerebral herniation.
Blood glucose at same time as CSF so can be compared
Normal lumbar puncture result
clear appearance
glucose 70% of plasma
protein 0.3 g/l
WCC 2 per mm^3 (neuts)
Bacterial meningitis LP result
Cloudy
Glucose low (< 1/2 plasma) bacteria using up the glucose
Protein high (> 1 g/l) bacteria releasing proteins
WCC 10 - 5,000 polymorphs/mm³ the immune system releases neutrophils in response to bacteria
Viral meningitis LP result
Clear/cloudy
Glucose 60-80% of plasma glucose* viruses don’t really use glucose
Protein normal/raised viruses may release a small amount of protein
WCC 15 - 1,000 lymphocytes/mm³ the immune system releases lymphocytes in response to viruses
Tuberculous LP result
Slight cloudy, fibrin web
glucose Low (< 1/2 plasma)
Protein high >1g/l
WCC 30-300 lymphocytes/mm3
The Ziehl-Neelsen stain is only 20% sensitive in the detection of tuberculous meningitis and therefore PCR is sometimes used (sensitivity = 75%)
Bacterial meningitis 0-3 months
BELS
- Group B Streptococcus (most common cause in neonates)
- E. coli
- Listeria monocytogenes
- Strep pneumoniae
Bacterial meningitis 3 months-6 years
- Neisseria meningitidis
- Streptococcus pneumoniae
- Haemophilus influenzae
Bacterial meningitis 6-60 years
- Neisseria meningitidis
- Streptococcus pneumoniae
Bacterial meningitis >60 years
- Streptococcus pneumoniae
- Neisseria meningitidis
- Listeria monocytogenes
Meningitis in immunocompromised
listeria monocytogenes
Community meningitis initial management
Benzylpenicillin IM or IV
< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg
Meningitis initial empirical therapy < 3 months
IV cefotaxime + amoxicillin (or ampicillin)
Meningitis initial empirical therapy 3 months-50 years
IV cefotaxime
Meningitis initial empirical therapy > 50 years
IV cefotaxime + amoxicillin (or ampicillin)
Meningitis management - listeria
IV amoxicillin (or ampicillin)
+ gentamicin
When should dexamethasone be given for meningitis
Give if lumbar puncture reveals:
- frankly purulent CSF
-CSF white blood cell count greater than 1000/microlitre
- raised CSF white blood cell count with protein concentration greater than 1 g/litre
- bacteria on Gram stain
Withhold if:
- septic shock
- meningococcal
- septicaemia
immunocompromised
Management meningococcal meningitis
IV benzylpenicillin or cefotaxime
Post exposure prophylaxis bacterial meningitis
Ciprofloxacin single dose
This risk is highest for people that have had close prolonged contact within the 7 days prior to the onset of the illness
Signs of raised ICP
cushing’s reflex (raised BP, low HR) irregular breathing, bradycardia, widening pulse pressure (blood pressure)
focal neurological signs
papilloedema
significant bulging of the fontanelle
contraindications to LP
Brain - raised ICP, convulsions, focal neurology
- reduced or fluctuating level of consciousness (Glasgow Coma Scale score less than 9 or a drop of 3 or more)
- age-relative bradycardia and hypertension
- focal neurological signs
- abnormal posture or posturing
- unequal, dilated or poorly responsive pupils
- papilloedema
- abnormal ‘doll’s eye’ movements
- tense, bulging fontanelle
Cardio - shock
Respiratory - respiratory insufficiency (lumbar puncture is considered to have a high risk of precipitating respiratory failure in the presence of respiratory insufficiency).
Blood - Coagulation abnormality
- coagulation results (if obtained) outside the normal range
- platelet count below 100×109/litre
- receiving anticoagulant therapy
Typical history infective endocarditis
PC:
Fever
Fatigue
Night sweats
Muscle aches
Anorexia (loss of appetite)
o/e:
New or “changing” heart murmur
Splinter haemorrhages
Petechiae on the trunk, limbs, oral mucosa or conjunctiva
Janeway lesions
Osler’s nodes
Roth spots
Splenomegaly (in longstanding disease)
Finger clubbing (in longstanding disease)
risk factors infective endocarditis
Intravenous drug use
Structural heart pathology (see below)
Chronic kidney disease (particularly on dialysis)
Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)
History of infective endocarditis
define infetcive endocarditis
Infective endocarditis refers to infection of the endothelium (the inner surface) of the heart.
