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Rashes + skin infections Flashcards

1
Q

Describe this rash.
What condition does it relate to?

A

Chicken pox
Develops from red bumps, to fluid-filled blisters to crust and scabbed lesions - common on scalp, face and middle of the body.

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2
Q

What is chicken pox?

A

An acute disease, predominantly in childhood, caused by varicella-zoster virus.
The virus can persist in the sensory nerve ganglia of the dorsal root.
Can reactivate and cause shingles.

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3
Q

What are the clinical features of chicken pox?

A

Incubation period: 10-20 days
Fever initially, general signs of bacterial infection (myalgia, pain, loss of appetite)
Itchy rash starting of head/trunk before speading, intially macular then papular then vesicular
Systemic upset is usually mild

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4
Q

What is the transmission of chickenpox like?

A

Personal contact or airborne spread
Incubation - 2-3weeks
Infections from 2 days before rash until vesicles are dry/crusted over usually 5-7days after onset.

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5
Q

What are some common complications of chicken pox?

A

bacterial skin infection - young children
Lung involvement - adults - varicella pneumonia
Pregnancy -> severe maternal chickenpox and foetal varicella syndrome
Immunocompromised -> disseminated with varicella pneumonia, encephalistis, heaptitis and haemorrhagic complications.

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6
Q

How do we treat the symptoms of chicken pox?
When and what antiviral might be considered?

A

High risk individual and their close contacts can receive a two stage vaccination programme.
Antiviral medication - aciclovir ( if present within first 24hrs of rash),
Paracetamol
Shingles - antiviral tends to be aciclovir, NSAIDs, amitriptyline, oral corticosteroids

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7
Q

What condition has this type of rash?

A

Bacterial meningitis - commonly meningococcal septicemia
Starts as small pink/purple pinpricks and spreads into larger purple/pink blotches
Is a non-blanching rash.

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8
Q

What is the relevant epidemiology and prognosis of bacterial meningitis?

A

Life-threatening conditions
Most common in babies and children
UK 1 per 100,000
4-10% fatality in children and 25% mortality in adults.

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9
Q

What is the transmission route of bacterial meningitis?

A

Close contracts
Droplets
Direct contact with secretion

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10
Q

What are the clinical features of bacterial meningitis?

A

Symptoms - neck stiffness, vomitting, headache, altered consciousness, fever, photophobia, non-blanching rash and seizures.
Signs - kernigs test, brudzinski test.

Neonates - non specific - hypotonia, poor feeding , lethargy, hypothermia and bulging fontanelle.

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11
Q

What are the two common types of meningitis?

A

Neisseria meningitidis - menigococcus - can cause meningococcal septicemia resulting in the rash
Streptoccocus pneumoniae - pneumococcus
Neonates - Group B strep from vaginal canal.

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12
Q

In the community what should you do for a child with suspected meningitis?

A

If suspected and non-blanching rash adminstered urgent/STAT IM?IV benzypenicillin prior to urgent hospital transfer.

Only do not give if true penicillin allergy, then transfer immediately to hospital.

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13
Q

How common are complications from meningitis?
What are these complications?

A

Pneumococcal = 30%
Meningococcal = 7%
Include hearing loss, seizures+epilepsy, cognitive impairment and learning disability, memory loss, cerebral palsy (focal neurological deficit such as limb weakness or spasticity)

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14
Q

What factors affect the prognosis of bacterial meningitis?

A

Age - higher fatality at extremes
The causative organism
Presence of comorbidities
Severity of presentation

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15
Q

What conditions has this rash?

A

Erythema multiforme

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16
Q

Describe the rash seen in erythema multiforme.

A

Widespread, itchy, erythematous rash.
Norm on hands/feet then spreads to the tummy, chest, back or face.
Does not norm affect mucous membranes but can cause a sore mouth (stomatitis).
Typically self resolves within 1 to 4 weeks.
Typical ‘target lesion’ appearance - darkest red at centre

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17
Q

What is the typical cause of erythema multiforme?

A

Cutaneous type 4 hypersensitivity reaction
Usually caused by infection: herpes simplex virus or mycoplasma pneumonia.
Drug sensitivities: sulphonamides, barbiturates, antibiotics.

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18
Q

What is the treatment for erythema multiform typically like?

A

Treatment of the rash is normally not required.
Treatment of the underlying cause typically allows resolution of the rash.

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19
Q

What is impetigo?

A

A common superficial bacterial infection of the skin, norm cause of staphylococcus resulting in a golden crust.
Highly contagious
There are two main types: non-bullous and bullous impetigo.

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20
Q

What are the common complications of impetigo?

A

Usually mild
Complicates are rare - glomerulonephritis and cellulitis.

