DERMATOLOGY (5%) Flashcards
ACNE VULGARIS
ACNE = eruption VULGARIS = common
= “common eruption” of skin that occurs when hair follicles (pores) get blocked up/plugged with dead skin cells or oil
once the hair follicle is blocked ==> forms red raised bump on the skin
Acne = particularly common among teenagers because of skin changes that occur during puberty
- affects males more during puberty
- affects females more during later years
DIFFERENT TYPES OF ACNE
⦁ mild acne = whiteheads + blackheads
⦁ moderate acne = pustules
⦁ severe acne = cysts + nodules
3 MAIN LAYERS OF SKIN
⦁ epidermis (5 sublayers) = “Come Lets Get Some Beer”
- stratum corneum = outermost
- stratum lucidum = in palms + feet (thicker)
- stratum granulosum
- stratum spinosum = thickest layer
- stratum basale
⦁ dermis
- connective tissue
- sweat glands
- nerve endings
- lymphatic vessels
- blood vessels
- sebaceous glands - secretes sebum (oil) - helps transport nutrients and lubricates the skin
- hair follicles (shaft, root, bulb)
When arrector pili muscle contracts, sebum gets squeezed out
- Sebum softens the hair shaft and prevents it from getting brittle
- Sebum prevents moisture loss in the skin
- sebum is also slightly acidic, so helps to deter pathogens
⦁ hypodermis
- made of fat and connective tissue that anchors the skin to the underlying muscle
CAUSE OF ACNE - not fully understood - combination of factors
⦁ keratin plugs
⦁ sebum
⦁ bacterial overgrowth
- 4 factors involved ⦁ follicular hyperkeratinization ⦁ increased sebum production ⦁ Propionibacterium acnes within the follicle ⦁ inflammation
1) KERATIN PLUGS
- dead keratinocytes (dead skin cells) + keratin + melanin
- when hair follicles and keratinocytes overproduce keratin (hyperkeratosis), –> leads to more keratin plugs forming –> blocks opening of hair follicle (pore)
- clogged sebaceous glands due to increased proliferation of follicular keratinocytes
2) SEBUM
- released by sebaceous glands in response to increased androgen hormone production that is released during puberty
- also causes blockage of pore, just like keratin plug
- increased sebum production due to increased androgens - MC after puberty, or when increased androgen levels with PCOS or Cushing’s disease
3) BACTERIAL OVERGROWTH
- when excess of keratin plugs or sebum or both ==> can start to fill up a hair follicle (pore), but doesn’t quite plug it up all the way
- if hair follicle is still open to the surface of the skin (open comedo = blackhead)
- blackheads are black because the melanin in keratin plug gets oxidized when exposed to air - becomes darker than normal
- bacteria = Propionibacterium acnes (now called CUTIBACTERIUM ACNES) = always present in follicle - part of normal skin flora, usually don’t cause problems
- if follicle gets completely plugged up with keratin and sebum, then bacterium gets closed off
==> closed comedo where the bacteria continues to grow, as bacteria feasts on keratin and sebum. Bacteria overgrowth as it has nowhere else to go
Triglycerides in the sebum (large component of sebum) particularly is what the bacteria thrive on
- P. acne produces lipase, which converts sebum into inflammatory fatty acids that damages healthy cells –> leads to an inflammatory response
- bacterial overgrowth attracts immune cells, which start attacking bacteria ==> white pus (whitehead) with surrounding red inflammation
CAUSES OF ACNE
- genetic + environmental factors
⦁ hyperkeratosis (genetic component)
⦁ hormones (ex: PCOS - increased androgen levels) (ex: Cushing’s disease = increased androgens)
⦁ products (can block pores)
⦁ behaviors (ex: wearing a headband) (ex: excessive face washing –> irritation –> more acne)
⦁ psychological stress –> increased cortisol –> increased sebum secretion
⦁ certain foods (dairy or chocolate)
acne can affect one’s physical appearance / confidence –> leads to more stress –> leads to more acne / etc.
wearing a headband / helmet / hat etc = contact acne (ACNE VENENATA)
HORMONES - increased androgen levels
Acne vulgaris is thought to be an insulin-like growth factor 1 mediated disease
⦁ Milk products
⦁ hyperglycemia
⦁ smoking
- can all lead to increased insulin-like growth factor 1
Insulin-like growth factor is thought to activate the 5-alpha-reductase enzyme for conversion of testosterone to dihydrotestosterone. It also stimulates androgen release by the adrenal gland and gonads as well as androgen receptor signal transduction. These factors together may stimulate the eruption of acne lesions.
Elevated testosterone and exogenous supplementation of testosterone have also been associated with acne formation. Because hormone levels are elevated and labile in adolescents, this is a significant cause of acne in teens
Androgens, not estrogens, stimulate the growth and secretion of the sebaceous glands. In teenagers, comedonal acne correlates with the rise of dehydroepiandrosterone (DHEA) serum levels.
androgens are what kick off the sebaceous glands -> increased sebum production. DHEA (precursor of testosterone) is what increases sebum production –> seborrhea.
No androgens = no acne
ACNE VULGARIS MC OCCURS ON LOCATIONS OF ⦁ face / neck ⦁ shoulders ⦁ chest ⦁ back - sites of oil glands
- COMEDONES = small, noninflammatory bumps from clogged pores
⦁ blackheads = open comedones (incomplete blockage)
⦁ whiteheads = closed comedones (complete blockage)
4 TYPES OF ACNE VULGARIS (based on severity)
⦁ type I (mild acne) = no scarring, and has few small comedones, may have some papules / pustules
⦁ type II (moderate acne) = no scarring, larger comedones / larger amounts of papules / pustules
⦁ type III (moderately severe acne) = some scarring, have papular and pustular acne
⦁ type IV (severe) = severe scarring and nodulocystic acne - invades deeper into the dermis
TREATMENT - depends on severity
⦁ type I (mild acne)
- topicals such as benzoyl peroxide or salicylic acid - decreases P. acne concentration, removes the top keratin layer, reduces inflammation
- SE = erythema / dermatitis
- topical abx = clindamycin or erythromycin
- ** CLINDAMYCIN can be used with BENZOYL PEROXIDE to reduce resistance ***
- topical retinoids - help to alter pilosebaceous glands –> antibacterial, decreases comedone formation, reduces inflammation
- OCPs = decreases androgen –> reduces sebum production
⦁ mild to moderate = topical retinoids, topical antibiotics, benzoyl peroxide
⦁ type II (moderate acne) = topical retinoids, oral abx such as doxycycline / minocycline / bactrim
- spironolactone for hormonal regulation
⦁ type III and IV = isotretinoin (Accutane) = oral retinoid = synthetic vitamin A derivative - affects sebum secretion
- SE = teratogenicity
Spironolactone = decreases androgen –> reduces sebum production
ISOTRETINOIN - affects all 4 MOA of acne!
- teratogen
- SE = photosensitivity - specifically to UVA
- labs = CBC, lipid panel, LFTs
- hepatitis (increased LFTs)
- increased triglycerides / cholesterol
- arthralgias
- leukopenia (CBC)
- premature long bone closure
- dry skin
- monitor for SE of increased depression / suicidality
- 2 pregnancy tests prior to initiation of treatment + monthly pregnancy tests / labs, 2 forms of contraception - used at least 1 month prior to starting Accutane and 1 month after d/c accutane
the effect of most phototoxic medications is through their activation by UVA light (which comprises 95% of all UV light we receive from the sun).
TREATMENT FOR ACNE SCARS
- retinoids, peels, microdermabrasion, lasers
FOLLICULITIS
- superficial infection of hair follicle with singular or clusters of small papules or pustules with surrounding erythema
inflammation of the superficial or deep portion of the hair follicle
MC = Staph Aureus***
The classic clinical findings of superficial folliculitis are follicular pustules and follicular erythematous papules on hair-bearing skin
Nodules are a feature of deep follicular inflammation.
Folliculitis may be infectious or, less frequently, noninfectious (usually infectious)
Gram-negative folliculitis should be suspected in patients with acneiform lesions concentrated around the NOSE + MOUTH that are RESISTANT to long-term ANTIBIOTIC THERAPY
Gram-negative folliculitis often occurs in patients with a history of acne vulgaris who undergo long-term antibiotic therapy, as antibiotic treatment can disrupt the normal flora of the nasopharynx and allow colonization with gram-negative bacteria. Lesions tend to be fluctuant and concentrated around the nose and mouth.
TREATMENT
- warm compresses
⦁ Topical Mupirocin** = 1st line (or BP cream)
⦁ Clindamycin
⦁ Erythromycin
⦁ oral abx for refractory / severe cases = Cephalexin, Dicloxacillin (both used for impetigo)
⦁ If MRSA suspected = ** BACTRIM ** , doxycycline or clindamycin
HOT TUB FOLLICULITIS
CAUSE = ** PSEUDOMONAS AERUGINOSA **
(gram negative)
Commonly seen in people who bathe in a contaminated spa, swimming pool, or hot tub (especially if it is made of wood) ***
CLINICAL MANIFESTATIONS
⦁ small (2-10mm)
⦁ pink to red bumps - may be filled with pus or covered with a scab
⦁ appear 1-4 days after exposure to source
⦁ itchy, tender bumps located around hair follicles
TREATMENT
⦁ NONE***- reassurance! - usually resolves spontaneously within 7-14 days without treatment
⦁ oral ciprofloxacin if persistent
PSEUDOFOLLICULITIS BARBAE
also known as barber’s itch, folliculitis barbae traumatica, razor bumps, scarring pseudofolliculitis of the beard, and shave bumps
is a medical term for persistent irritation caused by shaving
Pseudofolliculitis barbae (PFB) or “razor bumps” is a chronic inflammatory condition of the skin caused by shaving or plucking hairs and sometimes genetic factors.
- very common in african americans
It begins in teen years as soon as shaving begins and lasts a lifetime.