Most commonly, it affects the heart valves.
It can be acute, subacute or chronic, depending on how rapidly and acutely the symptoms present and the causative organism.
Examples of structural heart pathology that can increase risk of infetcive endocarditis
Valvular heart disease
Congenital heart disease
Hypertrophic cardiomyopathy
Prosthetic heart valves
Implantable cardiac devices (e.g., pacemakers)
most common causative oragnism infective endocarditis? other causes
Staphylococcus aureus
Other causes include:
Streptococcus (notably the viridans group of streptococci)
Enterococcus (e.g., Enterococcus faecalis)
Rarer causes include Pseudomonas, HACEK organisms and fungi
Invetsigations ?infective endocarditis
- Three blood cultures, separated by 6 hours, taken from different sites
- Echo (trans-oesohageal ideal but trans-thoracic done mostly)
what scans can be done if prosthetic heat valve ?infective endocarditis
18F-FDG PET/CT
SPECT-CT
What criteria is used for diagnosis of infective endocarditis
modified duke criteria
what is the modified duke criteria
The Modified Duke criteria can be used to diagnose infective endocarditis. A diagnosis requires either:
- One major plus three minor criteria
- Five minor criteria
Major criteria are:
- Persistently positive blood cultures (typical bacteria on multiple cultures)
- Specific imaging findings (e.g., a vegetation seen on the echocardiogram)
Minor criteria are:
- Predisposition (e.g., IV drug use or heart valve pathology)
- Fever above 38°C
- Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions)
- Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis)
- Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)
Management infective endocarditis
Intravenous broad-spectrum antibiotics (e.g., amoxicillin and optional gentamicin) are the mainstay of treatment.
The choice of antibiotic may be more specific once the causative organism is identified on cultures.
Antibiotics are typically continued for at least:
4 weeks for with native heart valves
6 weeks for patients with prosthetic heart valves
Surgery may be required for:
- Heart failure relating to valve pathology
- Large vegetations or abscesses
- Infections not responding to antibiotics
Complications of infective endocarditis?
- Heart valve damage, causing regurgitation
- Heart failure
- Infective and non-infective emboli (causing abscesses, strokes and splenic infarction)
- Glomerulonephritis, causing renal impairment
when is prophylaxis for infective endocarditis given
case by case basis for surgical procedures etc for those at particularly high risk
what are janeway lesions vs oslers nodes
Osler’s nodes are on the tip of the finger or toes and painful. O for Owww.
Janeway lesions occur on palm and soles and are non-painful.
Complications bacterial meningitis
Hearing loss is a key complication
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Focal neurological deficits such as limb weakness or spasticity
What is scurvy? presentation
condition caused by a lack of vitamin C in the diet
Vitamin C is essential for the production of collagen
Symptoms of scurvy can include fatigue, weakness, joint pain, and bleeding gums. In severe cases, patients may experience anaemia and skin lesions.
cutaneous manifestations of scurvy
Perifollicular Petechiae: Small hemorrhagic spots surrounding hair follicles are one of the earliest signs of scurvy. They appear as reddish-brown or purple macules on the skin surface.
Follicular Hyperkeratosis: Swollen hair follicles with keratin plugs lead to a roughened skin texture resembling ‘goosebumps’ or ‘corkscrew hairs.’
Ecchymoses: Bruising occurs easily due to weakened blood vessel walls secondary to impaired collagen synthesis.
Gingival Changes: Swollen, spongy gums that bleed easily upon contact are common findings in patients with scurvy. In severe cases, gingival swelling may result in tooth mobility or loss.
MSK manifestations of scurvy
Arthralgia: Joint pain occurs due to inflammation of the synovial membrane secondary to subperiosteal haemorrhage.
Myalgia: Muscle pain and weakness are common complaints in patients with scurvy, often leading to a reluctance to move or ambulate.
Haemarthrosis: Bleeding into joint spaces can lead to painful and swollen joints.
