Dermatology Diagnosis+management Flashcards
Skin layering
Epidermis: outermost layering made of thin sheet of stratified squamous epithelium. As cells differentiate and migrate upwards in strata their nuclei are replaced by keratin. outermost layer is called the stratum corneum.
Dermis: deep to epidermis. Thicker and made up largely of connective tissue. Contains papillary (upper) and reticular (lower) layer as well as network of nerves and nerve endings for sensation of pain, pressure, touch and temperature. Also muscle fibres (erector pili), hair follicles, sweat glands and sebaceous glands and many blood vessels.
Papillary layer: upper region of dermis with rows of dermal papillae. Help bind skin layers together and also form ridges on fingertips and skin on palms of hands and feet forming your footprint and fingerprint. Patterns are unique to each individual.
Reticular layer: lower dermis filled with network of interlacing fibres (mostly collagen making skin tough) and also elastin fibres (reduce with age causing wrinkles)
Hypodermis: subcutaneous layer supports layers of skin: made of loose connective tissue and fat. Helps regulate temperature and serves as a store for energy sources. Also acts as a shock absorbing pad helping protect underlying tissue areas.
Outer layer dead dry cells sloughed off
External dead cells constantly separating from skin (desquamation) 4kg/year!
Each surface cell lasts 28 days then sheds and is replaced
Functions of skin
protective barrier; temp regulation; sensation; Vit D synth; immunosurveillance; UV protection; prevents moisture loss
Skin cell types and functions
Keratinocytes
Produce keratin as protective barrier
Langerhans cells
Present antigens and activate T lymphocytes for immune protection
Melanocytes
Produce melanocytes for skin pigmentation and protection from UV radiation damage
Merkel cells
Contain specialised nerve endings for sensation
Epidermal layers
Stratum basale (Basal cell layer) Actively dividing cells, deepest layer
Stratum spinosum (Prickle cell layer) Differentiating cells
Stratum granulosum (Granular cell layer) So called as they lose their nuclei and contain granules of keratohyalin. Secrete lipid into intracellular spaces
Stratum corneum (Horny layer) Layer of keratin, most superficial layer
Dermal neoplasia types
Non-malignant (BCC; SCC)
malignant melanoma
Actinic keratoses (premalignancy)
Identifying skin cancers
BCC: pearly/waxy bump or flat brown lesion; most easily treated and unlikely to spread
SCC: firm red pimple/nodules or scaly patch NOT SHIN. easily treated if detected early but more likely to spread than BCC
Melanoma: existing mole that bleeds, itches or changes shape/colour with large brownish patches or smaller spot with black/red or white patches. most serious form needs immediate diagnosis as later is difficult to treat and spreads easily
BCC and cause
> 75% skin cancers UK
Locally invasive but rarely metastasize due to slow growth
Slow and irregular growth (subclinical finger-like outgrowths)
Metastases can occur in larger tumours: 2% if diameter >3cm; 50% if diameter >10cm
Aetiology:
Unknown
More common on areas of chronic sun exposure such as face, head and neck
Thought to arise from hair follicles
EPIDEMIOLOGY:
Uncommon in dark skin
Most common cancer in EU, australia and US
BCC risk factors
Genetics UV exposure esp. In childhood Previous BCC Increasing age Male sex: this gap increases with age also Skin types I and II
BCC presentation and types
Usually head, neck area
Nodule with indurated edge (pearl), telangiectasia and ulcerated centre (rodent ulcer)
Types:
Nodular: classic. Solitary shiny red nodule. Can be cystic or ulcerated
Superficial: often multiple on upper trunk and shoulders
Morphoeic: sclerosing or infiltrative BCC
Pigmented: brown, blue or greyish in colour
Baso-squamous
BCC investigations and diagnosis
Refer all suspicious lesions
Biopsy must be done to confirm before treatment commences
CT/MRI for larger or deeper cases where bony involvement is suspected or where tumour may have invaded major nerves, orbit or parotid gland
Diagnosis:
Clinical exam
Exisional biopsy
BCC differentials
Intradermal naevus Sebaceous hyperplasia Fibrous papule Molluscum contagiosum Keratocanthoma
BCC management
Surgical removal (excision + 4mm margin)
Curettage and cautery/electrodesiccation
Cryotherapy/cryosurgery
Imiquimod 5% cream
Fluorouracil (5FU) 5% cream
PDT (light therapy + a topical photosensitising agent»_space; to destroy cancer cells)
Radiotherapy (RT): incomplete excision, recurrent BCC, nodular BCC of the head and neck under 2 cm, and BCC with invasion of bone or cartilage
Prognosis:
Recurrence rate about 5%
Actinic keratosis
Keratoses: thickened skin
Solar/Actinic: sunlight induced
Pathophysiology:
Sun damaged skin over years
UV induced DNA damage leads to dysplastic intra-epidermal proliferation of atypical keratinolcytes
Non- contagious
Epidermiology:
Rare in UK <40 years
More common in elderly, fair skinned, blue eyed red/blonde haired individuals
More common in men
More common in those working outdoors, sunbathers, sunbed use, recreational activities
AK presentation
Sun exposed areas: face, ears, lips, bald scalp, forearms, back of hands, lower legs
Variable appearance even with multiple lesions on same individual
Rough sandpaper like feel
Skin coloured, pink, reddish brown colour
Thick scaly, warty layer (yellow white scaly crust)
Can be itchy
Grade:
Slightly palpable (better felt than seen)
Moderately thick (easily felt and seen)
Very thick, hyperkeratotic and/or obvious
May also be field damage: large areas of multiple AKs on background of erythema and sun damage
AK progression
Small risk of SCC
Generally more risk of all skin cancer types
Increased risk in pts. Who have numerous AK patches or those on immunosuppresive drugs for other conditions
AK may not convert to SCC or cancers
May regress but may also recur
2WW dermal referral red flags and non urgent referral
Recent growth Recent tenderness Recent inflammation Nodular lesion/lump Bleeding Ulceration Lesions on lips
Non-urgent referral: Diagnostic uncertainty Widespread or numerous patches Severe actinic damage Immunosuppressed pts. Very young pts presenting with AK (xeroderma pigmentosum)
AK diagnosis and differentials
Diagnosis:
Clinical exam; ideally with dermatoscope
Biopsy if in doubt
Differentials:
BCC; SCC (indurated nodular lesions but more rapid growth tend to be eroded or ulcerated)
Seborrhoeic keratosis (greasy brown crusts with sharply demarcated borders and non-erythematous base, areas not exposed to sun)
Bowen’s disease
Amelanotic melanoma
Discoid lupus erythematosus (abnormal pigmentation, dilated follicles and atrophy)
Psoriasis
AK management
Advise: limit sun exposure; sun protection all day all times of year; pre-canceous lesion; safety net vigilance and report skin changes
Creams: 5-fluorouracil, 5FU (cytotoxic)
Imiquimod (CMI↑)
Diclofenac (unknown mechanism)
Retinoic acid (regulate the differentiation and growth of keratinocytes, anti-aging, …)
Cryotherapy: causes no scarring, but is painful Photodynamic therapy (PDT) >> better than cryo., but useful for single lesions
Surgical excision»_space; assessment of the whole lesion but leaves scar, may recur in surrounding damaged tissues
Prevention
Education ›››› Hats - Long sleeves – Sunscreens (SPF>30)
SCC
Malignant tumour of skin
Arises from keratinising cells of epidermis or it’s appendages
Locally invasive and metastasis often (fast growing)
Epidemiology:
2nd most common skin cancer (after BCC)
20% non melanoma skin cancers caused by SCC and 80% by BCC
Incidence is rising worldwide
SCC risk factors
Chronic UV exposure
Susceptibility to sun exposure: fair skin, blonde/red hair
Ionising radiation exposure
Chemical carcinogens: arsenic and chromium, soot, tar and pitch oils
HPV infection
Immunodeficiency
Chronic inflammation: near chronic ulcers, around chronic sinuses etc.