It is predominantly a disease of those with tightly curled and coiled coarse hair who attempt to remove it by shaving or plucking.
- common in African American populations
PFB is more commonly seen in persons of color given the biological difference of more tightly curved hairs growing out of curved hair follicles.
When shaving is too close (occurs by stretching the skin), the sharpened curved hair retracts below the surface of the skin and pierces the follicle wall from inside (transfollicular penetration). If shaving is infrequent, the hair may grow back in a curve towards the skin and can poke through from the outside (transepidermal or re-entry penetration).
- occurs when free ends of tightly coiled hairs re-enter skin and cause foreign body inflammatory response
⦁ extrafollicular penetration = curly hair coming out and coming back into the hair = more common
⦁ intrafollicular penetration = hair grows out of a different spot - out of the follicle
CLINICAL MANIFESTATIONS
⦁ firm papules with embedded hair
⦁ Painful bumps can appear and lead to long-lasting or permanent dark spots, scars, and even keloids in the sites of inflammation
⦁ The embedded hairs may develop into pustules or become secondarily infected with bacteria
⦁ The shaved cheeks and front of the neck are usually involved while the lip and back of the neck are usually spared
⦁ Similar bumps can occur in the bikini area or the armpits but are much less common.
DIAGNOSIS = made based on clinical appearance
TREATMENT
⦁ Most effective and safe = stop shaving (first line)
⦁ if must remove hair = shave in the direction of hair growth, not against the grain. use single blade razors to avoid too close of a shave, shave frequently
⦁ pre-soak area to soften hairs
⦁ laser hair removal
⦁ Adjunctive medical therapy
- Topical retinoids (Tretinoin) - Low potency topical corticosteroids (treat only for 3-4 weeks) - Topical antimicrobials (benzoyl peroxide 5% or clindamycin 1%)
ROSACEA
Chronic acneiform disorder of facial pilosebaceous units
an inflammatory facial skin disorder characterized by erythematous papules and pustules, but no comedones.**
- increased reactivity of capillaries to heat
PATHOPHYSIOLOGY
- ** dermal matrix degeneration **
- This leads to the pathologic pooling of blood and concentration of reactive oxygen species and inflammatory mediators in the dermis.
The exact etiology for rosacea is unknown. Some believe that it may be a T-cell mediated immune response to the presence of microbial agents (particularly the Demodex species, which are mites that typically infect human hair follicles). However, the evidence is conflicting
- onset: 30-50 years old
- predominantly affects females
EXACERBATING ROSACEA FACTORS ⦁ hot liquids ⦁ spicy foods ⦁ alcohol ⦁ exposure to sun + heat ⦁ exercise ⦁ stress
CLINICAL PRESENTATION OF ROSACEA
⦁ redness to cheeks, nose and chin
⦁ burning or stinging with episodes
⦁ skin dryness, edema
The nose, cheeks, forehead, chin, and glabella are the most commonly affected areas.
Clinical features include flushing, telangiectasias, erythema, papules and pustules, and rhinophyma.
More than 50% of patients with rosacea have ocular manifestations, and ocular findings may be the first manifestation of rosacea in some patients.
Variable erythema and telangiectasia are seen over the cheeks and the forehead. Inflammatory papules and pustules may be predominantly observed over the nose, the forehead, and the cheeks.
Prominence of sebaceous glands may be noted, with the development of thickened and disfigured noses (rhinophyma) in extreme cases. Unlike acne, patients generally do not report greasiness of the skin; instead, they may experience drying and peeling. The absence of comedones is another helpful distinguishing feature.
Rhinophyma may occur as an isolated entity, without other symptoms or signs of rosacea. Rhinophyma can be disfiguring
Manifestations of ocular rosacea range from minor irritation, foreign body sensation, dryness, and blurry vision to severe ocular surface disruption and inflammatory keratitis. Patients frequently describe a gritty feeling, and they commonly experience Blepharitis and conjunctivitis. Other ocular findings include lid margin and conjunctival telangiectasias, eyelid thickening, eyelid crusts and scales, chalazia and hordeolum, punctate epithelial erosions, corneal infiltrates, corneal ulcers, corneal scars, and vascularization
Ocular rosacea is most frequently diagnosed when patients also suffer from cutaneous disease. However, ocular signs and symptoms may occur prior to cutaneous manifestations in 20% of patients with rosacea
4 SUBTYPES OF ROSACEA ⦁ erythematotelangiectatic rosacea ⦁ papulopustular rosacea ⦁ phymatous rosacea (large nose - rhinophyma) ⦁ ocular rosacea
TREATMENT FOR ROSACEA
- minimize precipitating factors
- TOPICAL ANTIBIOTICS = 1st line therapy for mild to moderate rosacea
use gel or creams
⦁ Metronidazole - most common - 1st line
⦁ Erythromycin
⦁ Clindamycin
⦁ Azelaic acid - anti-inflammatory effects (reduces redness and inflammation for both acne + rosacea)
⦁ Brimonidine (Mirvaso) = alpha -2 agonist = vasoconstrictor; best for facial flushing / persistent redness) - brimonidine can also be used for acute angle closure glaucoma
⦁ Topical Ivermectin cream (Soolantra) = for ppl who get papulopustular acneiform rosacea due to being immunologically sensitive to mites
⦁ Laser
SYSTEMIC ANTIBIOTICS = for mod/severe rosacea
⦁ Tetracycline
⦁ Doxycycline (Oracea) / Minocycline
⦁ Erythromycin
FACIAL REDNESS/FLUSHING TX = BRIMONIDINE (MIRVASO)
PAPULOPUSTULAR DISEASE TX = metronidazole, azelaic acid, ivermectin (soolantra) = 1st line; can try sodium sulfacetamide
can do oral antibiotics for mod/severe = tetracyclines (doxy/tetra), oral metronidazole, oral ivermectin, sodium sulfacetamide
ERYTHEMA MULTIFORME
An acute, immune-mediated condition that affects the skin and mucous membranes (mouth + genitals)
Acute self-limited TYPE IV HYPERSENSITIVITY RXN
type IV = delayed or cell-mediated (cytotoxic T cells)
MC in young adults: age 20-40
Skin = largest organ in the body
⦁ epidermis
⦁ dermis
⦁ hypodermis
In the epidermis = keratinocytes produce protein keratin in the stratum basale or basal layer of the epidermis
- Basal cells = single layer of stem cells that continually divide and produce new keratinocytes
- new keratinocytes then migrate upwards to form other layers of the epidermis
- basement membrane sits underneath stratum basale that connects epidermis to dermis - forms epidermal-dermal junction
Mucosa lines the inside of the body, just as the skin lines the outside of the body
- Mucosa is named for the surface it covers (oral mucosa / nasal mucosa / bronchial mucosa / gastric mucosa / etc)
- Mucosa is made up of Epithelial Cells that sits on top of lamina propria (connective tissue)
- Basement membrane present in mucosa as well, that connects epithelial cells to lamina propria
Basal epithelial cells, as well as all other cells, will present MHC I molecule on their surface to present foreign particles to Cytotoxic T cells for destruction. If Cytotoxic T cell recognized cell as foreign = destroys it
ERYTHEMA MULTIFORME = TYPE IV HYPERSENSITIVITY REACTION = Cell mediated
- meaning that damage is due to the CYTOTOXIC T CELLS inappropriately attacking the basal epithelial cells –> cellular death + detachment at basement membrane
Cytotoxic T cells release proinflammatory mediators such as interferon gamma + TNF alpha, which attract other immune cells to the area –> more damage –> cellular death + detachment at basement membrane
leads to formation of VESICLES + EROSIONS in the skin and mucosa - red (erythema) + multiforme (presents in a variety of shapes and sizes)
CLINICAL PRESENTATIONS
⦁ red rash - macules / papules / vesicles / bullae of various shapes and sizes - NOT ITCHY*
⦁ ** MC LESION = TARGETOID LESION ** - between 2mm - 2cm
- have central necrosis of epidermis surrounded by concentric rings of erythema = looks like a “bulls-eye” or “target”
⦁ MC on HANDS + FOREARMS*
⦁ 50% of rash = ORAL LESIONS (PAINFUL)***
3 concentric zones of color from center to outer ring
1) central dusky/dark area that can be crust or vesicle
2) paler pink or edematous zone
3) peripheral red/dark ring
Fixed lesions (as opposed to urticaria, in which lesions typically resolve within 24 hours)
About 3 days prior, may begin having muscle aches, low-grade fever, and headache. Will begin itching and burning, then rash appears.
Erythema Multiforme can progress to Steven’s Johnson’s Syndrome + Toxic Epidermal Necrolysis
presence of erythematous patches with central clearing, known clinically as target lesions, are associated with erythema multiforme. Erythema migrans chronicum (Lyme Disease) also produces an annular erythematous rash with central clearing, but usually affects the thigh, groin, and axilla
CAUSES
- In approximately 50% of patients, no specific precipitating cause is identified
- in remaining cases, a variety of causes have been implicated
⦁ certain infections (herpes simplex, enteroviruses, Mycoplasma pneumoniae - especially children, Chlamydia, histoplasmosis) - ** MC = HERPES SIMPLEX VIRUS ***
- Other MC = Mycoplasma (especially in children)
- HIV, CMV
⦁ drugs (sulfonamides, penicillins, phenytoin, carbamazepine, ciprofloxacin, aspirin, corticosteroids, cimetidine, allopurinol, oral contraceptives)
- ** MC = SULFA DRUGS ****
- also Beta Lactams, Phenytoin, Phenobarbital, etc.
⦁ neoplasia (leukemia, lymphoma, multiple myeloma, internal malignancy)
⦁ sarcoidosis
⦁ foods (notably emulsifiers in margarine).