Subperiosteal Hemorrhage: Blood accumulates beneath the periosteum of long bones, causing pain and tenderness. In children, this may manifest as pseudoparalysis or refusal to bear weight on affected limbs.
typical history disseminated gonococcal infection
Various non-specific skin lesions
Polyarthralgia (joint aches and pains)
Migratory polyarthritis (arthritis that moves between joints)
Tenosynovitis
Systemic symptoms such as fever and fatigue
septic arthritis
The rash consists of a few skin lesions only, usually on the distal extremities, and may be missed. The lesions begin as petechial macules which progress to form papules and pustules as microabscesses form around embolized bacteria. They later develop a necrotic center.
Pathophysiology HSP
antigenic stimulus –> IgA antibody production –> IgA deposited in vascualr walls –> deposition in kidneys - golmerulonephritis, deposition in GI tract (pain, haemorrhage, intussception, deposition in skin - palpable purpura
complement system also activated
Presentation HSP
Purpura (100%)
Joint pain (75%) usually knees and ankles
Abdominal pain (50%)
Renal involvement (50%) - microscopic or macroscopic haematuria and proteinuria, oedema
most common trigger HSP
URTI 1-3 weeks prior, streptococcus
what type of hypersensitivity is HSP
type 3 - immune complex mediated
Invetsiagtions HSP
To rule out other things:
- Sepsis : blood culture, CRP
- Thromboytopaenia (inc leukaemia) : coagulation studies
- Other vasculidities: Autoantibody screen: antinuclear antibodies, antineutrophil cytoplasmic antibodies, and complement levels
To help support HSP diagnosis
- ESR raised in 75% of patients
- Serum IgA may be high
To test for complications:
- urinalysis : haematuria, proteinuria
- Serum creatinine and electrolyte levels
Elevated creatinine indicates renal impairment or renal failure
Electrolyte abnormalities may occur in patients with severe gastrointestinal symptoms.
- blood pressure
If non-typical presentation :
- skin/renal biopsy for confirmation of diagnosis
If severe abdo pain:
- abdo USS
Management HSP
Supportive (fluid, rest, symptomatic relief)
- paracetamol (avoid ibruprofen if abdo pain)
- steroids may be used in severe cases
Monitoring
- 6 months periodic urinalysis and BP monitoring
- abnormlaity on urinalysis –> test serum cretainine
- if persistent - refer to nephrologist
monitoring post HSP
- 6 months periodic urinalysis and BP monitoring
- abnormlaity on urinalysis –> test serum cretainine
- if persistent - refer to nephrologist
Presentation staphylococcal scalded skin
PC: abrupt fever, diffuse, blanching skin erythema usually beginning on the face and flexures associated with skin tenderness. Mucous membranes are NOT involved.
o/e: red rash, wrinkled tissue paper-like. Blisters then form superficially → rupture easily → skin peeling (Nikolsky sign is positive)
Are mucous membranes involved in staphylococcal scalded skin
no
epidemiology SSSS
occurs in children <5 years
Plan ?SSSS
Investigation
cultures should be obtained from blood, urine, nasopharynx, umbilicus or any suspected focus of infection
Management
Antibiotics antistaphylococcal antibiotics (nafcillin or oxacillin), and Vancomycin in areas with a high prevalence of CA-MRSA
diligent fluid and electrolyte management and wound care, generally in a burn unit
Presentation toxic shock syndrome
PC: diffuse erythematous rash, which eventually desquamates on the hands and feet.
o/e: fever, hypotension
Pathophysiology and causes toxic shock
staph aureus
Classically TSS has been associated with high absorbent tampon use, however nasal packing, surgical wounds, postpartum infection and abscesses are other causes.
microorganism toxic shock
staph aureus
Management toxic shock syndrome
removal of infection focus (e.g. retained tampon)
IV fluids
IV antibiotics
Presentation SJS
PC: start with non-specific symptoms of fever, cough, sore throat, sore mouth, sore eyes and itchy skin. → maculopapular rash with target lesions, may develop vesicles/bullae mucosal involvement, fever, arthralgia. <10% skin detachment. Nikolsky sign is positive in erythematous areas - blisters and erosions appear when the skin is rubbed gently
Presentation toxic epidermal necrolysis
PC: sudden onset diffuse erythema with painful skin and eventual sloughing, >30% skin detachment
cause SJS and TEN
almost always drug related
Anti-epileptics: phenytoin, carbamazepine, lamotrigine
Antibiotics: penicillins
Antivirals
Allopurinol
NSAIDs
Sulfonamides
The OCP
Can also be caused by infection but is rare
Difference between SJS and TEN
SJS <10% skin detachment
TEN >30% skin detachment
Management SJS and TEN
Management:
Identify and stop causative agent
IV fluid management and wound care, usually in a burn unit.