Premalignant conditions such as Bowen’s disease or Actinic keratoses
SCC presentation
Variable appearance
Typically non-healing ulcer or growth in sun exposed areas of head and neck
Indurated keratinising or crusted nodule with/without ulceration
Slow growing ulcer without keratinisation
Slow growing reddish plaque
SCC may make local metastases or spread to local lymph nodes
SCC differentials
Keratoacanthoma (can be difficult to differentiate even histologically).
BCC.
Malignant melanoma (particularly amelanotic malignant melanomas).
Solar keratosis.
Pyogenic granuloma.
Seborrhoeic warts (especially if traumatised or infected).
Plantar warts or Verrucas (Periungual SCC)
SCC investigations/ diagnosis
Clinical exam
Excisional biopsy (+safe margin) in small lesions, not cosmetically sensitive areas or near to vital structures
Incisional biopsy (punch biopsy) for large lesions in cosmetically sensitive areas or near vital structures
Enlarged nodes LAP: FNA or excisional biopsy
CT/ MRI bone or soft tissue spread, cervical lymph nodes, perineural invasion
TNM staging for SCC
Stage 0/Tis: primary tumour carcinoma is in situ; no regional LN metastases or distant
Stage 1/T1: tumour <2cm; no regional or distant metastases
Stage 2/T2: tumour between 2-5cm; no local or distant metastases
Stage 2/T3: tumour >5cm
Stage 3/T4: tumour invading deeper extradermal structures OR any stage with regional lymph node spreading
Stage 4: any stage with distant metastases
SCC management
Referral of suspicious SCC (urgent 2ww) Excisional biopsy +/- LAPs Curettage and cautery/electrodesiccation Cryotherapy/cryosurgery Pomade/Cream/Gel: Imiquimod cream, Fluorouracil cream, Diclofenac gel Photodynamic therapy (PDT) Electrochemotherapy Radiotherapy Mohs' micrographic surgery
Pigmentation pathology
Melanocytes found in equal number in black and white skin
However in black skin produce much more melanin
Results in darker pigmentation; greater UV protections
Non-cancerous growth of melanocytes results in MOLES (benign melanocytic naevi) and freckles (ephelides and lentigines)
Malignant melanoma
Malignant melanoma more common in women
Much less common than non-melanoma skin cancers (SCC, BCC)
Rare in children. Incidence increases with age in box sexes
Stages:
Stage 0: All melanoma cells confined to epidermis (melanoma in situ); can be cured via excision because has no potential to spread around the body
When the cancer has grown through the dermis it is termed an invasive melanoma
Melanoma clinical types
Lentigo maligna melanoma: a patch of lentigo maligna, develops a papule or nodule, signalling invasive tumour.
Superficial melanoma: a large flat irregularly pigmented lesion which grows laterally,
before vertical invasion develops. Superficial spreading melanoma (SSM) is the most common subtype.
3. Nodular melanoma: the most aggressive type. It presents as a rapidly growing
pigmented nodule which bleeds or ulcerates.
Rarely, they are amelanotic (non-pigmented) and can mimic pyogenic granuloma.
Acral lentiginous malignant melanoma: arises as pigmented lesions on the palm, sole
or under the nail and it usually presents late.
Melanoma risk factors
Naevi UV/sun exposure Skin coloud: pale type I/II skin. Fair hair, inability to tan or freckled complexion doubles risk of melanoma Family history Solar keratoses Past pesticide exposure Higher socio-economic group
Melanoma presentations
Any pigmented lesion
Asymmetrical
Irregular border, scalloped or poorly defined edges
Uneven or variable colouring
Diameter bigger than 6mm
Changing size, shape or colour
ubungual melanomas: pigmented highly defined stripes under the nail (may just be hyperpigmentation usually in darker skin) but always refer for biopsy to be sure!
Melanoma investigations and diagnosis/referral points
ABCDE: Asymmetry Border irregular Colour irregularity Diameter greater then 7mm Evolving
7 point checklist: 3+ needs 2ww urgent referral major (2 points each) - change in size - irregular shape - irregular colour Minor (1 pnt each) - >7mm diameter - inflammtion - oozing - change in sensation
Acne
Androgen driven increase in sebum production Causing obstructed follicles to fill with lipid rich material forming visible open and closed comedones
Blockage of sebaceous follicle by keratin and sebum
Colonisation of follicle promotes bacterial growth leading to proliferation Propionibacterium acnes (commonly found in large quantities)
Inflammation presents in form of papules, pustules, nodules and cysts
Acne clinical features
Open and closed non inflamed comedones (black and whiteheads; black=oxidised; white=not)
Inflamed papules and pustules
In severe acne, nodules and pseudocysts (cyst like fluctuant swelling)
Post inflammatory erythematous or pigmented macules or scars
Adverse social and psychological effects (permanent scarring)
Lesions usually present on forehead,nose and chin. More severe cases whole face, upper chest and back may be affected usually with periorbital sparing.
the more widespread the acne the more need to consider systemic ABs/treatment
Whiteheads form when pores are blocked with sebum and dead skin cells. The pore is closed
Papules are red, painful with inflammatory evidence; can disappear spontaneous or can develop to become a pustule (squeezy spot)
Pustules (AKA pimples) form few days after white blood cells in papule make it to skin surface
Develops most commonly in puberty years
Acne vulgaris
Vulgaris means common; most common form of acne
Nearly 90% teens suffer
Peak incidence 13-16 years
May continue to 20-40years
1% men and 5% women have lesions
Females with PCOS or those with excess cortisol are prone
Differentials: rosacea, folliculitis, perioral dermatitis
Acne vulgaris severity categories
Mild: predominantly non-inflamed lesions (open and closed comedones) with few inflammatory lesions, total count <30
Moderate: more widespread with increased number of inflammatory papules and pustules, TLC 30-125
Severe: widespread inflammatory papules, pustules and nodules or cysts. Scarring may be present, TLC >125.