- ’’ TARGET LESIONS - DULL, “DUSTY VIOLET” RED, PURPURIC MACULES/VESICLES/BULLAE IN THE CENTER SURROUNDED BY PALE EDEMATOUS RIM + PERIPHERAL RED HALO
- Often febrile / URI symptoms
ERYTHEMA MULTIFORME MINOR
⦁ milder condition
⦁ almost always triggered by a preceding infection*
⦁ targetoid lesions on PALMS + SOLES (acral)
⦁ lesions are symmetric and mostly on extremities (acral)
⦁ **NO MUCOSAL MEMBRANE LESIONS**
ERYTHEMA MULTIFORME MAJOR
⦁ 1+ mucosal sites are involved = typically oral mucosa + either ocular and/or genital mucosa
⦁ skin lesions more widespread
⦁ < 10% BSA: spreads acrally –> centrally
⦁ more severe, but still only rarely life-threatening
⦁ can progress to epidermal necrosis - usually occurs in oral mucosa - labial mucosa*, tongue, buccal mucosa, floor, soft palate
⦁ hemorrhagic crusting of vermillion lip border
⦁ MC associated with preceding mycoplasma or herpes simplex infection
⦁ ** no epidermal detachment ** (unlike SJS/TEN)
** Erythema multiforme is associated with (bacteria) Mycoplasma infection, which causes atypical pneumonia **
some patients can have recurrent episodes of erythema multiforme - ex: recurrent HSV sores of oral mucosa
** thought that HSV proteins are similar to proteins found in oral mucosa –> causing T cells to get confused and attack oral keratinocytes expressing those proteins
SJS + TENS = almost always due to a drug reaction, and are much more extensive to the skin/mucosa and are much more life threatening
SJS = < 10% BSA - preferential involvement of face + trunk (EM usually acral - palms + soles, may have mucosal involvement with EM major)
Toxic Epidermal Necrolysis (TEN) is a severe form of Stevens Johnson Syndrome where there is diffuse sloughing of skin and is distinguished by involvement of > 30% BSA
- Both are typically associated with an adverse drug reaction, especially sulfonamides, and ** EPIDERMAL DETACHMENT ** - Nikolsky Sign
DIAGNOSIS
⦁ clinical appearance of targetoid skin rash + bleeding + hemorrhagic crusting of the lips
⦁ Biopsy = Erythema multiforme targetoid lesions can be distinguished as an accumulation of lymphocytes on the dermo-epidermal junction.
the involvement of oral mucosa makes it hard for patient to eat + drink —> dehydration
TREATMENT
⦁ ** SYSTEMIC STEROIDS *** to reduce inflammation
⦁ maintain hydration - IV fluids
⦁ pain control - lidocaine / diphenhydramine mouthwash for oral lesions
⦁ treat infection if present
⦁ d/c offending agent if caused by medication
⦁ continuous antivirals to prevent recurrence due to HSV: valacyclovir 500mg TID x 10 days
- Erythema Multiforme usually self-resolves over weeks
Skin lesions usually evolve over 3-5 days + persist about 2 weeks
STEVENS JOHNSONS SYNDROME
Acute, immune-mediated condition that affects the skin and mucous membranes
TYPE IV HYPERSENSITIVITY REACTION (T-cell mediated hypersensitivity reaction)
- meaning that damage is due to the cytotoxic T cells (CD8 cells) inappropriately attacking the epithelial cells in the mucosa and epidermis
Cytotoxic T cells release proinflammatory mediators such as interferon gamma + TNF alpha, which attract other immune cells to the area –> more damage –> cellular death + detachment at basement membrane
leads to formation of VESICLES + EROSIONS in the skin and mucosa - red (erythema) + multiforme (presents in a variety of shapes and sizes)
leads to formation of VESICLES + EROSIONS in the skin and mucosa - red (erythema) + multiforme (presents in a variety of shapes and sizes)
- due to sloughing of the skin at the dermal-epidermal junction.
Drugs may bind to major histocompatibility complex (MHC) I and T-cell receptors, which causes expansion of cytotoxic T cells. These T-cells induce massive apoptosis of keratinocytes through a variety of cytotoxic proteins, including FAS LIGAND.
- Granulysin, in particular, is a cytolytic protein that is highly associated with cell death in TEN
Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are considered to be the same condition with differing severities of affected BSA
- Both SJS + TEN can be fatal if not treated, and fatality increases with severity
CLINICAL PRESENTATION
- fever + flu-like symptoms about 1 week prior to rash
such as cough, sore throat, red eyes, tender pink skin
⦁ red rash - macules / papules / vesicles / bullae of various shapes and sizes - NOT ITCHY***
⦁ ** MC LESION = TARGETOID LESION ** - between 2mm - 2cm
- have central necrosis of epidermis surrounded by concentric rings of erythema = looks like a “bulls-eye” or “target”
SJS = more severe form of Erythema Multiforme - in which 10-30% BSA is involved
- may also be thought that SJS = <10% BSA, TEN = > 30% BSA, and 10-30% = overlap between SJS + TEN
⦁ almost always due to a drug reaction
⦁ is much more extensive to the skin/mucosa
⦁ is much more life threatening
- ’’ TARGET LESIONS - DULL, “DUSTY VIOLET” RED, PURPURIC MACULES/VESICLES/BULLAE IN THE CENTER SURROUNDED BY PALE EDEMATOUS RIM + PERIPHERAL RED HALO
With the skin + mucosa compromised, the body can DEHYDRATE, and external pathogens can invade and cause an infection –> can lead to SEPSIS
SJS = preferential involvement of face + trunk
⦁ * 1+ mucous membrane involvement
⦁ with epidermal detachment (NIKOLSKY SIGN)*
NIKOLSKY SIGN = the separation of papillary dermis from basal layer when gentle lateral pressure is applied; this is a helpful diagnostic feature of SJS + TEN
CAUSES
- MC after drug eruptions- especially with
SULFA + ANTICONVULSANT MEDS - where metabolite peptides are recognized as foreign by cytotoxic T cells
⦁ Sulfa drugs** + Penicillins ****
⦁ Anticonvulsant Meds - Phenytoin, Carbamazepine, Lamotrigine (Lamictal), Phenobarbital
⦁ NSAIDS (Aspirin, Piroxicam, nevirapine, and diclofenac)
⦁ Allopurinol***
⦁ Other antibiotics - Beta Lactams, Ciprofloxacin
- Infections are less common ⦁ Mycoplasma*** ⦁ HIV ⦁ HSV*** ⦁ CMV ⦁ Malignancy - (leukemia, lymphoma, multiple myeloma, internal malignancy) ⦁ Idiopathic
DIAGNOSIS
- can be diagnosed by medical history and physical examination, and confirmed by a skin biopsy (punch)
SJS + TEN = associated with a high mortality rate.
TREATMENT
- similar to the protocol for treating patients with extensive burns.
- hospitalization
- immediately d/c triggering medications
Immune- Modulators to help stop the hypersensitivity reaction
⦁ IV steroids
⦁ IVIG
⦁ antihistamines
Supportive Therapy
⦁ IV fluids
⦁ Pain Meds
⦁ Wound care
Scarring can be left for quite some time after healing
TOXIC EPIDERMAL NECROLYSIS (TEN)
Acute, immune-mediated condition that affects the skin and mucous membranes
TYPE IV HYPERSENSITIVITY REACTION (T-cell mediated hypersensitivity reaction)
- meaning that damage is due to the cytotoxic T cells (CD8 cells) inappropriately attacking the epithelial cells in the mucosa and epidermis
Cytotoxic T cells release proinflammatory mediators such as interferon gamma + TNF alpha, which attract other immune cells to the area –> more damage –> cellular death + detachment at basement membrane
leads to formation of VESICLES + EROSIONS in the skin and mucosa - red (erythema) + multiforme (presents in a variety of shapes and sizes)
- due to sloughing of the skin at the dermal-epidermal junction.
Drugs may bind to major histocompatibility complex (MHC) I and T-cell receptors, which causes expansion of cytotoxic T cells. These T-cells induce massive apoptosis of keratinocytes through a variety of cytotoxic proteins, including FAS LIGAND.
- Granulysin, in particular, is a cytolytic protein that is highly associated with cell death in TEN
Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are considered to be the same condition with differing severities of affected BSA
- Both SJS + TEN can be fatal if not treated, and fatality increases with severity
TEN = more severe form of SJS - in which > 30% BSA is involved
⦁ * 1+ mucous membrane involvement
⦁ with epidermal detachment (NIKOLSKY SIGN)*
NIKOLSKY SIGN = the separation of papillary dermis from basal layer when gentle lateral pressure is applied; this is a helpful diagnostic feature of SJS + TEN
CLINICAL PRESENTATION
- fever + flu-like symptoms about 1 week prior to rash
⦁ red rash - macules / papules / vesicles / bullae of various shapes and sizes - NOT ITCHY***
⦁ ** MC LESION = TARGETOID LESION ** - between 2mm - 2cm
- have central necrosis of epidermis surrounded by concentric rings of erythema = looks like a “bulls-eye” or “target”
SJS = more severe form of Erythema Multiforme - in which <10% BSA is involved
- SJS = < 10% BSA, TEN > 30% BSA, and 10-30% = overlap between SJS + TEN
⦁ almost always due to a drug reaction
⦁ is much more extensive to the skin/mucosa
⦁ is much more life threatening
- ’’ TARGET LESIONS - DULL, “DUSTY VIOLET” RED, PURPURIC MACULES/VESICLES/BULLAE IN THE CENTER SURROUNDED BY PALE EDEMATOUS RIM + PERIPHERAL RED HALO
With the skin + mucosa compromised, the body can DEHYDRATE, and external pathogens can invade and cause an infection –> can lead to SEPSIS
** Sepsis = MC cause of death in patients with TEN **
SJS = preferential involvement of face + trunk
⦁ * 1+ mucous membrane involvement
⦁ with epidermal detachment (NIKOLSKY SIGN)*
NIKOLSKY SIGN = the separation of papillary dermis from basal layer when gentle lateral pressure is applied; this is a helpful diagnostic feature of SJS + TEN
- ASBOE-HANSEN sign is the lateral extension of bullae with pressure and is a diagnostic feature of toxic epidermal necrolysis.