Presentation erythema nodosum
PC: tender, erythematous nodular lesions over the shins (can be elsewhere). Resolves within 6 weeks
pathology erythema nodosum
inflammation of the subcutaneous fat
causes of erythema nodosum
infection
- TB
systemic disease
- sarcoidosis
- IBD
malignancy/lymphoma
drugs
- penicillins
- sulphonamides
- combined oral contraceptive pill
Approach to erythema nodosum
Approach:
Try to identify the underlying cause.
DHx: recent changes to drugs?
Investigation:
CXR for TB/sarcoidosis
what is erythroderma?
Erythroderma is a term used when more than 95% of the skin is involved in a rash of any kind.
causes erythroderma
eczema
psoriasis
drugs e.g. gold
lymphomas, leukaemias
idiopathic
trigger erythrodermic psoriasis
This may be triggered by a variety of factors such as withdrawal of systemic steroids.
management erythroderma
hospitalisation for monitoring and to restore fluid and electrolyte balance, circulatory status, and body temperature.
what is acute generalised exanthematous pustulosis?
Drug eruption
most often called by b lactam abx
presentation AGEP
PC: high fever, sterile pustules, oedema, similar to acute pustular psoriasis
Onset less than 4 days
presentation drug reaction with eosinophilia and systemic symptoms
Onset 15-40 days
PC: morbilliform, oedema, lymphadenopathy, purpura, scaling, maculopapular
onset DRESS
15-40 days
cause DRESS
drug eruption
Aciclovir
Sulfa drugs
management DRESS
Withdrawal of the drug +/- systemic steroids in severe cases
Supportive care: fluids, nutrition, electrolytes
Topical steroid and emollient dressings 50:50
Presentation erythema multiforme
PC: target lesions on back of or palms and soles → torso. The more severe form, erythema multiforme major is associated with mucosal involvement.
Cause erythema multiforme
Cause: hypersensitivity, most commonly triggered by infections
viruses: herpes simplex virus (the most common cause), Orf*
idiopathic
bacteria: Mycoplasma, Streptococcus
drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill, nevirapine
connective tissue disease e.g. Systemic lupus erythematosus
sarcoidosis
malignancy
management erythema multiforme
EM major requires discontinuing the offending agent and fluid
management, analgesics, wound care.
Although often given, systemic steroids are of unproven benefit.
what are the 5 childhood exanthems
1 measles
2 scarlet fever
3
4 rubella
5 erythema infectionosum (parvovirus)
6 roseola infantum
which of the childhood exanthems require school exlusion? how long for?
measles 4 days
rubella 5 days
scarlet fever 24 hours after abx
how does scarlet fever spread
Scarlet fever is spread via the respiratory route by inhaling or ingesting respiratory droplets or by direct contact with nose and throat discharges, (especially during sneezing and coughing).
what is scarlet fever
Scarlet fever is a reaction to erythrogenic toxins produced by Group A haemolytic streptococci (usually Streptococcus pyogenes).
epidemiology scarlet fever
It is more common in children aged 2 - 6 years with the peak incidence being at 4 years.
pathogen scarlet fever
streptococcus pyogenes
features scarlet fever
fever: typically lasts 24 to 48 hours
malaise, headache, nausea/vomiting
sore throat
‘strawberry’ tongue
rash
fine punctate erythema (‘pinhead’) which generally appears first on the torso and spares the palms and soles
children often have a flushed appearance with circumoral pallor. The rash is often more obvious in the flexures
it is often described as having a rough ‘sandpaper’ texture
desquamination occurs later in the course of the illness, particularly around the fingers and toes
features of the rash in scarlet fever
fine punctate erythema (‘pinhead’)
rough ‘sandpaper’ texture
plan ?scarlet fever
investigation
1. throat swab
management
empirical (dont wait until swab back)
1. oral penicillin V for 10 days
2. patients who have a penicillin allergy should be given azithromycin
what should chidlren with a penicillin allergy be given for scarlet fever?
