Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3151 Therapeutics > Skin & Soft Tissue Infections > Flashcards

Skin & Soft Tissue Infections Flashcards

1
Q

How does the skin serve as a protective barrier to infection?

A
  1. Physical barrier
  • barrier from physical, microbial, chemical assaults
  • prevent excessive water loss
  1. Chemical barrier
  • acidic pH 4-5 (FFAs from phospholipids)
  • acidic environment keep bacteria and candida low, regulate desquamation
  • continuous renewal of epidermal layer, results in shedding of keratocytes and skin microbiota
  • sebaceous secretions inhibit growth of many bacteria and fungi
  • normal commensal skin microbiome prevents overgrowth and colonization of pathogenic strains
  1. Immunological barrier
  • innate (physical barrier + AMPs antimicrobial peptides, cytokines, cells with PRR)
  • AMP kills pathogens, influences cellular processes to promote wound healing, initiation of adaptive immune response, controls inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What factors impair skin barrier function?

A

Age
Infection
Physical damage
Physical environment
Ischemia - lack of perfusion
Diseases (e.g., DM)
Drugs
pH
Excessive soap and detergent use
Too much moisture and humidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the classification of SSTIs that occur at each anatomical site?
(Epidermis, Dermis, Hair follicles, Subcutaneous fat, Fascia, Muscle)

A

Epidermis - Impetigo

Dermis - Ecthyma, Erysipelas

Hair follicles - Furuncle, Carbuncle

Subcutaneous fat - Cellulitis

Fascia - Necrotizing fasciitis

Muscle - Myositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some other protective mechanisms of the skin?

A
  • Continuous renewal of epidermal layer, results in shedding of keratocytes and skin microbiota
  • Sebaceous secretions inhibit growth of many bacteria and fungi
  • Normal commensal skin microbiome prevents overgrowth and colonization of pathogenic strains
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are some risk factors for SSTI?

A

Disruption of the skin barrier

  • Traumatic: lacerations, recent surgery, burns, abrasions…
  • Non traumatic: pressure ulcers, tinea pedis, dermatitis, toe web intertrigo, chemical irritants
  • impaired venous and lymphatic drainage: obesity, saphenous venectomy
  • peripheral artery disease

Conditions / underlying diseases that predispose to infection

  • DM, cirrhosis, neutropenia, HIV, transplant, immunosuppression

History of cellulitis

Also look out for: animal exposure, water exposure, travel history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How can SSTI be prevented?

A

Management of predisposing risk factors => identify at time of initial diagnosis to decrease risk for recurrence

Good care to maintain skin integrity

  • good wound care
  • treatment of tinea pedis
  • preventing dry, cracked skin
  • good foot care for DM patients to prevent wound and ulcers

Acute traumatic wound should be irrigated, foreign objects removed, devitalized tissues debrided

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. Confirm presence of infection

When is culture required?

A

Bacteria culture is NOT required for mild and superficial infections (no systemic symptoms)

Blood culture is only required for severe cases with marked systemic symptoms of infection or immunocompromised patients

  • E.g., lab (TW, CRP, creatinine phosphokinase, lactate, gram stain and culture)
  • If sinister pathology suspected: radiography, CT with contrast, MRI, ultrasonography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. Confirm presence of infection

How should cultures of pus, exudates or tissues from wounds be taken?

A

Avoid wound swabs - colonizers, contaminants => polymicrobial

Cultures should be collected:

  • from deep in the wound after surface cleansed
  • from base of a closed abscess, where bacteria grow
  • by curettage, rather than wound swab or irrigation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. Confirm presence of infection (diagnosis - clinical presentation)

Describe the clinical presentation of Impetigo

A

Epidermis, superficial infection

Begin as erythematous papules, evolve into vesicles and pustules that rupture with dried discharge forming honey-coloured crusts on an erythematous base

Usually on exposed areas of the body (face, extremities)

Lesions well localized, frequently many, bullous, or non-bullous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. Confirm presence of infection (diagnosis - clinical presentation)

Describe the clinical presentation of Ecthyma

A

Dermis, deeper variant of impetigo that extend through the epidermis and deep into dermis

Begin as vesicles/pustules, evolve into “punched out” ulcers (ulcerative form of impetigo)

Pruritis is common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. Confirm presence of infection (diagnosis - clinical presentation)

Describe the clinical presentation of Furuncle and Carbuncle

A

Furuncle: Infection of the hair follicle with purulent material, extends through the dermis into s/c tissue, small abscess forms

Carbuncle: furuncles coalesce, extent into s/c tissues

*PURULENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. Confirm presence of infection (diagnosis - clinical presentation)

