Cellulitis; Pressure Sores; Head lice; Folliculitis; Contact Dermatitis Flashcards
What are the different classes of cellulitis
Class I:
- There are no signs of systemic toxicity and the person has no uncontrolled co-morbidities
Class II:
- The person is either systemically unwell or systemically well but with a co-morbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection
Class III:
- The person has significant systemic upset such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize
Class IV:
- The person has sepsis syndrome or a severe life-threatening infection such as necrotizing fasciitis
Which patients do you admit for cellulitis? [6]
- Has Eron Class III or Class IV cellulitis.
- Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
- Is very young (under 1 year of age) or frail.
- Is immunocompromized.
- Has significant lymphoedema.
- Has facial cellulitis (unless very mild) or periorbital cellulitis.
Describe how you manage Eron Class I / II cellulitis [1]
- oral flucloxacillin as first-line treatment for mild/moderate cellulitis
- oral clarithromycin, erythromycin (in pregnancy) or doxycycline is recommended in patients allergic to penicillin.
How do you manage Class III/IV Cellulitis? [2]
Eron Class III-IV
* admit
* NICE recommend: oral/IV co-amoxiclav, oral/IV clindamycin, IV cefuroxime or IV ceftriaxone
General points
* mark the area of erythema to detect spreading cellulitis
* if possible elevate the leg
* consider paracetamol or ibuprofen for pain or fever
Flucoxacillin
Co-amoxiclav
Define what is meant by a pressure sore [1]
Localised injuries to the skin and underlying tissue due to prolonged pressure
Describe the pathophysiology of pressure sores [3]
sequence of events initiated by unrelieved pressure:
- Ischaemia: when external pressure exceeds capillary closing pressure, it leads to occlusion of blood vessels causing ischaemia in the affected area. This deprives tissues of oxygen and nutrients leading to cell death and necrosis.
- Reperfusion injury: Upon relief from sustained pressure, reperfusion occurs. However, this sudden influx of blood can cause further damage due to oxidative stress and inflammation.
- Tissue distortion: Continuous mechanical stress can distort and damage cells directly.
Describe the stages in the development of pressure sores [4]
Non-blanchable erythema::
- Initial presentation involves reddening of the skin that does not turn white (non-blanchable) when pressed.
- The affected area may feel differently than surrounding skin – warmer or cooler, firmer or softer.
Partial-thickness skin loss:
- With continued pressure, there is partial-thickness loss involving epidermis or dermis.
- It presents as a shallow open ulcer with a red-pink wound bed without sloughing.
Full-thickness skin loss:
- Prolonged unrelieved pressure results in full-thickness tissue loss exposing subcutaneous fat but not muscle or bone. Slough may be present along with undermining or tunneling.
Full-thickness tissue loss with exposed bone, muscle or tendon:
- This is the most severe form of pressure sore where there is extensive destruction and necrosis extending to underlying structures.
Beyond the 4 stages of pressure sores, what two categories of pressure sore exist? [2]
Unstageable Pressure Sores:
- This classification is used when the base of the ulcer is covered by slough (yellow, tan, grey, green or brown) and/or eschar (tan, brown or black) in the wound bed, making it impossible to determine its depth.
Suspected Deep Tissue Injury (SDTI):
- SDTI is characterised by a purple or maroon localised area of discoloured intact skin or a blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue.
What investigations do you perform for pressure sores? [3]
Wound Swab
FBC; U&E; CRP & albumin levels
Radiological imaging - if ?osteomyelitis
Which score / scores are used to identify patients at risk of pressure sores? [2]
Braden or Waterlow scale
How do you prevent / manage pressure sores [4]
Regular repositioning every 2 hours for bed-bound patients and hourly for those in chairs.
Maintain skin integrity by keeping skin clean and dry. Use mild soap and warm (not hot) water for cleaning
Dressings:
- Alginate dressings are useful for exuding wounds;
- Hydrocolloid dressings can be used for non-exuding wounds.
Administer analgesics as required. Regularly reassess pain levels.
Long-standing pressure sores can occasionally give rise to [] - a type of squamous cell carcinoma.
Cancerous changes: Long-standing pressure sores can occasionally give rise to Marjolin’s ulcers - a type of squamous cell carcinoma.
In addition to the typical presentations of head lice, there are other possible features associated with head lice infestation:
Secondary bacterial infection:
- Persistent scratching can lead to excoriation and subsequent bacterial superinfection, manifesting as impetigo or cellulitis.
Cervical lymphadenopathy:
- Swollen lymph nodes in the neck area may occur due to local inflammatory response or secondary infection.
Psychological distress:
- Patients, particularly children, may experience embarrassment, anxiety or sleep disturbances due to the infestation.
One of the primary challenges in diagnosing head lice (Pediculus humanus capitis) lies in distinguishing it from other conditions that present with similar symptoms, such as itching and visible evidence on the scalp.
What are the main three differential diagnoses? [3]
seborrhoeic dermatitis, dandruff, and folliculitis.
How do you differentiate head lice to seborrhoeic dermatitis, dandruff, and folliculitis?
seborrhoeic dermatitis:
- Redness, greasy or oily areas of skin, white or yellowish crusty scales
- head lice itchier
Dandruff
- White flakes on shoulders of dark clothing, itchy scalp.
Folliculitis
- Red and inflamed hair follicles, pus-filled blisters that break open and crust over.
- Typically more painful than pruritic
Which pathogen is the most common cause of follicullitis? [1]
Staphylococcus aureus
Describe the basic pathophysiology of follicultiis
- Bacterial colonisation within the hair follicle (especially if there is any damage or disruption to skin barrier)
- An inflammatory response is triggered; leads to follicular wall rupture causing it to break down and release its contents (including bacteria) into the surrounding dermis.
- Leads to a cycle of ongoing tissue damage and repair
Asides from pain, itching and small red inflamed papules, what is a key localised symptom seen in folliculitis? p[1]
Follicular hyperkeratosis: This describes thickening or roughness of the skin surrounding the hair follicle, which can be a feature in chronic cases.
Name this subtype of folliculitis [1]
Pseudofolliculitis barbae: This is a specific type of folliculitis that commonly affects men with curly hair.
- It presents as inflammation and bumps in the beard area due to ingrown hairs.
Hot tub folliculitis is associated with an infection from which pathogen? [1]
Pseudomonas aeruginosa:
- It typically presents as a sudden onset of widespread follicular-based papules and pustules, often on the trunk and limbs.
What is the name for this form of folliculitis? [1]
Folliculitis decalvans
- A chronic form of deep folliculitis that leads to scarring and permanent hair loss, usually on the scalp. Patients may present with painful, red plaques containing pustules around hair follicles.
How do you differentiate acne vulgaris to folliculitis?
Acne vulgaris predominantly affects the face and upper trunk where there is a high density of sebaceous glands.
folliculitis can occur anywhere on the body where hair follicles are present.