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21
Q

What is the difference between non-bullous and bullous impetigo?

A

Non-bullous - around nose or mouth, exudate from lesions forms a dry gold crust, no system symptoms

Bullous - also staph, aureus, epidermolytic toxins break down proteins in the skin, causes fluid filled vesicles to form on the skin, these grow and burst forming golden crust. Painful and itchy. Often have systemic symptoms. Severe = scalded skin syndrome

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22
Q

What is the relevant stats epi,prog and prev surrounding impetigo?

A

Affects all age groups - most common in young children
Up to 3% of up to eyrs and up to 1.5% of 5-15yrs.

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23
Q

How is impetigo managed in primary care?

A

Highly contagious - children should be off school.
Non-bullous - topical fusidic acid, anti-septic cream (hydrogen peroxide 1%)
Oral flucloxacillin if more severe

Bullous - flucloxacillin IV or oral.

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24
Q

What conditions is this rash indicative of?

A

Impetigo

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25
Describe the impetigo rash
Typically yellow/golden crusts around the mouth /nose Bullous - more vesicles that them become golden crusts Sever presentation - scalded skin syndrome.
26
What is Lyme disease?
Infections by bacteria Borrelia Burgdorferi, transmitted from a bite from an infected bite.
27
What disease is this rash typical off?
Lymes disease
28
Describe the rash seen in Lymes disease
Bullseye rash appearance - erythema migrans. Norm at foot/ankle = site of bite. Start 2/2.5 inches then grows. Usually appears within 3 to 4weeks of the bite, but can take up to four months. Often alongside fever, joint pain, fatigue, and headache.
29
What are some complications of Lymes disease?
Bells Palsy Pericaridits Heart Block
30
How should erythema migrans/lymes disease be treated?**
No focal symptoms -> oral doxycyline Focial symptoms/neurological complaints -> ceftriaxone if disseminated disease Lyme disease 12yrs+ = Doxycycline 100mg BD for 21 days.
31
What disease is this rash indicative of?
eczema herpeticum
32
How does herpes simplex virus affect eczema rash? How does this present?
HSV - super added infection Appears as grouped vesicles and punched-out erosion within areas of particularly flared eczema. If disseminate can cause widespread lesion that combined to give large, denuded and bleeding areas. Can be further complicated by staph or strep.
33
What are the clinical features of eczema herpeticulum?
Secondary HSV infection on top of eczema or dermatitis. Can be triggered by trauma or cosmetic procedures. After 5-12days from exposure - rapidly worsening and painful eczema. Vesciular - blood stained, clear or yellow Punched out erosion Possible fever, lethargy, lymphadenopathy or distress. Need to be cautious of eye involvement. Viral or bacterial swab from one of the blisters can confirm the infection.
34
How severe is eczema herpeticum?
Medical emergency Especially in children under 2yrs of age Should be managed with immediate hospital admission.
35
What are some risk factors for eczema herpeticum?
Severe atopic skin disease - eczema, dermatitis. Burns, friction, chemical exposure to skin.
36
What conditions aligns with this skin change?
Cellulitis
37
Describe the skin changes seen in cellultitis
Swelling, erythema, warmth and tenderness are the common hallmarks of a cellulitis infection. usually unilateral - commonly on the shin Often well defined regions - can spread Systemic upset - fever, malaise, nausea.
38
What are the signs and symptoms of cellulitis?
Hallmark - swelling, erythema, warmth and tenderness. Commonly unilateral with well defined but enlarging borders, may have blisters and bullae in more severe disease. Often have systemic upset such as fever, malaise and nausea.
39
What is cellulitis?
Bacterial infection of the dermis and deeper subcutaneous tissues Commonly streptococcus pyrogenes or staphylococcus aureus. Often, they enter due to disruptions in the cutaneous barrier
40
What are the risk factors for cellulitis?
Trauma Ulceration Obesity In patients with reduced sensation (Diabetic Neuropathy) or reduced circulation (CHF) Venous insufficiency or PAD Lymphoedema Pregnancy Alcoholism Skin conditions that disrupt the integrity of the skin barrier - eczema, venous ulcers, psoriasis
41
When should a patient with cellulitis be admitted?
1. Severe cellulitis with systemic symptoms (fever, low BP) 2. More vulnerable to life-threatening infection - very young and frail or co-morbidities.
42
What is the management of uncomplicated cellulitis in primary care?
Offer oral antibiotic treatment - the first line tends to be flucloxacillin or co-amox if near nose/eyes. Paracetamol or ibuprofen for pain +/- fever. Drink adequate fluids Elevate leg for comfort and to relieve oedema (where applicable) Avoid compression garments Safety net to reasses if worsens rapidly or significantly at any time or does not start to improve within 2-3 days.
