burns Flashcards
immediate first aid for burns
airway, breathing, circulation
burns caused by heat: remove the person from the source. Within 20 minutes of the injury irrigate the burn with cool (not iced) water for between 10 and 30 minutes. Cover the burn using cling film, layered, rather than wrapped around a limb
electrical burns: switch off power supply, remove the person from the source
chemical burns: brush any powder off then irrigate with water. Attempts to neutralise the chemical are not recommended
how to assess the extent of the burn
Wallace’s Rule of Nines: head + neck = 9%, each arm = 9%, each anterior part of leg = 9%, each posterior part of leg = 9%, anterior chest = 9%, posterior chest = 9%, anterior abdomen = 9%, posterior abdomen = 9%
Lund and Browder chart: the most accurate method
the palmar surface is roughly equivalent to 1% of total body surface area (TBSA). Not accurate for burns > 15% TBSA
how to assess the depth of the burn
1) Superficial epidermal - First degree-Red and painful
2) Partial thickness (superficial dermal) Second degree-Pale pink, painful, blistered
3) Partial thickness (deep dermal)-Second degree Typically white but may have patches of non-blanching erythema. Reduced sensation
4) Full thickness-Third degree White/brown/black in colour, no blisters, no pain
when to refer to secondary care
all deep dermal and full-thickness burns.
superficial dermal burns of more than 3% TBSA in adults, or more than 2% TBSA in children
superficial dermal burns involving the face, hands, feet, perineum, genitalia, or any flexure, or circumferential burns of the limbs, torso, or neck
any inhalation injury
any electrical or chemical burn injury
suspicion of non-accidental injury
initial management of burns
initial first aid as above
review referral criteria to ensure can be managed in primary care
superficial epidermal: symptomatic relief - analgesia, emollients etc
superficial dermal: cleanse wound, leave blister intact, non-adherent dressing, avoid topical creams, review in 24 hours
what is the most common malignancy associated with acnathosis nigricans
gastrointestinal adenocarcinoma
what is acanthosis nigricans
Describes symmetrical, brown, velvety plaques that are often found on the neck, axilla and groin.
causes of acanthosis nigricans
- type 2 diabetes mellitus
- gastrointestinal cancer
- obesity
- polycystic ovarian syndrome
- acromegaly
- Cushing’s disease
- hypothyroidism
- familial
- Prader-Willi syndrome
- drugs: oral contraceptive pill, nicotinic acid
pathophysiology of acanthosis nigricans
insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1)
whats is nickel dermatitis
llergic contact dermatitis and is an example of a type IV hypersensitivity reaction. It is often caused by jewellery such as watches
how to diagnosie nickel dermatitis
allergic contact dermatitis and is an example of a type IV hypersensitivity reaction. It is often caused by jewellery such as watches
tender, erythematous nodules over her forearms.
hypercalcaemia
sarcoidosis
what is erythema nodosum
inflammation of subcutaneous fat
usually resolves within 6 weeks
lesions heal without scarring
causes if erythema nodosum
1) infection
- streptococci
- tuberculosis
- brucellosis
- chlamydia
- leprosy
2) systemic disease
- sarcoidosis
- inflammatory bowel disease
- Behcet’s
3) malignancy/lymphoma
4) drugs
- penicillins
- sulphonamides
- combined oral contraceptive pill
- amoxicillin
5) pregnancy
features of pyoderma gangrenosum
typically on the lower limbs
initially small red papule
later deep, red, necrotic ulcers with a violaceous border
may be accompanied systemic symptoms e.g. Fever, myalgia
causes of pyoderma gangrenosum
idiopathic in 50% inflammatory bowel disease: ulcerative colitis, Crohn's rheumatoid arthritis, SLE myeloproliferative disorders lymphoma, myeloid leukaemias monoclonal gammopathy (IgA) primary biliary cirrhosis
management for pyoderma gangrenosum
the potential for rapid progression is high in most patients and most doctors advocate oral steroids as first-line treatment
other immunosuppressive therapy, for example ciclosporin and infliximab, have a role in difficult cases
if meninngococcal septicaemia is suspect what do you do
parentral ABx
what is purpura
describes bleeding into the skin from small blood vessels that produces a non-blanching rash.