CAUSES
- MC after drug eruptions- especially with
SULFA + ANTICONVULSANT MEDS
⦁ Sulfa drugs** + Penicillin ****
⦁ Anticonvulsant Meds - Phenytoin, Carbamazepine, Lamotrigine (Lamictal), Phenobarbital
⦁ NSAIDS (Aspirin, Piroxicam, nevirapine, and diclofenac)
⦁ Allopurinol
⦁ Other antibiotics - Beta Lactams, Ciprofloxacin
- Infections are less common ⦁ Mycoplasma*** ⦁ HIV ⦁ HSV ⦁ CMV ⦁ Malignancy - (leukemia, lymphoma, multiple myeloma, internal malignancy) ⦁ Idiopathic
DIAGNOSIS
- can be diagnosed by medical history and physical examination, and confirmed by a skin biopsy (punch).
- Nearly all patients with TEN develop oral, ocular, or genital mucositis, which helps diagnose the condition.
- ASBOE-HANSEN sign is the lateral extension of bullae with pressure and is a diagnostic feature of toxic epidermal necrolysis.
SJS + TEN = associated with a high mortality rate.
TREATMENT
- similar to the protocol for treating patients with extensive burns = refer to burn unit!!!!
- hospitalization
- immediately d/c triggering medications
Immune- Modulators to help stop the hypersensitivity reaction
⦁ IV steroids
⦁ IVIG
⦁ antihistamines
Supportive Therapy
⦁ IV fluids
⦁ Pain Meds
⦁ Wound care
- consult ophtho if eyes are affected
Scarring can be left for quite some time after healing
ALOPECIA AREATA
also known as spot baldness
is an autoimmune disease in which hair is lost from some or all areas of the body, usually from the scalp due to the body’s failure to recognize its own body cells and destroys its own tissue as if it were an invader
Alopecia areata is an autoimmune disease characterized by destruction of hair follicles and the acute development of bald patches on the body.
Often it causes bald spots on the scalp, especially in the first stages.
The first symptoms of alopecia areata are small bald patches.
The alopecia can be reversible or irreversible depending on if there is fibrosis of the scalp.
The hair that does regrow may be gray or depigmented
Any area of the body can be affected including the scalp, beard, axilla, and pubic hairs.
A quarter of alopecia patients will have other autoimmune diseases such as type 1 diabetes mellitus, thyroid disease or vitiligo
PHYSICAL EXAM = Typically well-circumscribed round or oval patches of hair loss with smooth and normal-appearing scalp. The periphery of the hair loss typically is studded with “exclamation point hair,” or fractured hairs which look like an exclamation point.
Differential diagnosis includes secondary syphilis, trichotillomania and fungal infection.
DIAGNOSIS = usually clinical but trichoscopy or biopsy can be done
TREATMENT = topical or injectable steroids (ILK)
The disease can resolve spontaneously and simple observation is done in minor cases
ANDROGENIC ALOPECIA
D
ALOPECIA TOTALIS
more severe case of alopecia in which the entire scalp experiences hair loss
less likely to resolve adequately
Diagnosis is usually clinical but trichoscopy or a biopsy can be done
ALOPECIA UNIVERSALIS
more severe case of alopecia in which the entire epidermis experiences hair loss
less likely to resolve adequately
Diagnosis is usually clinical but trichoscopy or a biopsy can be done
ONYCHOMYCOSIS
Onychomycosis = fungal infection of the nail.
Onychomycosis can be caused by fungi, yeasts, and nondermatophyte molds.
Fingernail onychomycosis is most commonly caused by yeast.
Onychomycosis is more common in adults than in children and is more common in men than in females.
There are several subtypes of onychomycosis, but the most common clinical subtype is distal lateral subungual onychomycosis.
Over 80% of onychomycosis cases in the United States are caused by Trichophyton rubrum.
Risk factors for onychomycosis include ⦁ increased age, ⦁ swimming, ⦁ tinea pedis, ⦁ psoriasis, ⦁ diabetes, ⦁ immunodeficiency ⦁ living with individuals with onychomycosis.
Distal lateral subungual onychomycosis often begins on the great toe spreading from a distal corner to the cuticle.
The nail appears yellowish or brownish and is often thickened and rough.
Although onychomycosis is primarily a cosmetic concern for most patients, occasionally severe disease can cause discomfort or pain.
DIAGNOSIS
⦁ KOH prep
⦁ periodic-acid-Schiff staining
TREATMENT
- topical or systemic antifungals
- systemic = higher cure rate with shorter course, but more serious SE
⦁ 1st line = Terbinafine (Lamisil) 250mg x 12 weeks
- watch liver enzymes
⦁ 2nd line = Itraconazole 200mg x 12 weeks
- watch liver enzymes
⦁ 3rd line = Diflucan 150mg x 6-9 months
- no labs
Onychomycosis
Patient will be complaining of thickened and discolored toenails
Diagnosis is made by KOH preparation of nail scraping
Treatment is oral terbinafine
Comments: Serum aminotransferases should be monitored before starting treatment with terbinafine and during the treatment due to hepatotoxicity
PARONYCHIA
Infection of the nail margin
MC occurs after skin trauma (biting nails, cuticle damage) - infection in the skin around the fingernails or toenails often caused by ingrown nails
MC bacterial agent = STAPH AUREUS (especially if rapid - acute)***
- others = GABHS
- Candida if slow growing (chronic)***
CLINICAL MANIFESTATION
- painful, red, swollen area around the nail at the cuticle site / around the base or the sides of the nail.
MANAGEMENT
- warm soaks (to reduce pain + swelling)
- ABX (cephalexin / Keflex)
- I+D (to drain pus)
***Most important thing = differentiate paronychia from a felon (entire finger is swollen, red, and very tender = starting to compromise vascular flow to the area)
An 11-blade scalpel or 18-gauge needle should be inserted into the eponychium and paronychium parallel to the nail until pus begins to drain
ERYTHEMA INFECTIOSUM (FIFTH’S DISEASE)
SLAPPED CHEEK DISEASE
PARVOVIRUS B19
APLASTIC CRISIS
LACY RETICULAR RASH ON FACE - spreads to body 24 hrs later
Caused by Parvovirus B19* - single stranded DNA virus
- transmission = respiratory droplets (or blood)
- 4-14 day incubation period
a mild febrile illness with rash. It often occurs in outbreaks among school-aged children, although it can occur in adults as well
⦁ MC in children < 10 y/o
CLINICAL PRESENTATION
1) coryza (non-allergic rhinitis) + fever, runny nose, headache, sore throat x about 1 week ==>
==> “slapped cheek” on face with circumoral pallor (central clearing) x 2-4 days ==>
==> about 24hrs later- LACY RETICULAR RASH on extremities (especially upper extremities) - rash spares palms + soles
- the rash resolves by 2-3 weeks; rash may last few days to several weeks
- rash = frequently pruritic
2) Arthropathy / Arthralgias in older children + adults (usually occurs in adult women)*** (Also seen with RUBELLA - german measles)
3) Associated with fetal loss in pregnancy - fetal hydrops, CHF, and spontaneous abortion - mild febrile exanthematous disease, little or no prodrome
- low grade fever, varying degrees of conjunctivitis, upper respiratory complaints - runny nose, cough, coryza, myalgia in older children / adults, itching, nausea, diarrhea
- SLAPPED FACE - fiery red erythema of cheeks
- bilaterally symmetrical appearance. 24 hours later, rash appears on arms/legs/trunk
a child with fever that later develops red rash on their cheeks that fades as a lacy reticular rash spreads across the body
** Reappearance of rash - after it clears, this may occur if skin is irritated/traumatized by sunlight, heat, cold or friction
- illness usually mild - may include ⦁ low grade fever ⦁ URI symptoms (cough / coryza) ⦁ mild malaise (but may not have any of these symptoms)
Rash = flat, LACY, reticular, often pruritic - located on cheeks, trunk and extremities
Children are NOT contagious once the rash appears
** Parvovirus B19 may cause APLASTIC CRISIS (Reticulocytopenia - decreased # of immature RBCs) - in children with weakened immune systems - Sickle Cell Disease***, G6PD deficiency, HIV, Leukemia, thalassemia etc (NOT megaloblastic anemia - only in patients with chronic hemolytic anemia)
aplastic crisis is an infection caused by parvovirus B19. It causes production of RBCs in the marrow to be shut down for up to 10 days.
The aplastic crisis is temporary cessation of red cell production. Because of the markedly shortened red cell survival time in patients with sickle cell disease, a precipitous drop in hemoglobin occurs in the absence of adequate reticulocytosis
DIAGNOSIS
- Diagnosis is based primarily on clinical observations, history, and physical exam.
- Elevated titer of IgM anti-parvovirus antibodies
- PCR in serum
- Serology: associated with enlarged nuclei** with peripherally displaced chromatin
TREATMENT
- symptomatic treatment = NSAIDS, antipyretic
HAND-FOOT-MOUTH DISEASE
COXSACKIE VIRUS A
ASEPTIC MENINGITIS
- caused by the COXSACKIE VIRUS - part of the enterovirus family
⦁ spread via fecal - oral route or oral-oral route (saliva / sputum)
- highly contagious intestinal virus - part of Picornaviridae family
- single stranded RNA virus
Picornaviruses = nonenveloped, single stranded, positive sense, linear, RNA virus with icosahedral capsid structure.