patients who have a penicillin allergy should be given azithromycin
when can a child return to school scarlet fever
children can return to school 24 hours after commencing antibiotics
most common complication scarlet fever
otitis media
complications of scarlet fever
otitis media
rheumatic fever
acute glomerulonephritis
invasive complications e.g. bacteraemia, meningitis, necrotizing fasciitis
what is rheumatic fever
an autoimmune condition triggered by streptococcus bacteria. It is caused by antibodies created against the streptococcus bacteria that also target tissues in the body.
when does rheuamtic fever present vs infection
occurs 20 days after infection
incubation period scarlet fever
2-4 days
Jones criteria fir
The mnemonic for the Jones criteria is JONES – FEAR.
evidence of recent streptococcal infection, plus:
Two major criteria OR
One major criteria plus two minor criteria
Major Criteria:
J – Joint arthritis
O – Organ inflammation, such as carditis
N – Nodules
E – Erythema marginatum rash
S – Sydenham chorea
Minor Criteria:
Fever
ECG Changes (prolonged PR interval) without carditis
Arthralgia without arthritis
Raised inflammatory markers (CRP and ESR)
what systems and corresponding symptoms does rheuamtic fever affect
Joints
- arthritis (maj)
- arthralgia (min)
Skin
- nodules (maj)
- erythema marginatum (maj)
Heart
- carditis (maj)
- ECG Changes (prolonged PR interval) (min)
Neuro
- sydenham chorea
Invetsigation ?rheuamtic fever
- Throat swab for bacterial culture
- ASO antibody titres
- Echocardiogram, ECG and chest xray can assess the heart involvement
A diagnosis of rheumatic fever is made using the Jones criteria
complication rheuamtic fever
Recurrence of rheumatic fever
Valvular heart disease, most notably mitral stenosis
Chronic heart failure
how is rheuamtic fever managed
specialist
NSAIDs (e.g. ibuprofen) are helpful for treating joint pain
Aspirin and steroids are used to treat carditis
Prophylactic antibiotics (oral or intramuscular penicillin) are used to prevent further streptococcal infections and recurrence of the rheumatic fever. These are continued into adulthood.
Monitoring and management of complications
causative organism erythema infectionosum
Parvovirus B19
Presentation erythema infectionosum
mild fever, coryza, non-specific viral symptoms. After 2-5 days diffuse bright red rash on both cheeks (slapped cheeks). A few days later a reticular mildly erythematous rash affecting the trunk and limbs appears that can be raised and itchy. Reticular means net-like.
characteristic of rash erythema infectionosum
diffuse bright red rash on both cheeks
A few days later a reticular mildly erythematous rash trunk and limbs raised and itchy. Reticular means net-like.
management erythema infectionosum
Self limiting - symptoms usually fade over 1 – 2 weeks
who is at risk of complications erythema infectiosum
Immunocompromised pts, pregnant women and patients with haematological conditions such as sickle cell anaemia, thalassaemia, hereditary spherocytosis and haemolytic anaemia
most common complication erythema infectionosum
Aplastic anaemia - serology testing for parvovirus to confirm the diagnosis and checking of the full blood count and reticulocyte count for aplastic anaemia
when is erythema infectionosum contagious
It is infectious prior to the rash forming, but once the rash has formed they are no longer infectious and do not need to stay off school.
No school exclusion
presentation roseola infantum
high fever that lasts for 3-5 days then disappears. There may be coryzal symptoms, sore throat and swollen lymph nodes during the illness.WHEN THE FEVER SETTLES…, the rash appears for 1 – 2 days. The rash consists of a mild erythematous macular rash across the arms, legs, trunk and face and is not itchy.
incubation period roseola infantum
1-2 weeks
causative organism roseola infantum
HHV-6
management roseola ifnantum
Children make a full recovery within a week
main complication roseola infantum
febrile convulsions due to high temperature.