Smaller petechiae (1-2 mm in diameter) may also be seen. It is typically caused by low platelets but may also be seen with bleeding disorders, such as von Willebrand disease.
why should you be cautious if a child comes with new purpuric rash
meningococcal septicaemia or acute lymphoblastic leukaemia.
causes of purpura in childre
Meningococcal septicaemia
• Acute lymphoblastic leukaemia
- Congenital bleeding disorders
- Immune thrombocytopenic purpura
- Henoch-Schonlein purpura
- Non-accidental injury
causes of purpura in adulrs
Immune thrombocytopenic purpura
- Bone marrow failure (secondary to leukaemias, myelodysplasia or bone metastases)
- Senile purpura
- Drugs (quinine, antiepileptics, antithrombotics)
- Nutritional deficiencies (vitamins B12, C and folate)
petechia or purpura in raised SVC pressure
Raised superior vena cava pressure (e.g. secondary to a bad cough) may cause petechiae in the upper body but would not cause purpura.
what does dermatophyte fungal skin infection result in
pityriasis versicolor
acne rosacea is triggered by
sun exposure, hot drinks or exercise,
what is pityriasis rosea
Pityriasis rosea describes an acute, self-limiting rash which tends to affect young adults.
can last upto 3 months
The aetiology is not fully understood but is thought that herpes hominis virus 7 (HHV-7) may play a role.
features of pityriasis rosea
recent viral infection herald patch (usually on trunk)
followed by erythematous, oval, scaly patches which follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer.
This may produce a ‘fir-tree’ appearance
management of pityriasis rosea
self-limitingm - usually disappears after 6-12 weeks
can give emollients / antihistamines / topical corticosteroids if itchy
what os hirsutism
androgen-dependent hair growth in women
what is hypertrichosis
androgen-independent hair growth
causes of hirsutism
MOST COMMON POLYCYSTIC OVARIAN SYNDROME
Cushing's syndrome congenital adrenal hyperplasia androgen therapy obesity: thought to be due to insulin resistance adrenal tumour androgen secreting ovarian tumour drugs: phenytoin, corticosteroids
How to assess hirsutism
Ferriman-Gallwey scoring system: 9 body areas are assigned a score of 0 - 4, a score > 15 is considered to indicate moderate or severe hirsutism
management of hirsutism
advise weight loss if overweight
cosmetic techniques such as waxing/bleaching - not available on the NHS
consider using combined oral contraceptive pills such as co-cyprindiol (Dianette) or ethinylestradiol and drospirenone (Yasmin). Co-cyprindiol should not be used long-term due to the increased risk of venous thromboembolism
facial hirsutism: topical eflornithine - contraindicated in pregnancy and breast-feeding
causes of hypertrichosis
drugs: minoxidil, ciclosporin, diazoxide
congenital hypertrichosis lanuginosa, congenital hypertrichosis terminalis
porphyria cutanea tarda
anorexia nervosa
what is kertocanthoma
large nodule
friable
no regional lymphadenopathy
resolve with scarring
what is dermatitis herpetiformis
Chronic itchy clusters of blisters.
papuloivesicular eruptions
Linked to underlying gluten enteropathy (coeliac disease).
features of BCC
Most common form of skin cancer.
Commonly occur on sun exposed sites apart from the ear.
Typically slow growing with low metastatic potential.
sub types of BCC
nodular, morphoeic, superficial and pigmented.
management of BCC
Standard surgical excision, topical chemotherapy and radiotherapy are all successful.
As a minimum a diagnostic punch biopsy should be taken if treatment other than standard surgical excision is planned.
what is SCC
Again related to sun exposure.
May arise in pre - existing solar keratoses.
May metastasize if left.
Immunosupression (e.g. following transplant), increases risk.
Wide local excision is the treatment of choice and where a diagnostic excision biopsy has demonstrated SCC, repeat surgery to gain adequate margins may be required.
treatment for malignant melanoma
Suspicious lesions should undergo excision biopsy. The lesion should be removed in completely as incision biopsy can make subsequent histopathological assessment difficult.
main diagnositc features of malignant melanoma
Change in size
Change in shape
Change in colour
secondary features of malignant melanoma
Diameter >6mm
Inflammation
Oozing or bleeding
Altered sensation
what is the criteria used to excise the margins for malignant melanoma
Margins of excision-Related to Breslow thickness
Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm
what is kaposi sarcoma
- Tumour of vascular and lymphatic endothelium.