- MC in children < 5 y/o
- MC in late summer / early fall
2 types of Coxsackie Virus = A + B
BOTH A + B CAN CAUSE ⦁ Aseptic meningitis *** ⦁ rashes ⦁ common cold symptoms - or no symptoms
PRIMARILY COXSACKIE A VIRUS = what causes hand-foot-mouth disease
Coxsackie A virus = hand-foot-mouth disease, herpangina, viral conjunctivitis
Coxsackie B virus = Pericarditis, Myocarditis, pleurodynia - can infect the heart, pleura and pancreas (type I DM association)
Coxsackievirus is a viral infection most commonly associated with subacute granulomatous De Quervian thyroiditis.
SIGNS / SYMPTOMS OF HAND-FOOT-MOUTH
⦁ mild fever / URI symptoms followed by rash
⦁ rash = flat discolored spots and bumps that may blister
⦁ rash involves the skin of hands, feet, mouth as well as occasionally the buttocks / genitalia
⦁ sore throat
⦁ decreased appetite because of sore throat/oral lesions
⦁ fatigue / malaise
Coxsackie A is one of the few causes of rash involving the palms and soles.
Hand-foot-mouth disease = mostly affects infants / children, but can occur in adults as well
mild fever, URI symptoms, decreased appetite starting 3-5 days after exposure
—> 1-2 days after fever/URI symptoms = oral exanthem - vesicular lesions with erythematous halos + ulcers in the oral cavity - especially the buccal mucosa and tongue
–> skin exanthem 1-2 days later = oval-shaped vesicular, macular or maculopapular lesions on distal extremities - often includes the palms + soles
COMPLICATIONS
⦁ aseptic (viral) meningitis - rare
⦁ encephalitis - rare
⦁ fingernail / toenail loss may occur
DIAGNOSIS
⦁ clinical - based on age / hx - symptoms / pe - mouth sores + rash
⦁ may do throat swab or fecal testing for coxsackie virus
LABS
⦁ elevated CRP
⦁ leukocytosis (elevated WBC)
⦁ atypical lymphocytes
TREATMENT
⦁ symptomatic = antipyretic (Tylenol / ibuprofen) + mouth numbing (magic mouthwash)
MEASLES (RUBEOLA)
PAROMYXOVIRUS
FEVER + 3C’s (3 days) = cough, coryza, conjunctivitis,
then 1-2 days later
KOPLIK SPOTS
BRICK RED RASH - STARTS AT HAIRLINE (7 days)
- rash darkens + coalesces
Measles = one of the most contagious infectious diseases
Remains a leading cause of death, especially among children, and particularly in areas with low rates of vaccination
Caused by ** MEASLES VIRUS **
= PARAMYXOVIRUS family (also causes Mumps)
Transmission = AIRBORNE PARTICLES = what makes it so contagious - tiny particles released into the air when someone coughs or sneezes –> can remain in that air space / nearby surfaces for up to 2 hours
- if someone breathes in that air, or touches space and then touches eyes / nose / mouth
Measles is so contagious that if one person is contagious, 90% of non-immune people around will also get infected
Measles quickly invades the epithelial cells of trachea or bronchi
Measles uses Hemagluttinin (H protein) to bind to cells
Measles virus = single stranded RNA virus with helical capsid symmetry with envelope = negative sense (has to be transcribed by RNA polymerase into a positive sense mRNA strand) –> then ready to be translated into viral proteins and be sent out to other cells –> carried from local tissue in the lungs to lymph nodes –> blood –> various organ systems (lungs / intestines / brain)
Incubation period of Measles = 10-14 days
Prodromal period of Measles = typically about 3 days
⦁ High Fever (unlike Rubella = mild fever) + 3 Cs
⦁ Cough
⦁ Conjunctivitis (of sclera)
⦁ Coryza (swelling of nasal mucosa = stuffy nose)
Then = Enanthem Rash 1-2 days later
- Rash on mucous membranes
- looks like “ SALT GRAINS” on a wet background =
- ** KOPLIK SPOTS ** - commonly seen on inside of cheeks = ** small red spots in buccal mucosa with pale blue / white center ***
Exanthem period of Measles = about 4 days
⦁ Morbiliform (maculopapular) BRICK-RED rash - STARTS AT HAIRLINE / FACE –> spreads to extremities (Cephalocaudal)
(opposite of Roseola = starts on trunk, spreads to face)
⦁ Some patients also get Photophobia *** - Vitamin A supplement can help with this
Recovery period of Measles = 10-14 days - usually left with a persistent cough
Once someone has Measles and recovers from it = have lifelong immunity!
Because Measles can spread to various organ system like Lungs, Intestines, Brain = can lead to serious complications such as Pneumonia, Diarrhea and Encephalitis –> can all lead to Death
⦁ Giant Cell Pneumonia = rare respiratory disease that is seen after Measles that occurs in immunocompromised
Measles also suppresses the immune system x 6 weeks = can lead to bacterial superinfectious such as Otitis Media and Bacterial Pneumonia
- these complications = worst among Infants (highest mortality rate with Measles)
** COMPLICATION IN CHILDREN < 2 **
⦁ SUBACUTE SCLEROSING PANENCEPHALITIS 7-10 years later after Measles infection = chronic inflammation of the entire brain
⦁ symptoms are subtle at first = mood changes, but can eventually become severe (seizures, coma, death)
DIAGNOSIS
⦁ Serology - look for Measles antibodies in blood serum
PREVENTION
⦁ Measles vaccine = Live attenuated vaccine (weakened) = given at 12-15 months old, then again at 4-6 y/o
⦁ 95% efficacy rate
⦁ can be given to HIV patients without signs of immunodeficiency
⦁ cannot be given in pregnancy
MEASLES VACCINE
⦁ is a live vaccine - can therefore cause mild measles symptoms
⦁ A morbilliform rash is a common side effect - spread across patient’s CHEST, is not itchy or painful
⦁ will present 7-14 days after vaccine is given
Another source of protection for young infants = Mother’s Anti-Measles Antibody (Immunoglobulin) = transferred via placenta - lasts until about 9 months old
TREATMENT
⦁ no specific anti-viral treatment
⦁ medications aimed at treating superinfections, maintaining hydration, fever + pain relief
⦁ Vitamin A = boosts antibody response and decreases risk of complications
GERMAN MEASLES (RUBELLA)
TOGAVIRUS 3 DAY RASH BLUEBERRY MUFFIN RASH POSTAURICULAR LYMPHADENOPATHY FORCHHEIMER SPOTS milder fever than rubeola CATARACTS + DEAFNESS + PDA CONGENITAL RUBELLA SYNDROME
- caused by the RUBELLA VIRUS
Rubella virus = RNA virus belonging to the TOGAVIRUS family that has a linear, positive single-stranded RNA structure and an icosahedral capsid symmetry
TRANSMISSION
⦁ Respiratory droplets
** 3 DAY RASH ** with rubella (german measles)
- Children are routinely immunized at 12 months, then again - booster at age 4-6 (kindergarten shots)
Rubella vaccine = live attenuated (weakened) vaccine = do NOT give during pregnancy!!!
Administration of rubella immunoglobulin is not indicated for a pregnant patient, as sufficient evidence for an ability to reduce congenital rubella syndrome has not been demonstrated.
according to the Advisory Committee on Immunization Practices (ACIP), a woman who intends to get pregnant should receive the vaccine 28 days before attempting to become pregnant. There is also no indication for using immunoglobulin for prevention.
Early in pregnancy = test that blood has POSITIVE rubella antibody titer = baby doesn’t have rubella
Rubella causes severe disease in neonates, but mild disease in children
SYMPTOMS
- in neonates, congenital rubella can cause Triad of:
1) cataracts (or retinopathy or microphthalmia)
2) deafness (sensorineural)
3) PDA = “continuous machinery murmur” (or pulmonary artery stenosis/hypoplasia)
*** Classic Triad of: Cataracts + Deafness + PDA
⦁ fever** / cough / anorexia ⦁ microcephaly ⦁ mental retardation* ⦁ "blueberry muffin" rash due to ** EXTRAMEDULLARY HEMATOPOIESIS ** - formation of blood cells outside the medulla of the bone (usually in liver or spleen - can be pathologic process)
Fever = lower compared to measles
Rash = usually lasts about 3 days
Rubella + CMV = two infections that are associated with a “blueberry muffin” rash.
- in children = mild disease
⦁ fever / cough / anorexia - sore throat
⦁ POSTAURICULAR LYMPHADENOPATHY* or POSTCERVICAL LYMPHADENOPATHY* or OCCIPITAL LYMPHADENOPATHY***
⦁ malar facial rash - starts on face, then spreads to trunk and extremities —> starts to desquamate
** RASH STARTS ON FACE, MOVES TO BODY ** within 24 hours = rash lasts 3 days
compared to rubeola (measles), rubella rash spreads more quickly (3 days) and does not darken or coalesce
⦁ ** FORCHHEIMER SPOTS ** = small red macules or petechiae on soft palate (also seen in scarlet fever)
- in adolescents / adults = prodrome of ⦁ low-grade fever ⦁ sore throat - anorexia, cough ⦁ ocular pain *** ⦁ polyarthralgia *** JOINT PAIN ⦁ postauricular / occipital lymphadenopathy ***
** JOINT PAIN + PHOTOSENSITIVITY ** may be seen, especially in young women (adolescents / young adults)
JOINT PAIN also seen in adult/adolescent women with fifth’s disease (erythema infectiosum)
Rubella causes a macular type of facial rash that starts desquamating when it moves to the trunk.
Rubella is a viral infection that presents with a postauricular lymphadenopathy and a fine rash that begins on the head and moves down.