Immunocompromised patients may be at risk of rare complications such as myocarditis, thrombocytopenia and Guillain-Barre syndrome.
what is pityriasis rosea?
acute, self-limiting rash which tends to affect young adults. The aetiology is not fully understood but is thought that herpes hominis virus 7 (HHV-7) may play a role.
features pityriasis rosea
herald patch –> then erythematous, oval, scaly patches which follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer. This may produce a ‘fir-tree’ appearance
management pityriasis rosea
self-limiting - usually disappears after 6-12 weeks
what may be confused for pityriasis rosea
gittate psoraisis
what is bullous pemphigoid
autoimmune condition causing sub-epidermal blistering of the skin
presentation bullous pemphigoid
PC: itchy, tense blisters typically around flexures
the blisters usually heal without scarring
there is stereotypically no mucosal involvement (i.e. the mouth is spared)
investigation bullous pemphigoid
immunofluorescence shows IgG and C3 at the dermoepidermal junction
management bullous pemphigoid
referral to a dermatologist for biopsy and confirmation of diagnosis
oral corticosteroids are the mainstay of treatment
topical corticosteroids, immunosuppressants and antibiotics are also used
what is pemphigus vulgaris
an autoimmune disease caused by antibodies directed against desmoglein 3, a cadherin-type epithelial cell adhesion molecule. It is more common in the Ashkenazi Jewish population.
difference between bullous pemphigoid and pemphigus vulgaris
BP = no mucosal involvement
PV= mucosal involvement
in reality this isn’t clear cut
invetsiagtion pemphigus vulgaris
skin biopsy
acantholysis on biopsy
management pemphigus vulgaris
steroids are first-line
immunosuppressants
presentation pemphigus vulgaris
PC: mucosal ulceration is common and often the presenting symptom. Oral involvement is seen in 50-70% of patients
skin blistering - flaccid, easily ruptured vesicles and bullae. Lesions are typically painful but not itchy. These may develop months after the initial mucosal symptoms. Nikolsky’s describes the spread of bullae following application of horizontal, tangential pressure to the skin
presentation chicken pox
widespread, erythematous, raised, vesicular (fluid filled), blistering lesions. The rash usually starts on the trunk or face and spreads outwards affecting the whole body over 2 – 5 days. Eventually the lesions scab over, at which point they stop being contagious.
Fever is often the first symptom
Itch
General fatigue and malaise
infectivity of chicken pox, when? how?
Chickenpox is highly contagious and spread through direct contact with the lesions or through infected droplets from a cough or sneeze. Patients become symptomatic 10 days to 3 weeks after exposure. The stop being contagious after all the lesions have crusted over.
complications chicken pox
Bacterial superinfection
Dehydration
Conjunctival lesions
Pneumonia
Encephalitis (presenting as ataxia)
what increases the risk of bacterial superinfection chicken pox
NSAIDs
when is aciclovir used for chicken pox
immunocompromised patients, adults and adolescents over 14 years presenting within 24 hours, neonates or those at risk of complications.
management of itch in chicken pox
calamine lotion and chlorphenamine (antihistamine).
infection control chicken pox
Patients should be kept off school and avoid pregnant women and immunocompromised patients until all the lesions are dry and crusted over. This is usually around 5 days after the rash appears.
pathogen hand foot and mouth
intestinal viruses of the Picornaviridae family (most commonly coxsackie A16 and enterovirus 71)
clinical features hand foot and mouth
mild systemic upset: sore throat, fever
oral ulcers
followed later by vesicles on the palms and soles of the feet
management hand foot and mouth disease
symptomatic treatment only: general advice about hydration and analgesia
reassurance no link to disease in cattle
children do not need to be excluded from school
the HPA recommends that children who are unwell should be kept off school until they feel better
they also advise that you contact them if you suspect that there may be a large outbreak.
infection control hand foot and mouth
children who are unwell should be kept off school until they feel better
what is molloscum contagiosum
skin infection caused by molluscum contagiosum virus (MCV), a member of the Poxviridae family.
how does molloscum contaginosum spread
directly by close personal contact, or indirectly via fomites (contaminated surfaces) such as shared towels and flannels.
epidemiology molloscum contagiosum
children (often in children with atopic eczema), with the maximum incidence in preschool children aged 1-4 years
presentation molloscum contagiosum
characteristic pinkish or pearly white papules with a central umbilication,
which are up to 5 mm in diameter. Lesions appear in clusters in areas anywhere on the body (except the palms of the hands and the soles of the feet). In children, lesions are commonly seen on the trunk and in flexures, but anogenital lesions may also occur. In adults, sexual contact may lead to lesions developing on the genitalia, pubis, thighs, and lower abdomen. Rarely, lesions can occur on the oral mucosa and on the eyelids.
mamagement molloscum contagiosum
Reassure people that molluscum contagiosum is a self-limiting condition.