Describe the clinical presentation of cutaneous abscess

A

Skin abscess: localized collection of pus within the dermis and deeper skin tissues

Manifest as painful, tender, fluctuant, and erythematous nodules

*PURULENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. Confirm presence of infection (diagnosis - clinical presentation)

Describe the clinical presentation of Erysipelas

A

Dermis

Affects upper dermis, more superficial, involves lymphatics

Fiery red, tender, painful plaque (raised) with well-demarcated edges

Common on face, lower extremities

*NON-PURULENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. Confirm presence of infection (diagnosis - clinical presentation)

Describe the clinical presentation of Cellulitis

A

S/C tissue, involve deeper and subcutaneous fats

Usually acute, diffuse, spreading, non-elevated, poorly demarcated edges
Rapid onset/progression
Unilateral
Fever in 20-70% of patients

Common in lower extremities, though may appear on any area of the skin

*PURULENT or NON-PURULENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. Confirm presence of infection (diagnosis - clinical presentation)

What are some cellulitis mimickers?

A

Deep venous thrombosis
Calciphylaxis
Stasis dermatitis
Hematoma
Erythema migrans

*if cant differentiate, may give a short course to monitor for response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. Confirm presence of infection (diagnosis - clinical presentation)

What are some complications that can arise if cellulitis progresses?

A

Bacteremia
Endocarditis
Toxic shock (overgrowth of staphs/streps => release toxins)
Glomerulonephritis
Lymphedema
Osteomyelitis
Necrotizing soft-tissue infections (Necrotizing fascia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
  1. Identify pathogens

Name the likely pathogens for Impetigo

A

Impetigo
- Staphylococci or Streptococci
- Bullous form caused by toxin-producing strains of S. aureus

18
Q
  1. Identify pathogens

Name the likely pathogens for Ecthyma

A

Ecthyma
- Group A Streptococci

19
Q
  1. Identify pathogens

Name the likely pathogens for Nonpurulent (Erysipelas, Cellulitis)

A

Nonpurulent
- Beta-hemolytic streptococcus, usually GAS (Strep. Pyogenes)
- S. aureus less frequent
- Others based on exposure: aeromonas (fresh water), vibrio vulnificus (sea water), pseudomonas (water exposure, hot tub)

20
Q
  1. Identify pathogens

Name the likely pathogens for Purulent (Furuncle, Carbuncle, Skin abscesses, Cellulitis)

A

Purulent
- S. aureus
- Some beta-hemolytic strep
- Gram-negative and anaerobes may be common in pt with skin abscess involving perioral, perirectal, vulvovaginal area

21
Q
  1. Identify pathogens

What is the difference between CA-MRSA and HA-MRSA?

What is used to treat CA-MRSA?

Why is CA-MRSA not a concern in Singapore?

A

CA-MRSA and HA-MRSA are genetically distinct

CA-MRSA

  • Panton-Valentine Leucocidin (PVL) - enzyme breaks down WBC, infection has more abscess and pus
  • SCCmec IV

CA-MRSA treatment

  • Oral non-beta lactams (e.g., clindamycin, co-trimoxazole, doxycyline), IV vancomycin

CA-MRSA has low incidence in Singapore

Risk factors include:

  • international schools
  • participants of contact sports, military personnel, IV drug abusers, prison inmates
  • overcrowded facilities, close contact, lack of sanitation
22
Q
  1. Selection of antimicrobial and regimen

Impetigo and Ecthyma

Discuss the antibiotic selection for Impetigo with mild limited lesions

A

Impetigo - Staph or Strep
Ecthyma - GAS

Impetigo (mild limited lesions):
- Topical Mupirocin BID x5d

23
Q
  1. Selection of antimicrobial and regimen

Impetigo and Ecthyma

Discuss the EMPIRIC antibiotic selection for Impetigo and Ecthyma

A

Impetigo - Staph or Strep
Ecthyma - GAS

Empiric - Cover staph + strep
- PO Cephalexin 500mg q6h
- PO Cloxacillin 500mg-1g q6h
- PO Clindamycin 300-450mg q6h (if allergic to penicillin) - SE: CDAD

*Treatment duration for oral: 7 days

24
Q
  1. Selection of antimicrobial and regimen

Impetigo and Ecthyma

Discuss the CULTURE-DIRECTED antibiotic selection for Impetigo and Ecthyma (if Strep Pyogenes)

A

Impetigo - Staph or Strep
Ecthyma - GAS

Culture directed (GAS):
- PO Penicillin V 500mg q6h
- PO Amoxicillin 500mg-1g q8h
*natural penicillin and aminopenicillin don’t cover MSSA