** STARTS ON FACE, MOVES DOWN TO BODY ** (unlike roseola = starts on trunk, moves to face!)
DIAGNOSIS
⦁ clinical
⦁ Rubella-specific IgM antibodies via enzyme immunoassay (MC used)
** DIFFERENCE BETWEEN RUBELLA (german measles) and RUBEOLA (measles) = fever is higher in rubeola (measles), and rash lasts longer in rubeola (measles) = about 7 days instead of 3 days, and also rash darkens and coalesces (comes together to form one larger lesion)
MANAGEMENT = supportive
⦁ anti-inflammatories
⦁ generally no complications in children with Rubella, compared to Rubeola (measles)
If pregnant = can cause complications as a TORCH infection
TERATOGENIC - ESPECIALLY IN 1ST TRIMESTER
⦁ congenital syndrome** = sensorineural deafness + cataracts + TTP (blueberry muffin rash) + mental retardation + heart defects (PDA or Pulmonic valve stenosis / hypoplasia) - part of TORCH syndrome
** PDA **
ROSEOLA
(SIXTH’S DISEASE)
HHV 6 OR 7
high fever x 3-5 days that resolves –> rash
RASH STARTS ON TRUNK –> SPREADS TO FACE
MC caused by HHV-6** (can be caused by HHV6 or 7) - just like pityriasis rosea
- also known as exanthem subitum.
- infection is very common
- MC occurs < 5 y/o (MC in 6 months - 3 years)
- seroprevalence in most countries approaches 100% in children over 2 years old
- Complications are uncommon (seizures can occur during febrile period)
TRANSMISSION = respiratory droplets (saliva!)
- Virus is acquired from close contact with saliva from parents or sibling
- 10 day incubation period
** major cause of infantile FEBRILE SEIZURES **
CLINICAL MANIFESTATIONS
⦁ **Abrupt onset of high fever (101 - 106) that lasts 3-5 days, then fever resolves, then erythematous maculopapular rash appears several hours later
⦁ fever resolves before onset of a ROSE, PINK nonpruritic maculopapular, blanchable rash on trunk / back that spreads to face
⦁ rash lasts up to 1-2 days
⦁ only childhood viral exanthem that STARTS ON TRUNK*** and THEN SPREADS TO FACE **
- child appears “well + alert” during febrile phase; may be irritable
- rash spontaneously resolves - may not appear for 1-2 days until after fever breaks
- fever gets so high, can lead to seizures
- usually kids are brought in for the rash, not the fever
kid often given amoxicillin for fever, then rash breaks out - ppl think their kid is allergic to amoxicillin
- lights up bright red in warm environment (bath)
TREATMENT
- supportive = anti-inflammatories, antipyretics (to prevent febrile seizures) [ ibuprofen for both! ] or acetaminophen / Tylenol for antipyretic properties
- tepid baths (do not put child in cool or cold water)
- may apply cool packs to groin/underarms in older kids
CELLULITIS
Cellulitis = - acute, spreading infection of dermal + subcutaneous tissues through a skin portal
- can occur in all ages*
COMMON CAUSES (adults) ⦁ staph ⦁ group A strep (GABHS = Strep Pyogenes)
CAUSES (kids)
⦁ h. flu
⦁ strep pneumo
Skin infection with underlying drainage, penetrating trauma, eschar, or abscess is most likely caused by STAPH; on the other hand
Strep is the most likely pathogen when these factors (drainage, penetrating trauma, eschar, abscess) are not present.
- hx of trauma
- may be unaware of wound of entry
- may include dog, cat or human bite
- common in patients with diabetes or PVD, but can happen in anyone
Common risk factors include recent surgery, trauma, or animal bite (dog / cat / insect)
MC will have a hx of trauma
MC site of cellulitis = lower leg
- surgery may exacerbate spread of disease - particularly venous stripping
PHYSICAL EXAM: SIGNS / SYMPTOMS ⦁ warmth ⦁ erythema ⦁ edema ⦁ tenderness of affected area ⦁ Flat margins + NOT well-demarcated (unlike erysipelas)
Maceration of the web spaces on the feet may be seen in cases of uncomplicated cellulitis
Cellulitis is an acute bacterial skin and skin structure infection of the dermis and subcutaneous tissue; commonly characterized by pain, erythema, warmth, and swelling. Margins are flat and not well demarcated
- cellulitis with violaceous color + bullae suggests infection with strep pneumoniae
if a pt comes in with cellulitis = take black sharpie and mark area affected - make sure not rapidly spreading, and that treatment is working
COMPLICATIONS
⦁ Necrotizing Fasciitis - necrosis of subcutaneous tissue.
⦁ Sepsis
⦁ Endocarditis
DIAGNOSIS
⦁ CULTURE = if purulent
- no work up required for uncomplicated cases that meet the following criteria
⦁ small area of involvement
⦁ minimal pain
⦁ no systemic signs of illness (fever / chills / dehydration / altered mental status / tachypnea / tachycardia / hypotension )
⦁ no risk factors for serious illness (eg, extremes of age, general debility, immunocompromised status).
IF COMPLICATED = SIGNS OF SYSTEMIC INVOLVEMENT
⦁ CBC
⦁ CMP
⦁ blood cultures
TREATMENT
- staph + strep coverage X 7-10 days
MILD
⦁ Keflex = 1st line (suspected MSSA)
⦁ Dicloxacillin
- Clindamycin or Erythromycin if allergic to PCN
If strep pyogenes = amoxicillin
IV (MSSA)
⦁ Ceftriaxone (Rocephin)
⦁ Ampicillin - Sulbactam (Unasyn)
⦁ Ancef (Cephalexin)
MRSA
⦁ bactrim, clinda, doxy
Cat / Dog / Human bite = Augmentin
⦁ Cat 2nd line = Doxy (if allergic to PCN)
⦁ Dog / Human 2nd line = Clindamycin + Cipro or Bactrim
If puncture wound (ex: through shoe) = cover for pseudomonas (cipro)
COMPLICATED
- hospitalization for IV antibiotics (to cover MRSA+)
⦁ Vanco
⦁ Zyvox (Linezolid)
Patient will present as → a 64-year-old female with a 4 cm × 7 cm edematous, red, hot tender area on the left thigh. The lesion has gotten larger over the past 6 hours. She tells you she has also had a low-grade fever and some chills. On physical exam, there is a poorly demarcated 12 cm red and tender plaque on her right calf. Some parts resemble an orange peel. There is a superficial cut in the middle of the plaque.
IMPETIGO
- common, contagious, superficial skin infection
- highly contagious, superficial vesiculopustular skin infection
Typically occurs at sites of superficial skin trauma (ex: insect bite)
- primarily occurs on exposed surfaces (ex: ** FACE ** or extremities)
RISK FACTORS
⦁ warm / humid conditions
⦁ poor personal hygiene
CAUSE
⦁ strep pyogenes (GABHS)
⦁ staph aureus - produces exfoliative toxin A
⦁ combo
- high incidence in children
- self limiting (will eventually go away), but if not treated = may last weeks to months
** POST - STREP GLOMERULONEPHRITIS ** - caused by group A strep
⦁ Occurring most commonly in children age 5-12 years
⦁ Patients develop symptoms 3- 6 weeks after streptococcal impetigo
⦁ Symptoms of PSGN include gross hematuria, facial edema, renal insufficiency, brown colored urine, and hypertension
PE
⦁ nonbullous and/or bullous
⦁ have vesicles and bullae containing clear yellow or slightly turbid fluid without surrounding erythema
⦁ superficial small vesicle or pustules 1-3 cm lesions
⦁ ** GOLDEN - YELLOW, HONEY CRUSTED LESION **
TYPES OF IMPETIGO
⦁ NONBULLOUS = MC type - impetigo contagiosa = vesicles, pustules = characteristic “honey colored crust”. Is associated with regional lymphadenopathy. MC etiology = ** STAPH AUREUS ** (2nd MC = GABHS)
⦁ BULLOUS = vesicles rapidly form large bullae –> lead to think “varnish-like crusts”. Have fever, diarrhea
- MC = ** STAPH AUREUS**
- this form of impetigo is rare - usually seen in newborns / young children if at all
⦁ ECTHYMA = ulcerative pyoderma caused by
** GABHS ** - heals with scarring. Not common
TREATMENT
⦁ BACTROBAN (MUPIROCIN) OINTMENT - mild = MC treatment - apply TID x 10 days
⦁ Bacitracin
⦁ Wash area gently with soap / water. good skin hygiene
If extensive disease or having systemic symptoms (fever) = systemic abx - CEPHALEXIN / DICLOXACILLIN / CLINDAMYCIN
⦁ oral abx - ** Cephalexin (Keflex**), dicloxacillin (especially effective against Staph), clindamycin, erythromycin, azithromycin, clarithromycin
⦁ In severe cases = oral antibiotics to cover for MRSA = Bactrim, doxycycline, clindamycin
LIPOMA
- benign SUBCUTANEOUS tumor of adipose tissue
- soft, rounded and movable against overlying skin
Lipomas are composed of fat cells that have the same morphology as normal fat cells
MC locations = trunk or extremities
SIGNS / SYMPTOMS ⦁ soft ⦁ symmetric ⦁ painless ⦁ easily mobile ⦁ palpable mass in subcutaneous tissue
Lipomas are generally slow growing—if the presenting lesion is fast growing, suspect another diagnosis
Lipomas are usually soft, homogeneous, oval, and nontender, with a rubbery or doughy consistency; if hard, suspect another diagnosis
The overlying skin is typically mobile and normal in appearance; if erythematous, suspect another diagnosis such as infection
PHYSICAL EXAM
“ Slippage sign” = gently sliding the fingers off the edge of the tumor –> the tumor will be felt to slip out from under fingers
DIAGNOSIS = ** CLINICAL **
- biopsy if rapidly growing
TREATMENT
⦁ NONE NEEDED!!!
⦁ may perform surgical removal for cosmetic reasons, or if lipoma becomes bothersome, too large, painful
**Some individuals have Familial Lipoma Syndrome = an autosomal dominant trait appearing in early adulthood, where an individual may have hundreds of Lipomas
A lipoma is a benign tumor composed of adipose tissue (body fat). It is the most common benign form of soft tissue tumor. Lipomas are soft to the touch, usually movable, and are generally painless.
Many lipomas are small (< 1 cm) but can enlarge to sizes > 6cm. Lipomas are commonly found in adults from 40-60 years of age, but can also be found in younger adults and children. Some sources claim that malignant transformation can occur, while others say this has yet to be convincingly documented.
PILONIDAL DISEASE (PILONIDAL CYST)
- Cyst near the natal cleft of the buttocks that often contains hair or skin debris
- tender abscess with drainage on or near the GLUTEAL CLEFT near the midline of the coccyx or sacrum with small MIDLINE PITS
Pilonidal disease results from an abscess, or sinus tract, in the upper part of the natal (gluteal) cleft
CAUSE
- usually happens when hair punctures the skin and becomes embedded
RISK FACTORS
MC in white males who are obese, hairy patients
- can occur from prolonged sitting or local trauma
- occurs in hairy, young men**
- rare in patients > 40
⦁ white males ⦁ obese ⦁ hairy ⦁ prolonged sitting ⦁ local trauma / irritation ⦁ younger patients
CLINICAL PRESENTATION
⦁ pain
⦁ erythema / swelling of the skin
⦁ drainage of foul smelling pus or blood from the opening of the skin
- *** part of FOLLICULAR OCCLUSION TETRAD **
1) HS
2) acne conglobata
3) dissecting cellulitis of scalp
4) pilonidal cyst
DIAGNOSIS = CLINICAL
TREATMENT / PREVENTION
1) I+D the cyst - may need to leave open or pack
2) if cyst reoccurs = surgical excision of cyst + tracts)
3) Antibiotics - usually only given in the setting of cellulitis = Cefazolin (1st gen) + Metronidazole (Flagyl)
Patient will present as → a 15-year-old male with pain, discomfort and swelling above the anus and near his tailbone that comes and goes. He reports that the pain worsens when he sits or bends forward. Medical history is significant for metabolic syndrome. He is a high school student who spends hours playing on his Xbox. On physical exam, there is a tender and fluctuant mass that is erythematous. There is also purulent discharge from a sinus tract.
BROWN RECLUSE SPIDER BITE
Loxosceles recluse - (brown recluse) spider
Found mostly in the midwestern, southern and southeastern United States
These spiders like to hide in quiet, cluttered places like closets, woodpiles, attics, and storage spaces
Most bites occur when the spider feels threatened by sudden movement, such as when a person puts on clothing or a shoe in which the spider is resting
Brown violin on the abdomen
SIGNS / SYMPTOMS
⦁ Local burning + erythema at bite site x 3-4 hrs
⦁ Brown recluse spider bites often develop a(n) ERYTHEMATOUS HALO around the bite within 24-72 hours, and may have SURROUNDING NECROSIS
⦁ can cause BLISTERING or NECROSIS at the site of the bite, erythema, and some systemic symptoms
⦁ The classic recluse spider bite possesses the “red, white and blue” sign: red erythema around a rim of blanched skin that encircles a central blue-purple papule, vesicle or bulla.
⦁ Necrosis typically begins 2-3 days after the bite, followed by ESCHAR formation and a deep ULCER
⦁ “Loxoscelism” consists of local vesicle formation, progressing to tissue necrosis and systemic symptoms
o Necrotic wound
- Local tissue reaction causes local burning at the site for 3-4 hours → blanched area (due to vasoconstriction) → central necrosis, erythematous margin around an ischemic center “red halo” → 24-72 hours after hemorrhagic bullae that undergoes Eschar formation → necrosis
SYSTEMIC SYMPTOMS maculopapular rash, fever, headache, malaise, arthralgia, nausea and vomiting. ⦁ maculopapular rash*** ⦁ fever*** ⦁ headache*** ⦁ malaise ⦁ arthralgia ⦁ N / V
TREATMENT
- wound care = clean with soap + water
- apply cold packs to bite site; avoid freezing the tissue
- keep body part in elevated or neutral position
- local symptomatic measures
- sometimes delayed excision
Most wounds heal spontaneously within days to weeks
o Pain Control: NSAIDS or opioids if more severe
- tetanus prophylaxis if needed
o Dermal Necrosis
- debridement in some cases if it will lead to better wound healing
- Dapsone (aczone) has been used in past
- antibiotics if secondary infection develops (treat like cellulitis)
Patient with brown recluse spider bite will present as → a 32-year-old man who was cleaning out his dark, undisturbed attic. That day he noticed an erythematous lesion with a clear center on his arm. Since then the lesion has necrosed in the center, giving rise to a crater-like eschar lesion
BLACK WIDOW SPIDER BITE
Black widow spiders are endemic to Eastern and Southwest U.S.A
Usually had a recent event outdoors within last 8 hours: outdoor activities - hiking / camping, outdoor furniture use, gardening, sleeping outside, etc.
These spiders are found mostly along the East Coast and in the Southwestern United States.
The black widow is well known for its black glossy color and red hourglass marking on its abdomen
Red hourglass on the abdomen
They can leave 2 fang marks and their venom, containing α-latrotoxin, can lead to release of acetylcholine, which is responsible for the bite symptoms.
They are not aggressive, prefer dark and quiet habitats like garages, and are WEB-BUILDERS.
Most bites occur during accidental or purposeful provocation of the spider or disruption of its web
SYMPTOMS = Latrodectism These spiders produce a neurotoxic venom (containing α-latrotoxin) that is responsible for the majority of systemic symptoms after a spider bite. The neurotoxin triggers the release of acetylcholine (cholinergic = sympathetic), which may result in ⦁ elevated blood pressure ⦁ muscle cramping / pain / spasms / rigidity **** ⦁ convulsions ⦁ lacrimation ⦁ salivation ⦁ seizures ⦁ headache *** ⦁ fever ⦁ tremors ⦁ N/V *** ⦁ SOB
Muscle pain MC affects extremities, back + abdomen
Neurologic manifestations - May not see much at bite site: toxic reaction = nausea, vomiting, HA, fever, syncope, and convulsions
** May not see much at bite site **
- Deaths are relatively rare
Cutaneous manifestations are usually unimpressive, but may present with significant
⦁ erythema
⦁ pain and
⦁ localized sweating
PHYSICAL EXAM
- blanched circular patch with a surrounding red perimeter and central punctum (target lesion)
Two fang marks can be at the site of the bite.
TREATMENT
⦁ 1st line = supportive - wound care + symptomatic treatment
- give antivenin if not responding to this
⦁ benzodiazepine / muscle relaxers for muscle cramps / spasms / rigidity
⦁ NSAIDS or opioids or other analgesics
⦁ antivenom can be given - after antihistamine - reserved for patients who are not responsive to above medications
Treatment is usually supportive because symptoms self-resolve in most cases within 1-3 days
Treatment involves supportive care, including a benzodiazepine to manage muscular cramps. Black widow spider antivenom may also be administered (pre-medicate with antihistamine to reduce adverse reactions).
- anti-venom available for elderly and kids
Patient with black widow spider bite will present as → a 21-year-old who returns from a camping trip early complaining of a dull numbness affecting his upper left extremity. He recalls a sharp pinprick sensation before the development of symptoms. The patient now describes a cramping pain and muscle rigidity of the back and chest area. A red, indurated area is found on the distal left arm. The patient has profuse sweating, nausea, vomiting, and shortness of breath.
PITYRIASIS ROSEA
- ETIOLOGY = unclear, but likely a viral source
- HHV 6 or 7**
- is self-limiting
- may have an accompanying UPPER RESPIRATORY INFECTION
- often occurs a few days after a viral illness, but can also occur more frequently in immunocompromised
- not contagious
- primarily occurs in older children / young adults
- increased prevalence in the spring/fall
- can mimic syphilis (order RPR if patient is sexually active)
CLINICAL MANIFESTATIONS
**First sign = “HERALD PATCH” (solitary salmon-colored macule on trunk 2-6cm in diameter)
–> then multiple new lesions appear a few days to 1-2 weeks later = smaller, pruritic, 1cm round/oval salmon-colored papules with white circular scaling in a ***“CHRISTMAS TREE DISTRIBUTION” on the back
- lesions are often oval with long-axis paralleling the lines of skin stress; oval, erythematous papules and small plaques
- mostly on the trunk, but may have some satellite lesions on the arm (usually proximal) - the face is usually spared
- lesions resolve in 6-12 weeks
- may be pruritic. Pruritus = MC complaint
- not contagious
ESSENTIAL CLINICAL FEATURES
⦁ discrete circular lesions
⦁ scaling on most lesions
⦁ peripheral COLLARETTE scaling*** with central clearance on at least two lesions.
OPTIONAL CLINICAL FEATURES
⦁ truncal and proximal limb distribution
⦁ most lesions appearing along cleavage lines
⦁ herald patch for at least 2 days before the rash or other lesions begin.
In many individuals with pityriasis rosea, the characteristic rash develops after vague, nonspecific symptoms that resemble those associated with an upper respiratory infection - Pityriasis rosea may have an accompanying upper respiratory infection.
Pityriasis rosea can be mistaken for secondary SYPHILIS - very similar looking rash, except syphilis also will appear on palms/soles of hands/feet
- secondary syphilis must be excluded to diagnose pityriasis rosea
- VDRL testing (venereal disease research lab test)
- FTA-Abs test (fluorescent treponemal antibody absorption = blood test - checks for antibodies to Treponema pallidum spirochete bacteria - causes syphilis)
DIAGNOSIS
⦁ A biopsy of pityriasis rosea will have extravasated erythrocytes within dermal papillae
TREATMENT
- none needed!
⦁ if needed for pruritus = give medium potency topical steroids, PO antihistamines, oatmeal baths
⦁ Acyclovir/Valacyclovir or Phototherapy for severe cases
BURNS
Burns cause damage and inflammation of the skin
The skin play an important role in protecting the underlying muscles / bones / ligaments / organs, etc.
