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.