Spontaneous resolution usually occurs within 18 months
Encourage people not to scratch the lesions. If it is problematic, consider treatment to alleviate the itch
If lesions are troublesome or considered unsightly, use simple trauma or cryotherapy
infection control molloscum contagiosum
sensible to avoid sharing towels, clothing, and baths with uninfected people (e.g. siblings)
Exclusion from school, gym, or swimming is not necessary
what is eczema herpeticum
Viral skin infection in patients with eczema caused by the herpes simplex virus (HSV) or varicella zoster virus (VZV)
pathogen eczema herpeticum
Herpes simplex virus 1 (HSV-1) is the most common causative organism
can also be caused by VZV
presentation eczema herpeticum
widespread, painful, vesicular rash with systemic symptoms such as fever, lethargy, irritability and reduced oral intake. There will usually be lymphadenopathy (swollen lymph nodes).
in a pt with eczema
plan ?eczema herpeticum
Viral swabs of the vesicles can be used to confirm the diagnosis, although treatment is usually started based on the clinical appearance.
Treatment is with aciclovir. A mild or moderate case may be treated with oral aciclovir, whereas more severe cases may require IV aciclovir.
abx for bacterial superinfection if req
can be v ill and LT if not treated properly
presentation rosacea
typically affects nose, cheeks and forehead
flushing is often first symptom
telangiectasia are common
later develops into persistent erythema with papules and pustules
rhinophyma
what makes rosacea worse
sunlight
occular involvement rosacea?
blepharitis
management rosacea
simple measures
- sunscreen
- camouflage creams
predominant erythema/flushing:
- topical brimonidine
mild-to-moderate papules and/or pustules:
- topical ivermectin
moderate-to-severe papules and/or pustules:
- topical ivermectin + oral doxycycline
what is brimonidine
topical alpha-adrenergic agonist
this can be used on an ‘as required basis’ to temporarily reduce redness
it typically reduces redness within 30 minutes, reaching peak action at 3-6 hours, after which the redness returns to the baseline
when should you rf someone w rosacea
- if symptoms have not improved with optimal management in primary care
(laser therapy may be appropriate for patients with prominent telangiectasia) - patients with a rhinophyma
what is rhinopyma
disfiguring nasal deformity due to the proliferation of sebaceous glands and underlying connective tissue
what is shingles?
Shingles (herpes zoster infection) is an acute, unilateral, painful blistering rash caused by reactivation of the varicella-zoster virus (VZV). Following primary infection with VZV (chickenpox), the virus lies dormant in the dorsal root or cranial nerve ganglia.
features shingles
Features
prodromal period
burning pain over the affected dermatome for 2-3 days
pain may be severe and interfere with sleep
around 20% of patients will experience fever, headache, lethargy
rash
initially erythematous, macular rash over the affected dermatome
quickly becomes vesicular
characteristically is well demarcated by the dermatome and does not cross the midline. However, some ‘bleeding’ into adjacent areas may be seen
most commonly affected dermatomes shingles
The most commonly affected dermatomes are T1-L2.
management shingles
- remind patients they are potentially infectious
may need to avoid pregnant women and the immunosuppressed
should be advised that they are infectious until the vesicles have crusted over, usually 5-7 days following onset
covering lesions reduces the risk
+ anaglgesia
paracetamol and NSAIDs are first-line
if not responding then use of neuropathic agents (e.g. amitriptyline) can be considered
oral corticosteroids may be considered in the first 2 weeks in immunocompetent adults with localized shingles if the pain is severe and not responding to the above treatments
+ antivirals
within 72 hours for the majority of patients, unless the patient is < 50 years and has a ‘mild’ truncal rash associated with mild pain and no underlying risk factors
one of the benefits of prescribing antivirals is a reduced incidence of post-herpetic neuralgia, particularly in older people
aciclovir, famciclovir, or valaciclovir are recommended
complication shingles?
post-herpetic neuralgia
the most common complication
more common in older patients
affects between 5%-30% of patients depending on age
most commonly resolves with 6 months but may last longer