- forms a barrier from infectious pathogens
- also prevents major water loss from the body
Skin = 3 layers
⦁ epidermis
⦁ dermis (papillary + reticular)
⦁ hypodermis
EPIDERMIS
- thin outermost layer of skin
- made up of several layers of keratinocytes
- keratinocytes make + secrete glycolipids = which prevent water from easily seeping into / out of the body
DERMIS
- thicker layer
- contains nerves + blood vessels
- 2 layers within the dermis
⦁ papillary layer
- contains fibroblasts - produce collagen (CT protein)
- fibroblasts arranged in papillae, which contain blood vessels + nerve endings
- nerve endings in this layer = detect pain + fine touch
⦁ reticular layer
- even thicker than papillary layer
- collagen is packed very tightly - good support
- these fibroblasts secrete elastin - make skin stretchy and flexible
- oil / sweat glands / hair follicles / lymphatic vessels / nerves / blood vessels present in reticular layer
- nerve endings in this layer = detect pressure + vibration
HYPODERMIS
- made of fat + CT
- insulates and pads the deeper tissue
- anchors skin to underlying muscle
PATHOPHYSIOLOGY OF BURNS
- when skin is burnt, cells and proteins within skin are damaged
- burn degree is determined by the # of skin layers affected
1ST DEGREE BURNS (SUPERFICIAL BURNS)
= sunburn: dominant in UVB (burns)
UVA = photoAging + tAnning
⦁ only affects the epidermis
2ND DEGREE BURNS
⦁ affects the epidermis + dermis
o 2ND DEGREE SUPERFICIAL PARTIAL THICKNESS BURN
⦁ affects the epidermis + papillary layer of dermis
o 2ND DEGREE DEEP PARTIAL THICKNESS BURN
⦁ affects the epidermis + goes through papillary layer of dermis and some of reticular layer of dermis
3RD DEGREE BURNS (FULL THICKNESS BURN)
⦁ affects the epidermis + dermis (goes through entirety of dermis)
4TH DEGREE BURNS
⦁ affects the epidermis + dermis + extend into hypodermis
COMMON COMPLICATIONS OF BURNS ⦁ infections (especially Pseudomonas) ⦁ water loss through damaged skin ⦁ hypothermia ⦁ hyperkalemia (capillary permeability) ⦁ Hypovolemic shock** ⦁ DIC***
Pseudomonas = gram negative, OXIDASE POSITIVE
- does not ferment lactose on MacConkey agar
- releases Exotoxin A
- look for inhalation injuries
- Macrophages remove dead cells
- Fibroblasts lay down new collagen to replace damage
the more extensive the area of new collagen, the more extensive the scar
SCAR FORMATION = ABSENT IN 1ST DEGREE BURNS
- PRESENT IN 2ND DEGREE PARTIAL THICKNESS +++
SYMPTOMS (depend on degree of burn) o 1st degree burns - superficial burn - epidermis ⦁ red ⦁ dry ⦁ painful / tender to the touch ⦁ blanches with pressure ⦁ Capillary Refill intact! ++++ / blanches! **** ⦁ heals within 7 days ⦁ no scarring!
o 2nd degree - superficial partial thickness burns
- epidermis + papillary dermis
⦁ red
⦁ BLISTERS **
⦁ wet / weeping
⦁ MOST PAINFUL DEGREE OF BURNS**
⦁ Very tender to touch
⦁ still blanches with pressure
⦁ Capillary Refill intact! ++++ / blanches! **
⦁ heals within 14-21 days
⦁ no scarring! - but may have some pigment change
o 2nd degree - deep partial thickness burns
- epidermis + some of papillary dermis
⦁ vary in color (yellow / white / red)
⦁ dry
⦁ BLISTERS **
⦁ may be painful, but not as severe as 2nd partial
- more Pressure + Discomfort
⦁ Absent capillary refill —— / non-blanching
⦁ heals in 3 weeks - 2 months
⦁ scarring = common (may need skin graft or excision to prevent contractures)
o 3rd degree - full thickness burn - extends through entire epidermis + dermis ⦁ waxy white ⦁ leathery, dry ⦁ PAINLESS ⦁ Absent capillary refill ------ / non-blanching ⦁ takes months to heal ⦁ does not heal well
o 4th degree burns - entire skin + fat / muscle / bone ⦁ charred black / eschar ⦁ dry ⦁ PAINLESS ⦁ Absent capillary refill ------ / non-blanching ⦁ does not heal well ⦁ usually needs debridement + tissue reconstruction
DIAGNOSIS OF BURNS
- usually based on appearance + extent of BSA
- sometimes can take tissue biopsy to determine which layers are affected
⦁ RULE OF 9s = used to diagnose burns in adults
- head = 9%
- chest = 9%
- abdomen = 9%
- upper back = 9%
- lower back = 9%
- right arm = 9%
- left arm = 9%
- anterior right leg = 9%
- posterior right leg = 9%
- anterior left leg = 9%
- posterior left leg = 9%
- groin = 1%
** SUPERFICIAL BURNS = DON’T COUNT IN BURN ASSESSMENT **
PALMAR METHOD = patient’s palm size = 1%
** LUND-BROWDER CHART = most accurate method for estimating TBSA in children + adults **
MINOR BURNS ⦁ < 10 TBSA in adults ⦁ < 5% TBSA in young/old ⦁ < 2% full thickness burn ⦁ must not involve face, hands, perineum, feet, cross major joints or be circumferential
MAJOR BURNS ⦁ > 25% TBSA in adults ⦁ > 20 % TBSA in young/old ⦁ > 10 % full thickness burn ⦁ Burns involving face, hands, perineum, feet, cross major joints or be circumferential
TREATMENT
- based on cause, location, and rule of 9s
1) flush burn with cool (but not ice-cold) running water
- wash wound only using mild soap + water, as disinfectants may inhibit healing.
- do NOT apply ice directly! (will stick to skin / peel off)
For Chemical Burns = irrigate profusely with running water x at least 20 minutes
For Blisters = LEAVE THEM ALONE!
- they help to prevent infection
- ruptured blisters can be removed, but leave intact blisters alone
Debridement = sloughed / necrotic skin may be debrided
- Escharotomy recommended for circumferential burns to prevent compartment syndrome
Fingers and toes should be wrapped individually to prevent maceration and gauze should be placed between them
2) Pain Management
- Acetaminophen / NSAIDS = alone or in combo with opioids
3) Topical Antibiotics
- should be applied to any non-superficial burn
- ** SILVER SULFADIAZINE = MC ** - on 2nd / 3rd
(Silvadene)
- do NOT use on face (SE of discoloration)
- do NOT use if sulfa allergy / pregnant / < 2 months old
For superficial burns = aloe vera or topical antibiotics (bacitracin)
- systemic abx not indicated in burn management
⦁ minor burns (1st degree + 2nd degree superficial)
- can heal after a few days with bandages + keeping burns clean with gentle soap / water
- can use topical antibiotics
⦁ serious burns (electrical burns / chemical burns / 2nd or 3rd degree burns in sensitive areas like face, hands or groin)
- IV fluids (needed in adults > 15% + kids > 10%)
o PARKLAND FORMULA = 4mL x kg x % TSA - given IV in first 24 hours - first 1/2 given in first 8 hours, remaining given over 16 hours
ex: 110lbs = 50kg
4mL / kg x 50kg = 200mL x 10% BSA = 2000mL IV in 24 hours = 2L in 24 hours = 1L given in 8 hours, then other L given over 16 hours
- hospitalization
- burn units
- replenish lost fluids/electrolytes
- antibiotics
surgical procedures (skin grafting, excision, amputation) may all be needed
***************************************************************** PAIN = 1st + 2nd partial CAPILLARY REFILL = 1st + 2nd partial BLISTERS = 2nd partial + 2nd deep WET / WEEPING = 2nd partial (rest = dry) LEATHERY = 3rd SCARRING = 2nd deep + 3rd + 4th MOST PAINFUL = 2nd partial
ACANTHOSIS NIGRICANS
- velvety thickening + hyperpigmentation of skin
ASSOCIATED WITH
⦁ Endocrine disorders
- diabetes
- insulin resistant syndrome - PCOS
- Acromegaly
- Cushing's Syndrome
⦁ Obesity
⦁ Internal malignancy (most commonly GI)
Obesity and diabetes mellitus = most frequently associated disorders with acanthosis nigricans.
Individuals with AN are at risk of developing metabolic syndrome.
- Rarely, acanthosis nigricans develops as a sign of internal malignancy (most commonly GI)
Abdominal adenocarcinomas, particularly gastric adenocarcinomas, represent the majority of acanthosis nigricans-associated tumors
Rarely, certain medications can cause AN = steroids, insulin, OCP, Niacin, testosterone, Aripiprazole (SGA)
o HISTORY
- insidious onset
- first visible change = darkening of pigmentation
o PHYSICAL EXAM
- hyperpigmentation
- velvety looking skin / hyperkeratotic
- skin line accentuation
- surface becomes wrinkled or creased
MC LOCATIONS ⦁ axilla ⦁ neck (back + sides) ⦁ groin ⦁ antecubital fossa ⦁ knuckles
if < 40 = usually diabetes or endocrinopathy
if > 40 = should rule out adenocarcinomas of the colon
if dark thickening in the mouth = think malignancy
DIAGNOSIS = CLINICAL
- can do skin biopsy if unsure
TREATMENT
- 1) rule out diabetes
- 2) treat underlying disorder - will then resolve
(weight loss or metformin / insulin)
- 3) usually no tx required
- can try topical retinoids / salicylic acid / lactic acid / peels / bleaching creams
Patient will present as → a 13-year-old obese male who is being seen for his routine physical. His skin examination reveals velvety, hyperpigmented, papillomatous lesions of the neck and axillae. The remainder of the examination is unremarkable. The patient has a strong family history of diabetes
