Skin Infections Flashcards
(69 cards)
1
Q
Complications of untreated skin and soft tissue infections (SSTI)
A
Sepsis
Underlying bone infection
2
Q
Primary SSTI
A
Previously healthy skin, usually single pathogen
3
Q
Secondary SSTI
A
Previously damaged skin, usually polymicrobial
4
Q
Complicated SSTI
A
Deeper layers (muscle, fascia), usually require surgical intervention OR immunocompromised pts
5
Q
Tinea unguinum
A
Nails
6
Q
Tinea manuum
A
Hands
7
Q
Predisposing factors to fungal infections
A
Diabetes Impaired circulation Immunosuppressive drugs Poor nutrition and hygiene Skin occlusion Warm and humid climates
8
Q
Tinea pedis
A
Men > women Whites > blacks Adults > children Athletes > non-athletes Shoes > sandals
9
Q
Presentation of tinea pedis
A
Soggy, malodorous, thickened skin Acute vesicular rash Fine scaling of the affected area with varying degrees of inflammation Cracks and fissures may also be present Typically involves lateral toe webs -Between 4th and 5th or 3rd and 4th toes Can spread to sole or instep -Rarely to the dorsum
10
Q
Presentation of tinea corporis
A
Smooth and bare skin
-Begin as small, circular, red, scaly areas
Spread peripherally and borders may contain vesicles or pustules
11
Q
Tx goals for fungal infections
A
Provide symptomatic relief
Eradicate infection
Prevent future infection
12
Q
Nonprescription tx for fungal infections
A
Appropriate for tinea pedis, corporis, cruris
Capitis and unguium require prescription tx
13
Q
Clotrimazole 1% and miconazole nitrate 2%
A
Inhibit biosynthesis of sterols and damage the fungal cell wall, altering permeability resulting in loss of essential intracellular elements
Apply BID for up to 4 wks
Nonprescription
Mild skin irritation can occur at application site
No drug-drug interactions with nl topical use
14
Q
Terbinafine 1% topical
A
Inhibits squalene epoxidase resulting in accumulation of squalene within fungal cell causing cell death
Apply BID for up to 4 wks
-Some trials showed resolution of tinea pedis after 7 days of tx
15
Q
Product selection of fungal infection tx
A
Ointments, creams, powders, and aerosols
Creams are the most efficient and effective
Sprays and powders are good adjuncts for prevention
16
Q
Terbinafine oral
A
First line for fungal nail infections
-250 mg daily for 6 wks-fingernails
-250 mg daily for 12 weeks- toenails
CBC and ALT/AST levels at baseline and every 4-6 wks during tx- rare but serious hepatic failure…don’t use with chronic or acute liver disease
17
Q
Psoriasis dx
A
Nail pitting, rash elsewhere on body, FHx of psoriasis
18
Q
Lichen planus dx
A
Nail atrophy, scarring at proximal aspect of nail
19
Q
Yellow nail syndrome dx
A
Multiple nails turn yellow, grow slowly, increased longitudinal and transverse curvature, intermittent pain and shedding, associated with chronic sinusitis, bronchiectasis, lymphedema
20
Q
Trauma of nails
A
Single nail affected, homogeneous alteration of nail color and altered shape of nail
21
Q
Folliculitis
A
Inflammation of hair follicle (stye)
22
Q
Furuncles
A
Infections of hair follicle that extends beyond follicle into subcutaneous skin layers
23
Q
Carbuncle
A
Group of furuncles forming a single area
24
Q
Abscess
A
Collections of pus within dermis or deeper tissues
25
Pathogen for folliculitis, furuncles, carbuncles, and abscesses
Typically S. aureus
| Underchlorinated pools and hot tubs have resulted in some Pseudomonas infections
26
Tx for folliculitis, furuncles, carbuncles, and abscesses
Warm, moist compresses for follicultiis and small furuncles
I & D should be performed if inflamed cysts, carbuncles, abscesses, and large furuncles
Usually do not require systemic abx unless extensive area affected or systemic signs of infection
T: >38 degrees C or < 36 degrees C
Tachypnea >20 breaths/min or PaCO2 <32 mm Hg
Tachycardia > 90 bpm
WBC > 12,000 or <4,000
27
Mild bacterial SSTI (folliculitis, etc.)
Purulent infection with no systemic signs of infection
28
Moderate bacterial SSTI (folliculitis, etc.)