*Treatment duration for oral: 7 days

25
Q
  1. Selection of antimicrobial and regimen

Impetigo and Ecthyma

Discuss the CULTURE-DIRECTED antibiotic selection for Impetigo and Ecthyma (if Staph aureus)

A

Impetigo - Staph or Strep
Ecthyma - GAS

Culture directed (MSSA):
- PO Cephalexin 500mg q6h
- PO Cloxacillin 500mg-1g q6h

*Treatment duration for oral: 7 days

26
Q
  1. Selection of antimicrobial and regimen

Purulent (Furuncle, Carbuncle, Skin abscesses, Purulent Cellulitis)

Mainstay of treatment is _________

A

Incision and drainage

27
Q
  1. Selection of antimicrobial and regimen

Purulent (Furuncle, Carbuncle, Skin abscesses, Purulent Cellulitis)

When is adjunctive systemic antibiotics required?

A
  • Unable to drain completely
  • Lack of response after drainage
  • Extensive disease involving several sites
  • Extremes of age
  • Immunosuppressed
  • Signs of systemic illness (SIRS: temp >38 or <36, HR >90, RR >24, WBC >12 or <4)
  • IV antibiotics for severe disease
28
Q
  1. Selection of antimicrobial and regimen

Purulent (Furuncle, Carbuncle, Skin abscesses, Purulent Cellulitis)

Discuss the treatment for MILD common purulent cause (S. aureus)

A

Purulent - mainly S. aureus (some beta hemolytic, gram negative and anaerobe if skin abscess involving perioral, perirectal, vulvovaginal area)

Mild infection: incision and drainage, warm compress

29
Q
  1. Selection of antimicrobial and regimen

Purulent (Furuncle, Carbuncle, Skin abscesses, Purulent Cellulitis)

Discuss the antibiotic selection for MODERATE common purulent cause (S. aureus)

  • Define MODERATE purulent
A

Purulent - mainly S. aureus (some beta hemolytic, gram negative and anaerobe if skin abscess involving perioral, perirectal, vulvovaginal area)

Moderate (w systemic symptoms): I&D + oral antibiotics
- PO Cephalexin 500mg q6h
- PO Cloxacillin 500mg-1g q6h
- PO Clindamycin 300-450mg q6h (if penicillin allergy)

*Treatment duration: 5-10 days

30
Q
  1. Selection of antimicrobial and regimen

Purulent (Furuncle, Carbuncle, Skin abscesses, Purulent Cellulitis)

Discuss the antibiotic selection for SEVERE common purulent cause (S. aureus)

  • Define SEVERE purulent
A

Purulent - mainly S. aureus (some beta hemolytic, gram negative and anaerobe if skin abscess involving perioral, perirectal, vulvovaginal area)

Severe - with severe systemic signs, failed I&D

Severe: I&D + IV antibiotics

  • IV Cefazolin 1-2g q8h
  • IV Cloxacillin 500mg-1g q4-6h
  • IV Clindamycin 600mg q8h
  • IV Vancomycin 15mg/kg q8-12h (if allergic to everyone else, or if pt has hospital associated risk factors for HA-MRSA, or pt come from another country that may have CA-MRSA)

*Treatment duration: 5-10 days

31
Q
  1. Selection of antimicrobial and regimen

Purulent (Furuncle, Carbuncle, Skin abscesses, Purulent Cellulitis)

Discuss the antibiotic selection if pt might have MRSA

A

Purulent - mainly S. aureus (some beta hemolytic, gram negative and anaerobe if skin abscess involving perioral, perirectal, vulvovaginal area)

Empiric (MRSA) - if pt has hospital associated risk factors for HA-MRSA, or pt come from another country that may have CA-MRSA

Less severe:

  • Co-trimoxazole (PO 960mg bid, IV 5mg/kg q8h)
  • Doxycyline (PO 100mg bid)
  • Clindamycin (PO 300-450mg q6h, IV 600mg q8h)

More severe:

  • IV Vancomycin 15mg/kg q8-12h
  • IV Daptomycin 4-6mg/kg q24h
  • IV Linezolid 600mg q12h

*Treatment duration: 5-10 days

32
Q
  1. Selection of antimicrobial and regimen

Purulent (Furuncle, Carbuncle, Skin abscesses, Purulent Cellulitis)

Discuss the antibiotic selection if pt might have gram negative or anaerobes

A

Purulent - mainly S. aureus (some beta hemolytic, gram negative and anaerobe if skin abscess involving perioral, perirectal, vulvovaginal area)

Empiric (gram-negative, anaerobes)
- PO Amoxicillin-Clavulanate 625mg TDS or 1g BD
- IV Amoxicillin-Clavulanate 1.2g q6-8h

*Treatment duration: 5-10 days

33
Q
  1. Selection of antimicrobial and regimen

Non-purulent (Erysipelas, non-purulent Cellulitis)