43
What is necrotizing fasciitis?
Destructive and rapidly progressive soft tissue infection - involves the deep subcunteanous tissue and fascia (occasionally muscles) Characterised by extensive necrosis and gangrere of the skin and underlying structures. Life-threatening
44
What are the common complications of necrotising fasciitis?
High mortality rate (30%) Sepsis Amputation Severe scarring and disfigurement
45
What are some risk factors for necrotising fasciitis?
Diabetes mellitus Trauma (external injuries or surgical wounds) Immunosuppressive drugs (prednisolone) Peripheral vascular disease.
46
What are the different types of necrotising fasilitis?
Type 1 - polymicrobial - multiple anaerobic species - norm trunk or perineum 70-90% of cases Type 2 - monomicrobial - streptococcus pyogenes - younger patients and limbs Type 3 - monomicrobial - clostrididum or virbrios - IV drug use Type 4 - fungal - candida - immunocompromised patients, particularly aggressive and extensive.
47
How does necrotising fasiitis commonly present?
Early clinical features: swelling (80%), pain (79%), erythema (70%), intubation. Characterised: pain that is severe and exaggerated compared to what would normally be suspected from a soft tissue infection. (may suside as disease progresses and nerve endings are destroyed) Common - rapid progression, blistering, bullae, grey/dusty skin = necrosis, D&V, sepsis, skin crepitus. failure to response to broad spec antibiotics.
48
What is the typical management of necrotising fasciitis?
Surgical debridement - inc fasciotomy - early as possible - continue until healthy tissue is found Antibiotic - depdent on organism - often broad spec anaerobic and gram neg - IV flucloxacillin, benzylpenicillin, metronidazole, clindamycin, gentamicin.
49
What conditions does this appearance indicate?
necrotising fascitis
50
Describe the skin changes seen in necrotising fasciitis?
Open skin wound Severe pain Fever, confusion, weakness, diarrhoea early skin erythema, quickly spreading in horse to days Skin redness to purple discoloration Gangrenous skin changes Loosening of skin and subcutaneous skin in association with deep fascial necrosis.
51
What is the management for eczema herpeticum?
1st line - Oral aciclovir - five daily for 10-14/7 2nd line - valaciclovir twice daily for 10-14days If vomiting or unable to take tables - IV acicilovir. If ocular - Ganciclovir ointment.
52
What are the two main types of necrotizing fasciitis?
Type 1 - anaerobes (bacterioides) and aerobes (S. aureus) common in co-morbid, elderly Type 2 - streptococcus pyogenes (group A strep) - younger healthy patients with a Hx of trauma - release of tozin by S.pyogenes means more likely to present with septic shock
53
How does a disseminated infection occur from necrotizing fasciitis?
Tissue necrosis at infected site enables access into blood stream leading to a systemic response.
54
What is at an increased risk of necrotizing fasciitis?
Immune suppression High number of tissue wounds Commonly: Diabetes and IVDU
55
What 2 clinical features will distinguish NF from cellulitis?**
NF - pain is disproportionate to clinical symptoms NF - more likely to have large bulla, potential haemorragic When inspecting wound may identify deeper layers such as underlying muscle - gangrenous appearance (black, foul odour)
56
What investigations should be done for necrotising fasciitis?
Bedside: obs, wound swab Bloods: FBC, U&Es, CRP, blood cultures (high risk of septicaemia), lactate (tissue necrosis),likely ABG/VBG Imaging: USS leg
57
Why is an ultrasound leg done in necrotising fasciitis?
1. identify fluid tracking along the deep fascial layers - differentiate from cellulitis 2. Rule out DVT 3. Assess for possible foreign bodies 4. identify fascila thickening, abnormal fluid and subcutaneous air - may help guide where to take fluid aspiration to aid diagnosis.
58
What is gas gangrene?
A form of necrotising fasciitis caused by clostridium species (C.perfringens) Bacteria produce gas within the tissue -> get tissue crepitus on light palpiation
59
What classification system is used to classify cellulitis?
Eron classification Stage 1 - no systemic signs, no uncontrolled co-morbs Stage 2 - systemically unwell or co-morbd that may comp/delay resolution Stage 3 - significant systemic upset, unstable co-morb interfere with response or life threatening infection due to vascular compromise Stage 4 - sepsis syndrome or a severe life-threatening infection such as necrotizinf fasciitis. stage 3/4 and sometimes stage 2 are hospitalised
60
What is the relevant treatment of cellulitis based on the Eron classification?
Class 1 - oral fluclox as first line, oral clarithromycin/erythromycin as second line Class 2 - may need admission check local guidelines Class 3/4 - admit and offer oral/IV co-amox or clindamycin

Med 1 Block (39 decks)

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