Purulent infection with systemic signs of infection
29
Severe bacterial SSTI (folliculitis, etc.)
Pt has failed I & D and oral abx
IC pts
Systemic signs of infection + HYPOTENSION
30
Primary tx for folliculitis, furuncles, carbuncles, and abscesses
I & D (this may be adequate alone) PLUS
TMP-SMX
Doxycycline
If no response after 2-3 days, look for complications and consider Vancomycin
For moderately ill pt with acute bacterial skin and skin structure infection requiring parenteral therapy but who can be managed as an outpt:
-Dalbavancin
-Oritavancin
31
Impetigo
Superficial skin infection seen most commonly in children 2-5 years
Common in hot, humid weather, and highly communicable
Pathogens typically:
-Beta-hemolytic streptococci (Strep pyogenes)
-S. aureus
Innoculation from scratches, abrasions, and insect bites usually on exposed areas of skin
Roughly 1/3 of cases are filled with yellow pus and rupture to form brown crust- S. aureus
32
Tx for impetigo
Gm stain and culture recommended (below crust if present, and avoid open pustules)
Topical therapy for 5 days with mupirocin 2% or retapamulin 1% is considered equivalent to oral abx in isolated impetigo
Retapamulin
-Inhibits nl bacterial protein
Mupirocin
-Inhibits nl bacterial protein synthesis
33
Impetigo tx with many lesions and oral therapy deemed
Pen VK
TMP-SMX
Benzathine Pen G
MRSA suspected or confirmed (or PCN allergy): Clinda, Doxy, of TMP-SMX
34
Erysipelas
Clearly demarcated borders
Lesions are raised above surrounding skin
Common in infants, children, and elderly
Intense red color, burning pain usually on LEs, dimpled appearance
AKA St. Anthony's Fire
35
Pathogens of erysipelas
```
Beta-hemolytic streptococcus (Strep pyogenes > Strep agalactiae)
Staph aureus (rare)
```
36
Mild erysipelas
Nonpurulent infections with no systemic signs of infection
37
Moderate erysipelas
Nonpurulent infection with systemic signs of infection
38
Severe erysipelas
Association with penetrating trauma or IV drug abuse
Evidence of or colonization with MRSA
Systemic signs of infection + HYPOTENSION
39
Workup for erysipelas
Hard to culture, low yield unless severe
Needle aspiration/punch biopsy variable
Diagnosed based on characteristic lesion
40
Tx for erysipelas
Pen VK or Amox
If hx of pcn skin rash and nothing to suggest an IgE-mediated reaction (anaphylaxis, angioneurotic edema): Cephalexin
If documented past hx of IgE-mediated allergic rxn to beta-lactam abx: Azithro, Linezolid
41
Cellulitis
Affects deeper dermis and subcutaneous fat
Does not appear raised and borders are not clearly demarcated
Areas are warm to touch, pts commonly experience hypotension and often AMS
Viewed as more serious than erysipelas due to potential for bloodstream infection
As in erysipelas, low yield on diagnostic measures unless sever
42
Pathogens for cellulitis
```
Strep pyogenes
Staph aureus (MRSA is a growing concern)
```
43
Mild cellulitis
Nonpurulent infection with no systemic signs of infection
44
Moderate cellulitis
Nonpurulent infection with systemic signs of infection
45
Severe cellulitis
Association with penetrating trauma or IV drug abuse
Evidence of or colonization with MRSA
Systemic signs of infection + HYPOTENSION
46
Tx of cellulitis
Pen G
If hx of pcn skin rash non-IgE-mediated allergic rxn: Cefazolin
If hx/evidence of past anaphylaxis: Vancomycin
Treat IV until afebrile, then outpatient pcn VK
47
Tx of cellulitis (acute bacterial skin and skin structure infections, moderately ill inpatient or outpatient who refuses hospitalization or is unlikely to comply with a multidose oral regimen)
Dalbavancin
| Oritavancin
48
Necrotizing SSTI
Rare but serious invasive and devastating infection that extends deep into fascia and muscle
Usually result from trauma or surgery
Monomicrobial or polymicrobial
Characterized by progressive destruction of tissue
49
Clinical sx differentiating necrotizing SSTI from typical skin infections
```
Severe, constant pain
Deep bullae
Skin necrosis or bruising
Gas in soft tissues
Numbness of skin
Edema
Systemic systems
Rapid spread
```
50
Type I necrotizing fasciitis
80% of necrotizing fasciitis