Acne management mild-moderate
Mild-mod:
Topical retinoid - adapalene (DIFFERIN) used alone or with benzoyl peroxide (EPIDUO) in strengths of 2.5%, 5% or 10% (CI in pregnancy and breastfeeding; must be on some form of contraception, apply at NIGHT due to sun sensitivity increase)
Topical ab (clindamycin 1%) always prescribed with benzoyl peroxide (antiseptic) apply once at night (DUAC) used at night as makes skin sensitive to the sun
Azelaic acid 20% is mildly effective as comedolytic, antibacterial and antiinflammatory agent
Treatment for 2-3 months then review and adjust accordingly
Acne vulgaris step up treatment
If no response/widespread area:
Lymecycline or doxycycline for max 3 months
Topical retinoid (if no CI) or benzoyl peroxide should always be co-prescribed with oral ABs to reduced risk of AB resistance
If no response to two different courses of ABs or if they start to scar; refer to dermatologist for isotretinoin consideration (GP cannot initiate this treatment)
Combined oral contraceptives, interfere with androgen production (if not CI) in combo with topical agents should be considered as alternative to systemics ABs in women (PROGESTERONE ONLY CAN WORSEN CONDITION; OTC TOPICAL STEROIDS hydrocortisone 1% CAN ALSO WORSEN)
*Topical steroids induce atrophy in skin; worsening acne as will weaken skin barrier and increase likelihood of damage; must be used very carefully for this reason
Acne dermatology referral
Severe or nodulocystic acne could benefit from oral isotretinoin
Severe social or psychological issues including morbid fear of deformity (dysmorphophobia)
Multiple treatments in primary care have failed
Laser treatment for acne not covered by NHS
Dermatology failure of treatment Qs
Does the pt adhere to the treatment? Possible adverse effects? Progression to more severe acne Use of comedogenic makeup/face creams Trial of alternative formulation or step up in treatment if appropriate (ask these stages first)
Rosacea
Chronic relapsing disease of recurrent erythema, telangiectasia, oedema, papules and pustules affecting forehead, cheeks, nose and often the chin
Affect fair skinned people relatively commonly accounting for 1% dermatology out pts in britain
Occurs in second half of life associated with facial flushing
More common in women tends to be more severe in men
Ocular changes usually bilateral result in mild blepharitis and conjunctivitis occur in more than 50% pts
Rosacea presentations
Blushing or flushing or persistent erythema
Red face and prominent blood vessels (telangiectasia fine, dilated blood vessels)
Red papules and pustules on nose, forehead, cheeks sna chin often follow (inflammatory or papulopustular rosacea) rarely trunk and upper limbs may involve
Facial skin thickening mostly nose
Dry and flaky skin burning stinging sensation
Aggravated by sun exposure hot spicy food or drink
Sensitive skin burning and stinging esp in makeup reaction sunscreens and facial creams
Red sore gritty eyelid margins including blepharitis
Rosacea clinical diagnosis
Papules and sometimes pustules. Dome shaped rather than pointy like acne and no black/white heads or nodules
May also result in red areas (erythematotelangiectatic rosacea), scaling (rosacea dermatitis) and swelling (phymatous rosacea)
Acne differentials
Acne vulgaris Seborrhoeic dermatitis Steroid rosacea (drug treatment) Flushing from other cause (allergies; malar flush; SLE) Skin ageing
Acne vulgaris advice and treatment
Advice:
Avoid triggers (heat, certain foods and excessive sun)
Never apply topical steroid to rosacea as will increase severity within few weeks
Treatment:
Topical/oral: ivermectin for 3 months trial reassess 10mg/g cream (SOOLANTRA) OD 8-12wks for mild-moderate papules and /or pustules
Brimonidine gel 0.5% reduce facial redness for 3-6hrs OD application.
Metronidazole cream or gel 0.75% TD or azelaic acid 15% TD can be used intermittently or long term for mild inflammatory cases in combo with oral ABs for more severe cases
Mod-severe papules and/or pustules prescribe combo of topical Ivermectin with oral doxycycline 40mg OD as modified release 8-12wks
Systemic ABs: Doxycycline
Likely to need many repeat treatments
Refer to dermatology if rhinophyma, ocular complications or failure to respond to treatment in GP
Urgent referral for if keratitis suspected (eye pain, blurred vision, sensitivity to light)
Routine referral for ocular symptoms severe or resistant to max treatment in primary care
Folliculitis
Inflamed hair follicles resulting in tender red spot often with surface pustule
Can be superficial or deep
Affects anywhere
Ance and acne variants are also types of folliculitis
Bacterial folliculitis usually due to staph. Aureus
Folliculitis types
Sycosis barbe (beard)
Beckhearts impetigo (superficial)
Gram -ve folliculitis (following acne treatment due to AB use)
Hot tub folliculitis from hot water, spa pool etc
Pseudofolliculitis from shaving/razors
Rosacea
Chronic relapsing disease of recurrent erythema, telangiectasia, oedema, papules and pustules affecting forehead, cheeks, nose and often the chin
Affect fair skinned people relatively commonly accounting for 1% dermatology out pts in britain
Occurs in second half of life associated with facial flushing
More common in women tends to be more severe in men
Ocular changes usually bilateral result in mild blepharitis and conjunctivitis occur in more than 50% pts
Rosacea presentations
Blushing or flushing or persistent erythema
Red face and prominent blood vessels (telangiectasia fine, dilated blood vessels)
Red papules and pustules on nose, forehead, cheeks sna chin often follow (inflammatory or papulopustular rosacea) rarely trunk and upper limbs may involve
Facial skin thickening mostly nose
Dry and flaky skin burning stinging sensation
Aggravated by sun exposure hot spicy food or drink
Sensitive skin burning and stinging esp in makeup reaction sunscreens and facial creams
Red sore gritty eyelid margins including blepharitis
Rosacea clinical diagnosis
Papules and sometimes pustules. Dome shaped rather than pointy like acne and no black/white heads or nodules
May also result in red areas (erythematotelangiectatic rosacea), scaling (rosacea dermatitis) and swelling (phymatous rosacea)
Acne differentials
Acne vulgaris Seborrhoeic dermatitis Steroid rosacea (drug treatment) Flushing from other cause (allergies; malar flush; SLE) Skin ageing
Acne vulgaris advice and treatment
Advice:
Avoid triggers (heat, certain foods and excessive sun)
Never apply topical steroid to rosacea as will increase severity within few weeks
Treatment:
Topical/oral: ivermectin for 3 months trial reassess 10mg/g cream (SOOLANTRA) OD 8-12wks for mild-moderate papules and /or pustules
Brimonidine gel 0.5% reduce facial redness for 3-6hrs OD application.
Metronidazole cream or gel 0.75% TD or azelaic acid 15% TD can be used intermittently or long term for mild inflammatory cases in combo with oral ABs for more severe cases
Mod-severe papules and/or pustules prescribe combo of topical Ivermectin with oral doxycycline 40mg OD as modified release 8-12wks
Systemic ABs: Doxycycline
Likely to need many repeat treatments
Refer to dermatology if rhinophyma, ocular complications or failure to respond to treatment in GP
Urgent referral for if keratitis suspected (eye pain, blurred vision, sensitivity to light)
Routine referral for ocular symptoms severe or resistant to max treatment in primary care
Folliculitis
Inflamed hair follicles resulting in tender red spot often with surface pustule
Can be superficial or deep
Affects anywhere
Ance and acne variants are also types of folliculitis
Bacterial folliculitis usually due to staph. Aureus
Folliculitis types
Sycosis barbe (beard)
Beckhearts impetigo (superficial)
Gram -ve folliculitis (following acne treatment due to AB use)
Hot tub folliculitis from hot water, spa pool etc
Pseudofolliculitis from shaving/razors
Folliculitis causes
Frequent shaving, waxing, hair removal (pseudofolliculitis)
Friction from tight clothes
Atopic dermatitis
Acne or other follicular skin disorders
Use of topical corticosteroids
Previous long term antibiotic use
Anaemia, obesity, diabetes, HIV/AIDS, viral hepatitis, cancer, other chronic illness
Bathing in inadequately cleaned hot tub/pool
Irritation folliculitis (pseudofolliculitis)
Shaving rash
No bacteria cause or other organisms present on swabbing
In beard areas is known as pseuofolliculitis barbe
Common in lower legs in women
Frequently itchy
Treatment is cessation of hair removal for 3-4 wks until follicles subside
To prevent recurrence use more gentle hair removal method
Folliculitis management
Warm compresses for itch and pain
Analgesics and antiinflammatories for pain
Antiseptic cleansers (hydrogen peroxide, chlorhexidine)
Topical antibiotics such as fusidic acid. To reduce bacterial resistance these should be applied for courses of no more than one wk
Incision and drainage of fluctuant lesions and abscesses (deep infection)
Systemic AB (oral or IV) flucloxacillin or erythromycin for extensive or severe infections (widespread) 7 day course
Folliculitis complications
Deep infection (boils/furuncle) One or more tender red spots, lumps, pustules S aureus cultured from skin lesions Usual course of 10 days Cellulitis and lymphangitis Osteomyelitis Septic arthritis
Define furuncles and carbuncles
Furuncles: skin abscesses caused by staph infections involving a hair follicle and surrounding tissue
Carbuncles: clusters of furuncles connected subcutaneously causing deeper suppuration and scrring. smaller and more superficial than subcutaneous abscesses
assessment of boils
Presence of discharge pus and fluctuance
Boil initially appear firm and tender, erythematous nodules which after several days enlarge and become painful and fluctuant (wave like feeling on palpation skin overlying fluid filled cavity with non-rigid walls)
Check for surrounding cellulitis
Check temperature, pulse, BP if clinically indicated (look out for sepsis)
Management of boil
May rupture spontaneously if small, once spontaneous drainage occurs lesion should be covered with sterile dressing
They heal over several days/weeks to leave violaceous macule and possible permanent scar
Oral AB - flucloxacillin
Incision and drainage at primary care (if small) or referral to surgical unit or emergency department according to local protocol
Swab lesion if: not responding to treatment; persistent or recurrent; multiple lesions; if pt is immunocompromised; known MRSA; has diabetes as ABs will not help
Bullous skin diseases (blistering)
round shiny lesions filled with fluids
often autoimmune related
examples: pemphigus vulgaris, pemphigoid and dermatitis herpetiformis
Pemphidoid vulgaris
Acquired autoimmune blistering disorder
Large tense subepidermal blisters on erythematous base
Autoantibodies IgG targeting components of basement memb can be detected
Usually disease of elderly rarely presents before 50 years
Usually occur on upper arms and thighs may spread to trunk
Mucous memb involvement seen in 50% cases
Oral lesions in about 1/3rd pts
Link to malignancy
Pemphigoid vulgaris management
Usually self limiting remits within 5years
Aim to suppress clinical signs to make disease tolerable for pt
Suppress infkammatory process: corticostewrods, BAs (tetracyclines, sulphones)
Immunosuppressive treatments: suppress production of pathogenic ABs eg high dose corticosteroids prednisolone 30-60mg /day, azathioprine, methotrexate, cyclophosphamide and cyclosporin
Dermatitis herpetiformis
Rare but persistent immunobullous disease linked to coeliac disease
Herpetiform (herpes simplex viral blisters) but not actually related to herpes virus
Not a viral infection
Predominantly affects caucasians aged 15-40 years but may occur in those younger or older and in other races
More females under age 20 affected than males
Genetic predisposition
Some pt have family history of other autoimmune conditions (thyroid disease) at least 75% pts with dermatitis herpetiformis have some degrees of enteropathy (vary from flat mucosa to partial villous atrophy)
Dermatitis herpetiformis management
Skin biopsy to confirm diagnosis
Screen for nutritional deficiencies
Offer same blood tests for coeliac disease to screen for nutrition def: FBC; LFTs; serum Ca; iron; zinc; B12; folate; TFTs; IgA anti-endomysial ABs
Gluten free diet
Sulphonamide AB - dapsone: used for symptomatic relief of rash and itch within a few days starting therapy. Monitor side effects (hemolysis) during treatment
Condyloma acuminatum
AKA genital warts or anogenital warts
Epidermal manifestation caused by HPV (95% by types 6 and 11)
Transmitted via sexual contact (60% transmission rate between partners)
HPV Types 16 and 18 have higher risk of neoplastic transformation
May also have risk of co-infection
HPV vaccination program in UK has reduced incidences significantly
Condyloma acuminatum risk factors
Smoking
Multiple sexual partners
History of other STIs
Anoreceptive intercourse. However perianal warts can occur in absence of anal intercourse
Manual sexual practices such as fisting and fingering
Immunosuppression
Condyloma acuminatum presentation
Lesion or multiple lesions which may form confluent mass
Warts on moist non-hairy skin are usually soft and non-keratinised while those on dry skin are likely to be keratinised and firm
Usually painless but can be disfiguring
Feel embarrassed
Warts can be broad based or pedunculated
May be pigmented or not
Often found on areas subject to traume during sex
Common sites: males; frenulum, corona, glans of penis inner foreskin, urethral meatus, penile shaft and scrotum
In females: labia, clitoris, urethral meatus, introitus, vagina and cervix
Both sexes: perineum, groin, pubis, perianal area and anal canal
Condyloma acuminatum investigations
Taking history on: Urethral or vaginal discharge Pelvic or scrotal pain Sexual activity in preceding 3 months Contraceptive and condom use Pregnancy possibility HIV risk activities Investigations: Diagnosed usually by clinical presentation Can take biopsy or viral typing in uncertain or recurrent cases or those with atypical features or high risk HPV malignancy Be suspicious of any pt >35 years or those with new symptoms Screen for other STI’s if appropriate
Condyloma acuminatum associated diseases
Cervical cancer
Vaginal, vulval and penile cancer
Anal cancers
Oral and oropharyngeal cancers
Condyloma acuminatum management
Pt education on condition and implications of long term health for them and their partners (reinforce with written info)
Advise use of condoms until lesions have resolved (protect against warts but not necessarily HPV)
Refer for counselling PRN
Screen and treat for other STIs if needed
Current partners and those in the previous 6 months should be assessed and educated with regards to STI prevention
Smoking cessation (evidence shows better response to treatment)
One third of warts regress spontaneously within 6 months
Podophyllotoxin for soft non-keratinised external warts. 0.15% cream or 0.5% solution TD for 3 days; four days rest. Can be repeated in weekly intervals PRN. Solution better for penile; cream better for vulval and anal lesions
Imiquimod 5% cream for keratinised lesions and non-keratinised external lesions. Thin application 3x wkly at night until lesions resolve for max 16 wks
Trichloroacetic acid less used due to corrosive action on skin but occasionally used in hospitals by specialists (pregnancy or indurated pts)
Ablation
Cryotherapy
Excision
Electrocautery or laser
*only surgical approaches have near 100% non-recurrence rate
*all treatments are associated with itching, pain, burning and erosions
*referral needed for cervical warts, intra-anal and pregnancy
*children showing genital warts raises safeguarding concerns however can be transmitted during birth or via non-sexual transmission from household members
*follow ups to assess response and side effects and check for new lesions regularly
Acanthosis nigricans
Characterised by hyperpigmentation and thickening (hyperkeratosis) of skin
Occurs mainly in folds of skin like axilla, groin, back of neck
Cause is unknown but appears related to insulin resistance
Has also been associated with benign and malignant conditions
Acanthosis nigricans types
Obesity associated (most common): may occur at any age but more common in adulthood and is associated with insulin resistance Syndromic acanthosis nigricans: defined as being associated with a syndrome such as hyperinsulinemia, Cushing’s, PCOS, total lipodystrophy, Crouzon syndrome Benign: AKA acral acanthotic anomaly. Thick lesion most prominent over the upper surface of hands and feet in pt who are otherwise healthy. Most common in darker skin types Drug induced: uncommon but medications include nicotinic acid, insulin, systemic corticosteroids and hormonal treatments Hereditary benign: autosomal dominant trait. Lesions may manifest at any age Malignant: associated with internal malignancy. Most common cancer is tumour of the gut (90% cases) esp. Stomach cancer. In 25-50% cases lesions are present in mouth on tongue and lips Mixed type: patients with one type acanthosis nigricans may develop new lesions of different cause eg obesity type then develops malignant type.
Acanthosis nigricans presentation and investigations
Thickened brown textures patches
In folds of axilla and neck most commonly
Papillomatosis (finger like growth) common on cutaneous and mucosal surfaces (oral cavity, nasal and laryngeal mucosa and oesophagus)
Itchy
Abrupt development of lesions in middle aged may indicate malignancy
Investigations:
Tests for underlying tumours or risk factors and refer immediately PRN
Acathosis nigricans treatment
Correct hyperinsulinemia with diet/mediations
Lose weight with obesity associated type
Excise or treat underlying tumour
Stop offending medicines in drug induced type
Hereditary type may spontaneously resolve eventually
steroid ladder
Mild: hydrocortisone: used on face, neck and infants
Moderate: clobetasone (Eumovate), betamethasone 0.025% (betonvate RD): used on infants for max 3 days, children and body
Potent: betamethasone (betnovate 0.1%), mometasone (Elocon): use on body
Very potent: clobetasol (dermovate): use on hands and feet
How to apply emollient and steroid creams
Clean area
Rinse with water
Apply emollient thin layer gently to skin in direction of hair growth
Wait 15-30mins before applying steroid creams also in direction of hair growth
* fingertip method: use finger to measure volume of cream needed per application! full tip of finger length = adult; half FTU = half fingertip length and so on
Atopic eczema/dermatitis
Characterised by papules and vesicles on erythematous base
Atopic is most common type of eczema
Usually develops in childhood and resolves during teen years (may recur)
80% cases before age 5
20% prevalence in <12 years in UK
Subtypes:
Intrinsic: atopic, seborrhoeic, pompholyx, discoid, venous
Extrinsic: contact allergic dermatitis, contact irritant dermatitis
Atopic eczema risk factors/cause
Family history of atopic eczema, allergic rhinitis, asthma
Primary genetic defect in skin barrier function appears to underlie cause but no one really knows
Exacerbating factors such as heat, allergens, infections, sweating and severe stress can trigger/cause
Atopic eczema presentation
Itchy
Erythematous dry scaly patches
More common on face, hands, extensor aspects of limb (infants) and flexor aspects in children and adults
Acute lesions are erythematous, vesicular and weepy (exudate)
Chronic scratching/rubbing can lead to excoriations and lichenification
May show nail pitting and ridging
Atopic eczema diagnostic criteria
if it doesn’t itch; it’s probably not eczema!
Itchy skin + 3 more of the following:
History of itchy skin creases such as folds of elbows or knees (or cheeks in <18months)
History of asthma, hay fever or atopic disease in first degree relative in children under age 4
General dry skin in preceding year
Visible flexural eczema
Onset in first two years of life (genetic factors; not acquired)
Atopic eczema severity assessments
Visual analogue scales (0-10) capturing the child/parent/carer’s assessment of severity, itch and sleep loss over the previous three days and nights.
Patient-oriented Eczema Measure (POEM).
Children’s Dermatology Life Quality Index (CDLQI).
Infants’ Dermatitis Quality of Life Index (IDQOL).
Dermatitis Family Impact (DFI) Questionnaire.
Atopic eczema differentials
Psoriasis Contact dermatitis Seborrhoeic dermatitis Fungal infections Lichen simplex chronicus Scabies
Atopic eczema investigations
Clinical examination and history
IgE and specific radioallergosorbent tests (RASTs) only to confirm atopic nature
Swabs for bacteriology if not responding to treatment to identify MRSA strain or detect addition strep. Infection
Atopic eczema management
Mild: emollients: mild potency topical corticosteroids
Moderate: emollients; moderate potency topicalcorticosteroids; topical calcineurin inhibitors (tacrolimus or pimecrolimus) and bandages (prescribed by specialists usually)
severe: emollients; potent topical corticosteroids; topical calcineurin inhibitors (tacrolimus or pimecrolimus); bandages; phototherapy; oral corticosteroids (prescribed by specialists usually)
Tacrolimus recommended for 2+ years
Pimecrolimus for ages 2-16 in moderate cases
Lichenification in eczema
results from repeated scratching; initially treated with potent steroid, bandages containing ichthammol paste etc. can be applied over steroid. Coal tar and ichthammol can be used in chronic cases
exudative eczema
initial potent steroid. Infection may also be present and need ABs. potassium permanganate solution can be used in exudative eczema for antiseptic and astringent effects
Severe refractory eczema:
specialist referral and care. May need phototherapy, systemic steroids or other drugs on the immune system (ciclosporin etc). Alitretinoin recommended for adults with severe chronic hand eczema not responding to potent topical steroids with Dermatology Life Quality Index score >15
managing eczema flare ups
Topical corticosteroids
Treat any associated infections (mod-severe usually 14 day course flucloxacillin)
Urgently refer or admit severe unresponsive disease or with suspected infection with herpes simplex virus
Frequent flare ups:
Change emollient to higher lipid content
Advise application more often and more quantity each time
Review factors provoking flares
Perioral dermatitis
Incidence 0.5-1%; hsa decreased in recent years likely due to greater awareness of problems from topical steroid use long term
Predominantly affects women aged 15-45 years
Male incidence increasing probably due to cosmetic use change
Perioral dermatitis cause
Underlying cause not found in all pts. And exact cause is unknown
Topical steroid preparations. No clear correlation exists between risk of condition and strength of steroid or duration of use
Cosmetics
High factor sun protection creams
Fluoridated toothpaste
Physical factors: UV, heat, wind
Candidiasis
Hormonal factors suspected: premenstrual deterioration also oral contraceptives potentially
Perioral dermatitis presentation
Skin lesions grouped follicular reddish purple, vesicles and pustules on an erythematous base around the mouth, nasolabial folds and cheeks
Pale area adjacent to border of mouth is characteristic (sparing of lip margins)
Occasionally the eruption can be more widespread (affecting eyelids and forehead)
Often sensation of burning and tension; itching is rare
Lupoid perioral dermatitis is severe variant with yellow granulomatous infiltrates
Complications mostly emotional and scarring related (with lupoid form)
Perioral dermatits management
Evaluate pt for underlying factors
Reassurance and education of condition; potential triggers (avoid alcohol and spicy foods, cosmetics, cleansers and moisturisers); time course of disease; wash hands after applying steroid cream
Topical antibiotics (clindamycin, erythromycin or metronidazole) can be used for mild cases
Mod-severe cases need systemic antibiotic for 4-6wks (oxytetracycline 500mg TD, lymecycline 408mg OD, erythromycin 500mg TD) or modified release doxycycline capsules 40mg OD
If unresponsive and granulomatous; oral isotretinoin may be considered
Pimecrolimus cream if other treatments fail may help
Photodynamic therapy may be effective (no large studies to evaluate this)
with treatment there can be initial worsening of symptoms before they improve esp if steroids are withdrawn
in cases of long term topical steroid misuse, gradual withdrawal with low dose 0.1-0.5% hydrocortisone cream can be initially trialed
contact and occupational dermatitis
Women more affected
4-7% dermatology app. Are for this
Hands affected in 75% contact and 90% occupational dermatitis
Prevalence lower in children but increasing
Pts in contact with chemicals may also be at risk of: contact urticaria, acne, folliculitis, skin infections, pigmentary disorders, mechanical skin disease (repetitive trauma), skin cancers
High risk occupations for dermatitis
Florists hairdressers/ barbers Cooks Beauticians and related occupations Metal working machine operatives Chemical, rubber, glass and ceramic process operatives Dental practitioners and dental nurses
Contact/occupational dermatitis types
Allergic contact dermatitis: type IV hypersensitivity reaction occurs after sensitisation and subsequent re-exposure to allergen
Irritant contact dermatitis: inflammatory response occurs after damage to skin usually by chemicals. Not allergy and can occur in anyone significantly exposed to irritants. May be acute or chronic/cumulative
contact/occupational dermatitis causes
common irritants and allergens (non-exhaustive list) Water (hard, chalky or heavily chlorinated) Detergents and soaps Solvents and abrasives Machining oils Acids and alkalis, including cement Reducing agents and oxidising agents including sodium hypochlorite Powders, dust and soil Plants Cosmetics Metals Topical medications Textiles Epoxy resin adhesives
Contact/occupational dermatitis presentation
Red skin Vesicles or papules on affected area Crusting and scaling skin Itching Fissures (chronic exposure) Hyperpigmentation (chronic) Pain or burning sensation from affected area Hands affected in 75% contact and 90% occupational dermatitis
Contact/occupational dermatitis complications and invesitigations
Secondary bacterial infections
Occupational skin disorders may impact quality of life and may need change of occupation
Investigations:
Full history including: job, materials involved, amount and duration of exposure, location of rash and distribution, timing of rash with relation to work and weather skin clears inbetween
Specialist patch testing (GOLD STANDARD)
Contact/occupational dermatitis management
Avoid irritants
Hand hygiene/protective equipment wearing
Severe or chronic forms may benefit from topical corticosteroid cream, strength and period of use being adjusted according to severity
Short course oral steroid may be used for acute severe episodes
Second line agents (psoralen combined with UV A - PUVA) treatment, ciclosporin and azathioprine may be used in specialist setting for chronic resistant dermatitis
Seborrhoeic dermatitis (cradle cap)
1-5% population globally
Incidence increased in immunocompromised pts (34-83%)
Suggested early marker of HIV/AIDs infection
Often severe condition
More common in males
Thought to be due to androgen effect on sebum production
Cause unclear but thought to be inflammatory reaction to yeast called malassezia spp
Aggravated by psychological and physical stressors
Seborrhoeic dermatitis presentation
Face: inflamed, greasy areas with fine scaling (nasolabial folds, nose bridge, eyelashes and eyebrows, blepharitis, ear particularly behind skin folds)
Scalp: dandruff flaking, ill-defined pink patches dry with yellowish or white bran like scale
Chest: usually greasy scaly papules; less commonly macules and papules similar to extensive pityriasis rosea
Sternum and upper back may show fine scaling
Flexures may have erythematous patches, papules or plaques presenting as intertrigo
Seborrhoeic dermatitis complications
Secondary bacterial infection
Severe SD or generalised seborrhoeic erythroderma is rare. May occur with immunosuppression or cardiac failure
Seborrhoeic dermatitis management
Regular antifungal medication with intermittent topical steroids.
Calcineurin inhibitors
Scalp:
First remove thick crusts or scales with olive oil or keratolytic prep such as salicylic acid or coal tar. Leave olive oil on affected areas for several hrs before washing off with normal coal tar shampoo
Medicated shampoos: containing ketoconazole 2% (nizoral) with sulfide shampoo (selsun)
Use at least 2x weekly for at least a month after which frequency may be reduced
Also used in beard
Steroid scalp applications reduce itching. Intermittent use for few consecutive days may be helpful (not in beard)
Face, ears, chest and back
Clean skin but avoiding soap
Ketoconazole or antifungal cream used OD for 2-4wks. Repeat PRN; reduce frequency when symptoms are controlled. Can use antifungal shampoos in addition
1% hydrocortisone cream applied once or twice daily for 1-2wks. Intermittent use may be needed if chronic (avoid long term)
Topical calcineurin inhibitors (pimecrolimus cream or tacrolimus ointment) may help (may allow sparing use of steroid creams)
For eyelids consider hygiene methods
Other treatments:
Oral antifungal medication - azoles (ketoconazole or itraconazole)
Oral tetracyclines used (off label) for antiinflammatory effects
Oral isotretinoin (off label)
UV light treatment
often responds well to treatment; often relapses so maintenance or intermittent treatment be be needed
Eczema herpetium
Medical emergency!
Rare widespread HSV infection occurs in atopic eczema patients (most often children)
Characterised by fever and clusters of itchy blisters or punched out erosions
Often seen as complication of atopic dermatitis
Repeated episodes of this condition are unusual
More commonly seen in infants and children with atopic eczema
Eczema herpetium causes
Herpes simplex virus type 1 or type 2
May also complicate recurrent herpes
When break down of skin barrier is not caused by atopic eczema is termed kaposi varicelliform eruption, can be due to: thermal burns, pemphigus vulgaris, darier disease, benign familial pemphigus, cutaneous T cell lymphoma and ichthyosis
Other virus’ can be due to coxsackivirus A16 (foot and mouth disease) causing similar eruptions (eczema coxsackium)
Eczema herpeticum presentation
Clusters of painful itchy blisters
Most often on face and neck but can affect anywhere
New patches form and spread over 7-10 days
Monomorphic blisters may be filled with yellow pus
Often blood stained
New Blisters have central dimples (umbilication)
May weep or bleed
Older blisters crust over foring sores (erosions)
Lesions heals over 2-6 wks
In severe cases small white scars may persist where skin has been destroyed
Eczema herpeticums diagnosis
Diagnosed clinically when pt has known atopic dermatitis and presents with acute painful blisters, fever and malaise
Viral culture
Direct fluorescent antibody scan
PCR sequencing
Tzank smear (showing epithelial multinucleated giant cells and acantholysis; cell separation)
Eczema herpeticums management
Considered a dermatological emergency
Prompt treatment with antiviral medications may eliminate need for hospitalisation
Oral aciclovir 400-800 mg 5xdaily; valaciclovir 1g TD for 10-14 days or until lesions heal
IV aciclovir if pt too sick to take tablets or infection deteriorates further
Secondary bacterial infections treated with systemic antibiotics
Topical steroids not generally recommended but may be needed to treat active atopic dermatitis
Consult ophthalmologist when eyelid or eye is involved
Discoid eczema and cause
Chronic dermatitis causing skin to become itchy, swollen, cracked in circular or oval patches
Cause:
Unknown although thought to be related to dry skin
History of atopic disease does NOT seem to be relevant to this condition
May be triggered by insect bites, burns, infections like Hep C, drugs (statins, TNF-alpha blockers) or weather changes
Discoid eczema presentation
Distinct oval or circular patches of eczema
Can affect any part of body although usually NOT face or scalp
First signs usually small group of spots or bumps on skin
These join up to form larger patches ranging from few mm to several cm large
Lighter skin will show red or pink patches
Darker skin will show dark brown or slightly palmers than normal surrounding skin
Dry, crusty
Swollen and blistered
May ooze fluid
Centre of patch may become clear leaving ring of discolouration which may be mistaken for ringworm
If infected: malaise, nausea, chills, fever
Discoid eczema management
Emollients and avoiding triggers
Topical corticosteroids
Antihistamines to reduce itching
Antibiotics for secondary infections
Psoriasis
Chronic inflammatory skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration
Chronic plaque psoriasis most common type
Other types include guttate (raindrop lesions), seborrhoeic (nasolabial and retroauricular), flexural, pustular (palmer-planter), and erythrodermic (total body redness)
Affects about 2% of population in UK;
Onset 30-50s
Increased prevalence increasing distance from equator
Pathophysiology:
Activated t cells infiltrate epidermis
Hyperproliferation of keratinocytes in epidermis
Increased epidermal cell turnover rate
Psoriasis risk factors
Genetic (40% family history) PSORS1 locus within major MHC on chromosome 6p21 (location of HLA genes) Obesity Smoking Alcohol Stress Infections
Psoriasis causes and complications
Causes:
Complex interaction between genetic, immunological and environmental factors
Precipitating factors include: trauma (may produce Koebner phenomenon), infection (tonsillitis), drugs, stress and alcohol
Complications:
Erythroderma
Psychological and social effects
Psoriasis presentation
Well- demarcated erythematous scaly plaques
Lesions can be itchy, painful or burning
Common on extensor surfaces and scalp
Auspitz sign (scratch and gentle removal of scales causes capillary bleeding)
50% associated with nail changes (pitting, onycholysis)
5-8% suffer from associated psoriatic arthropathy - symmetrical polyarthritis, asymmetrical oligomonoarthritis, lone distal interphalangeal disease, psoriatic spondylosis and arthritis mutilans
Psoriasis clinical subtypes
Plaque Palmo-plantar (feet and palms) Nail Scalp Inverse Guttate (small widespread plaques)
Psoriasis management
General measures to avoid known precipitating factors and emollients to reduce scaling Topical therapies (localised and mild cases): vit D analogues, topical corticosteroids, coal tar preparations, dithranol, topical retinoids, keratolytics and scalp preparations Phototherapy (extensive disease): UVB and photochemotherapy Oral therapies (extensive and severe or with systemic involvement): methotrexate, retinoids, ciclosporin, mycophenolate mofetil, fumaric acid esters and biological agents
Suturing
Aim is eversion of wound edges not inversion!
Move knots to the same side (don’t leave in the centre)
Place sutures to line up irregular wound edges first then suture between for full closure
Principles are:
To support tissues until healing process restores tensile strength
To minimise risk of bleeding and infection
To close dead space by approximating wound edges ensuring functional and aesthetically pleasing result
Wound types
Incision: sharp straight deep cut Punture: deep and narrow Abrasion: top layer of skin scraped off Laceration: irregular cut from tearing Avulsion: part of skin is loose/torn Amputation: part of body detached Burn: thermal electrical or chemical injury to skin Crush injury: body part subjected to high degree of force or pressure, usually after being squeezed between two heavy objects Bite: human/animal
Wound treating tips
- injuries involving glass, dog bites etc. should be X Rayed to check for residual foriegn body and fractures
- puncture wounds are deep and difficult to clear; cover with broad spectrum antibiotics
- hand wounds are most likely to get infected
- Sun exposure can cause hyperpigmentation and scarring - keep wound covered
- Small amount of foriegn body to remain is potentially normal/OK
Steri strips
Typically for cuts or wounds which aren’t too severe or minor surgery
Help heal wounds by pulling two sides of skin together without making contact with actual wound; reducing chance of introducing bacteria or other substances into cut
Sometimes a better option than stitches as they don’t need to be sewn into skin and are easily removable (good for children esp.)
Using steris
Are wound edges straight? Steris are best for shallow cuts with straight clean edges
Is bleeding light and measurable? Use sterile cloth to put pressure on the wound for 5mins at least. Don’t use strips if it’s still bleeding after this
Is the wound less than 5cm in length? Steris aren’t recommended for anything larger than this!
Is it in an area where skin doesn’t move a lot? Steri’s might not work as well on joints or other areas where it may have trouble staying in place
Using steri’s:
Make sure wound and surrounding area stays clean
Make sure steris area is kept dry for at least 24-48hrs once applied; special care when bathing or showering (cover with bandages etc)
Trim away edges of steris that come loose using scissors
Inspect wound every day to ensure no sign of infection
Don’t pull on loose steri ends (can reopen wound)
Don’t rub or pick the area (could introduce bacteria into or open wound again)
Glue
Medical glue used to close wounds
Can be used on it’s own or with stitches or adhesive tape
Forms protective waterproof covering over the wound
Mainly used for cuts that are minor, up to 5cm long, have straight edges and are easily pulled together
Can also close wounds on the face, head, some parts of arms and legs, trunk
Is not always suitable for joints as can move about too much
Will slough off within 5-10days
Appyling glue
Should not be put inside wounds
Hold skin together and put glue over the top of skin
Avoid touching for 24hrs
Keep wound dry for at least 5 days
Scar should take around 6months to fade
Pat dry if it’s wet, do not rub!
Don’t put plasters, creams, clothing, don’t brush hair in glued area, don’t pick glued area for first 5 days
Suturing general filament use on specific body areas
Face/lip: 6-0 monofilament, non-absorbable remove in 3-5 days
Scalp: 3-0, 4-0: Monofilament, non-absorbable remove in 7-10 days
Chest/abdomen/back: 3-0, 4-0 monofilament may be absorbable or not. remove in 10-14 days if non-absorbable
Limbs: 3-0 to 5-0: monofilament may be non or absorbable; remove in 10-14 days if needed
Hands: 4-0 or 5-0: monofilament usually non-absorbable remove in 10-14 days
Lidocaine
Max dose 1% is 3mg.kg
1% lidocaine (10mg per ml = 100mg in 10ml)
Usually comes in 5ml vial (5ml x 10mg = 50mg per vial)
Average 70kg person (3 x 70 = 210mg max)
210/50 = 4 vials max
If you have 0.25% = 2.5mg per 1ml (5 x 2.5 = 10mg per vial)
210/10 = 21 vials max
Warm liquid in hands by rubbing hands together: is rather acidic so can sting a bit when being given
facial injuries assessment overview
Check all bones for tenderness (move face; jaw etc.)
Infraorbital nerve: sensation and eye movements
Can touch gums to test sensation
Mouth injuries: any wound crossing vermillion border should be referred to maxfax for closure. Same for any cosmetically concerning cases
Nose injuries: NO nose XR for suspected fractures as unlikely to show up (unless very complex; then discuss with ENT before discharge). Have follow up with ENT Drs in around 7 days time; then will decide if they need imaging (less swelling; easier to see on XR). But still very important to rule out septal haematoma for nose injuries; look in nostrils (must be documented as can go on to cause significant infection!!)
Tetanus
Injecting drug users are high risk (particularly if SC or IM routes)
Any wound including burn is potent tetanus risk: always ensure there is sufficient tetanus protection (vaccinated)
Wounds most at risk are contaminated wounds (saliva, soil, dirt etc)
Standard active immunisation involved initial course of 3 IM doses of 0.5mL tetanus toxin given at 2,3,4 months old followed by boosters at 4 and 14 years
Full course of all 5 is considered to give lifelong immunity
Inadequate immunisation is likely in immigrants, elderly, patients with reduced immunity and those who refused vaccinations
Anti-Tetanus prophylaxis with wounds and when to consider
Need for immunisation after injury depends on pts immunity status and weather the wound is ‘clean’ or ‘tetanus prone’ such as:
Heavily contaminated (esp. With soil or faeces)
Devitalized tissue
Infection or wound >6hrs old
Puncture wounds and animal bites
If the pt receives full 5 dose vaccine: no need to give further vaccine
Consider giving anti-tetanus immunoglobulin (HATI) only if the risk is especially high (wound contaminated with manure etc.)
If immunisation status is unknown/uncertain then give dose of combined tetanus/diphtheria/polio vaccine and refer to GP for further doses if needed
For tetanus prone wounds also give one dose of HATI (250-500 units IM) at a different injection site
Antibiotics prophylaxis with wounds and when to consider
Most wounds won’t need antibiotics
They are frequently used for wounds >6hrs old, complex oral wounds and in high risk workers (gardeners, farmers, fishermen etc)
Antibiotics are indicated for penetrating injuries which cannot be properly cleaned
Bites
Can cause contaminated puncture wounds, contaminated crush injuries or both
All carry high infection risk (bacterial, viral, rabies etc)
Bacterial infection is likley in: punctures (cats/human bites), hand wounds, wounds older >24hrs, immunocompromised, alcoholics and diabetics
Bacterial organisms most likely to infect: streptococci, staph. Aureus, clostridium tetani, pasteurella multocida (cat bite or scratch), bactericides, Eikenella corrodes (human bites)
Bite investigations
Establish what animal
How long ago
Where bite occurred (surroundings)
XR if fracture suspicion, joint involvement (look for air), or radio-opaque foreign body (tooth)
Bites management (non-infectious)
Clean: explore fresh bite wounds with appropriate anaesthetic, debride and clean with normal saline or washing with tap water
Refer significant facial wounds or involving tendons or joint to specialist (usually plastics team)
Cosmetic considerations usually outweighs risk of infection for most facial wounds so aim for primary closure
Do not close puncture wounds that can’t be satisfactorily irrigated
Whether to give ABs prophylaxis for bite is controversial, consider for: punctures, crush injuries with devitalized tissues, bites to hands, wrist or genitals, primarily closed bites, human, cats and rat bites, bitten individuals who are immunocompromised
Co-amoxiclav is for broad spectrum cover (doxycycline and metronidazole or ceftriaxone alone for penicillin allergy)
Do not use erythromycin or flucloxacillin alone as prophylaxis
Infected bites managemente
Most occur >24hrs after injury and are due to staphylococci or anaerobes
Pain, inflammation and swelling +/- regional lymphadenopathy within 24hr suggests P. multocida infections
Take swab of all infected wounds
Treat with cleaning, elevation, analgesia and antibiotics (guided by micro results)
Oral Co-amoxiclav and outpt review at approx 36hr is appropriate for localised infections with no systemic involvement and no suspected underlying joint involvement
Refer pts with spreading infection for IV antibiotics and admission
Human and fight bites
Many human bites occur ‘in reverse’ when an individual punches another in the mouth, causing wounds on the dorsum of the hand over the MCPs
Underlying joint involvement is common and may progress to septic arthritis unless treated aggressively with exploration, irrigation and antibiotic —> refer all such patients
Consider Hep B, C and HIV, give appropriate prophylaxis