- Purple cutaneous nodules.
- Associated with immuno supression.
- Classical form affects elderly males and is slow growing.
- Immunosupression form is much more aggressive and tends to affect those with HIV related disease.
what is dermatofibroma
Benign lesion.
Firm elevated nodules.
Usually history of trauma.
Lesion consists of histiocytes, blood vessels and fibrotic changes.
what is pyogenic granuloma
Overgrowth of blood vessels.
Red nodules.
Usually follow trauma.
May mimic amelanotic melanoma.
clinical features of erythema nodosum
typically causes tender, erythematous, nodular lesions
usually occurs over shins, may also occur elsewhere (e.g. forearms, thighs)
Lesions continue to appear for 1-2 weeks and leave bruise-like
discolouration as they resolve
● Lesions do not ulcerate and resolve without atrophy or scarring
● The shins are the most common site
complications of erythema nodosum
is encapsulated fat necrosis, or ‘mobile encapsulated lipoma’
DD for erythema nodosum
rheumatoid nodule
lipidodermatosclerosis
treatment for erythema nodosum
Pain management may include extended rest, colchicine (1–2 mg/day), NSAIDs (non-steroidal anti-inflammatory drugs), and venous compression therapy
Systemic corticosteroids (1 mg/kg daily until resolution of erythema nodosum) may be prescribed if infection, sepsis, and malignancy have been ruled out
Oral potassium iodide as a supersaturated solution (400–900 mg/day) may be prescribed for one month if available
what is erythema multiforme
hypersensitivity reaction usually triggered by infections, most commonly herpes simplex virus (HSV) and drugs
It presents with a skin eruption characterised by a typical target lesion. There may be mucous membrane involvement. It is acute and self-limiting, usually resolving without complications.
risk factors for erythema multiforme
affects young adults (20–40 years of age), however, all age groups and races can be affected.
There is a male predominance.
genetic predisposition
triggers for erythema multiforme
infection - HSC. Type 1 more common
mycoplasma pneumoniae
Parapoxvirus (orf and milkers' nodules) Herpes varicella-zoster (chickenpox, shingles) Adenovirus Hepatitis viruses Human immunodeficiency virus (HIV) Cytomegalovirus Viral vaccines
dermatophyte fungal infections
drugs - barbituates, NSAIDs, penicillins, sulphonamides, nitrofurantoin, anticonvulsants
clinical features of erythema multiforme
The initial lesions are sharply demarcated, round, red/pink and flat (macules), which become raised (papules/palpable) and gradually enlarge to form plaques (flat raised patches) up to several centimetres in diameter. The centre of the papule/plaque darkens in colour and develops surface (epidermal) changes such as blistering or crusting. Lesions usually evolve over 72 hours.
target lesion
mucosal involvement Most commonly lips, inside the cheeks, tongue
Less commonly floor of the mouth, palate, gums.
listers break quickly to leave large, shallow, irregular shaped, painful ulcers that are covered by a whitish pseudomembrane. Typically the lips are swollen with haemorrhagic crusts. The patient may have difficulty speaking or swallowing due to pain.
extensive burns pathology
- Haemolysis due to damage of erythrocytes by heat and microangiopathy
- Loss of capillary membrane integrity causing plasma leakage into interstitial space
- Extravasation of fluids from the burn site causing hypovolaemic shock (up to 48h after injury)- decreased blood volume and increased haematocrit
- Protein loss
- Secondary infection e.g. – Staphylococcus aureus
- ARDS
- Risk of Curlings ulcer (acute peptic stress ulcers)
- Danger of full thickness circumferential burns in an extremity as these may develop compartment syndrome
healing of burns pathology
Superficial burns: keratinocytes migrate to form a new layer over the burn site
Full thickness burns: dermal scarring. Usually need keratinocytes from skin grafts to provide optimal coverage.
which qs will a burns unit ask
depth of burn
percentage area of the body affected
the age of the patient
degree of pain
medical history of the patient
managing of burns patient
paraffin gauze dressing
arrange for review in an outpatient at the nearest burns unit within 1 week
dressing change at least every 48 hours
management in a side room with berries nursing initially