Mixture of anaerobes (bacteroides, peptostreptoccocus) and facultative bacteria (streptococcus, enterobacteriaceae, S. aureus)
Slower spread of infection (3-5 days)
Fournier's Gangrene
51
Tx of type I necrotizing fasciitis
```
Debridement
Vancomycin or daptomycin +
Piperacillin-tazobactam
Cefepime and metronidazole if pcn rash
FQ and metronidazole if pcn allergy
```
52
Type II necrotizing fasciitis
Virulent strains of S. pyogenes
- AKA "flesh-eating bacteria"
- Rapidly extending necrosis (24-72 hrs)
53
Tx- type II necrotizing fasciitis
Debridement
PCN + clindamycin
Clinda is an important component of the regimen due to its suppression of streptococcal toxin and cytokine production
54
Type III necrotizing fasciitis
```
Clostridium myonecrosis
AKA "gas gangrene"
Less than 5% of cases
Advances very rapidly (several hours)
Presents with reddish-blue bullae
Pathogens: Clostridium perfringens (most common), Clostridium noyvi, Clostridium histolyticum, Clostridium septicum
```
55
Tx of necrotizing fasciitis
Debridement
| PCN + Clindamycin
56
Diabetic foot infections
Most common diabetic complication
-20% of all hospitalizations in diabetic pts
Usually caused by trauma or skin ulceration secondary to peripheral neuropathy
Causes loss of mobility and subsequent hospitalization
Severe cases often result in amputation
Diabetic pts who undergo LE amputation have a 5-yr mortality similar to most fatal cancers
57
Mild cases of diabetic foot infections
Monomicrobial
58
Moderate to severe diabetic foot infections
Often polymicrobial
59
Pathogens of diabetic foot infections
Staphylococci (MRSA increasing in incidence)
Streptococci
Pseudomonas aeruginosa
Anaerobes (Peptostreptococcus, Clostridium spp.)
Deep culture of wound basis necessary for accurate identification due to chronic nature
60
Signs of infection for diabetic foot infections
Local erythema
Pain
Warmth
Purulent d/c
61
Terbinafine oral tx- tinea capitis
```
250 mg daily for 2-4 wks
Age > 2
- <20 kg 65.5 mg q24 x 14 days
- 20-40 kg 125 mg q24 x 14 days
- > 40 kg 250 mg q24 x 14 days
```
62
Tx for mild diabetic foot infections (duration 1-2 wks)
Cephalexin
Augmentin
-MRSA, add TMP-SMX
63
Tx for moderate/severe diabetic foot infections (2-4 weeks or longer)
Augmentin
Cipro or Levo
-MRSA, add Doxy or Linezolid
MRSA risk (MRSA colonization/prevalence, PO tx failure): Vanocmycin
Pseudomonas risk (failed non-pseudomonal therapy, warm climate, high prevalence of Pseudomonas, frequent exposure to water, "may be advisable in severe infections"): Piperacillin-Tazobactam
64
Pressure sores
Most common among chronically debilitated persons, the elderly (70% involve persons greater than 70 yoa) and persons with serious spinal cord injury
Compounding the problems of shearing and friction forces are the macerating effects of excessive moisture in the local environment
-Incontinence and perspiration
-Increases the risk of pressure sore formation fivefold
65
Suspected deep-tissue injury
Area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. Area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared with adjacent tissue.
66
Stage 1 pressure ulcers
Pressure sore is generally reversible, is limited to the epidermis, and resembles an abrasion, intact skin iwth nonblanchable redness of a localized area, usually over a bony prominence. The area may be painful, firm, soft, warmer or cooler as compared with adjacent tissue
67
Stage 2 pressure ulcers
Sore also may be reversible, partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed. May also present as an intact or open/ruptured serum-filled blister, or as a shiny or dry shallow ulcer
68
Stage 3 pressure ulcers
Full thickness tissue loss. Subcutaneous fat may be visible, but bone, tendon, or muscles are not exposed. May include undermining and tunneling. Depth of the ulcer varies by anatomical location; may range from shallow to extremely deep over areas of significant adiposity
69
Stage 4 pressure ulcers
Full thickness tissue loss with exposed bone, tendon, or muscle; can extend into muscle and/or supporting structures (eg, fascia, tendon, or joint capsule) making osteomyelitis possible. Often includes undermining and tunneling. Depth of ulcer varies by anatomical location.