Discuss the antibiotic selection in MILD non-purulent SSTIs

  • Define MILD non-purulent
  • What to cover?
A

Non-purulent - Beta-hemolytic streptococcus, usually Strep. Pyogenes (S. aureus less frequent, Pseudomonas with water exposure)

Mild (no systemic signs of infection): cover Strep Pyogenes
- PO Penicillin V 500mg q6h
- PO Cephalexin 500mg q6h
- PO Cloxacillin 500mg-1g q6h
- PO Amoxicillin 500mg-1g q8h
- PO Clindamycin 300-450mg q6h (Penicillin allergy)

*Duration: 5-10 days, 14 days if immunocompromised

34
Q
  1. Selection of antimicrobial and regimen

Non-purulent (Erysipelas, non-purulent Cellulitis)

Discuss the antibiotic selection if MODERATE non-purulent SSTIs

  • Define MODERATE non-purulent
  • What to cover?
A

Non-purulent - Beta-hemolytic streptococcus, usually Strep. Pyogenes (S. aureus less frequent, Pseudomonas with water exposure)

Moderate (w systemic signs of infection, some purulence): include MSSA cover, may initiate IV alr

  • IV Cefazolin 1-2g q8h
  • IV Clindamycin 600mg q8h (Penicillin allergy)

*Duration: 5-10 days, 14 days if immunocompromised

35
Q
  1. Selection of antimicrobial and regimen

Non-purulent (Erysipelas, non-purulent Cellulitis)

Discuss the antibiotic selection if SEVERE non-purulent SSTIs

  • Define SEVERE non-purulent
  • What to cover?
A

Non-purulent - Beta-hemolytic streptococcus, usually Strep. Pyogenes (S. aureus less frequent, Pseudomonas with water exposure)

Severe (w systemic signs of infection, failed oral therapy, or immunocompromised): include broader coverage and explore possibility of necrotizing infections

=> Cover gram -ve, anaerobe, pseudomonas

  • IV Piperacillin/Tazobactam 4.5g q6-8h (cover gram +ve, gram -ve, anaerobes)
  • IV Cefepime 2g q8h (cover gram +ve, gram -ve)
  • IV Meropenem 1-2g q8h (cover gram +ve, gram -ve, anaerobes, ESBL)

*Duration: 5-10 days, 14 days if immunocompromised

36
Q
  1. Selection of antimicrobial and regimen

Non-purulent (Erysipelas, non-purulent Cellulitis)

Discuss the antibiotic selection if SEVERE non-purulent SSTIs if there are MRSA risk factor (what to add on?)

A

Non-purulent - Beta-hemolytic streptococcus, usually Strep. Pyogenes (S. aureus less frequent, Pseudomonas with water exposure)

Severe (w systemic signs of infection, failed oral therapy, or immunocompromised): include broader coverage and explore possibility of necrotizing infections

ADD

  • IV Vancomycin 15mg/kg q8-12h
  • IV Daptomycin 4-6mg/kg q24h
  • IV Linezolid 600mg q12h (If MRSA risk factor)

*Duration: 5-10 days, 14 days if immunocompromised

37
Q
  1. Selection of antimicrobial and regimen

What are some non-pharmacological management for non-purulent SSTIs?

A
  • Ensure rest and limb elevation (drainage of edema, inflammatory substances)
  • Treat underlying conditions (e.g., tinea pedis, skin dryness, limb edema)
38
Q
  1. Goal and monitoring therapeutic response for SSTI
A

Resolution of S&S
- Improvement by 48-72h after initiation (resolution not necessary)
- No progression of lesion or development of complication
- Switch to oral when pt is better
- If pt does not respond within 2-3 days, reassess indication and choice of antibiotics

Bacteriological Clearance
- Repeat culture not required for pt who responded

Absence of ADRs and allergies

39
Q

Discuss the use of topical antibiotics in SSTI

A

Controversial

Most mild cases are self-limiting and would not require antibiotics
Severe cases require oral/IV antibiotics

Local wound care is central in treatment

Topical antibiotic may add cost and ADR

40
Q

What is Mupirocin coverage, and what is it used for?

A

Mupirocin Coverage

  • highly effective against aerobic gram positive cocci, especially S. aureus (bactericidal at 2% ointment)
  • not effective against enterococci and gram negatives

Mupirocin Use

  • Nasal staphylococcal carriage
  • Impetigo (mild limited lesions) - BID x5d

Mupirocin resistance in MRSA is a major concern

  • In hospital, reserved for MRSA decolonization and superficial infection (e.g., hemodialysis catheter exist site infection)

3151 Therapeutics (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions