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PR3151 Finals > IC14 Skin and Soft Tissue Infection > Flashcards

IC14 Skin and Soft Tissue Infection Flashcards

1
Q

What are the 6 anatomical sites of the type of SSTI?

A

Superficial Infections:
1. Epidermis - Impetigo
2. Dermis - Ecthyma, Erysipelas

Deeper Infections:
3. Hair follicles - Furuncles, Carbuncles
4. Subcutaneous fat - Cellulitis
5. Fascia - Necrotizing fasciitis
6. Muscle - Myositis

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2
Q

How does the skin function as a protective barrier to infections? 6 reasons

A
  1. Physical Barrier against mechanical injury, UV
  2. Immunological barrier (Innate immunity - AMP, Cytokines, Cells with PRR)
  3. Chemical Barrier pH 4-5 acidic environment
  4. Continuous renewal of epidermal layer results in shedding of keratocytes and skin microbiota
  5. Sebaceous secretions inhibits growth of many bacteria and fungi
  6. Normal commensal skin microbiome prevents colonization and overgrowth of more pathogenic strains
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3
Q

What 9 factors can impair skin barrier function?

A
  1. Age
  2. Infection
  3. Physical damage - Pressure, friction, laceration
  4. Physical environment - urine, faeces, sweat, chronic wound fluid
  5. Ischaemia - Lack perfusion
  6. Diseases - DM
  7. Drugs - Immunosuppressants, SGLT2i
  8. pH - Detergents, excessive soap
  9. Humidity and moisture
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4
Q

What is the pathophysiology of SSTIs?

A

Disruption of normal host defenses allowing overgrowth and invasion of skin and soft tissues by pathogenic microbes

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5
Q

What are the risk factors for SSTI?

A
  1. Disruption of the skin barrier
    - Traumatic (Lacerations, recent surgery, burns, abrasions, crush injuries, open fractures)
    - Non-traumatic (Ulcers, tinea pedis, dermatitis)
    - Impaired venous and lymphatic drainage
    - Peripheral artery disease
  2. Conditions that predispose to infection
    - Diabetes
    - Cirrhosis
    - Neutropenia
    - HIV
    - Transplantation and immunosuppressive medications
  3. History of cellulitis
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6
Q

What are examples of traumatic skin disruption?

A

Lacerations, recent surgery, burns, abrasions, crush injuries, open fractures, injection drug use, human and animal bites, insect bites

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7
Q

What are examples of non-traumatic skin disruption?

A

Ulcers, tinea pedis, dermatitis, toe web intertrigo, chemical irritants

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8
Q

What are examples of impaired venous and lymphatic drainage?

A
  • Saphenous venectomy
  • Obesity
  • Chronic venous insufficiency
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9
Q

How to prevent SSTI?

A
  1. Manage risk factors
  2. Maintain skin integrity - Wound care, Tinea pedis treatment, prevent dry/cracked skin, Foot care (DM)
  3. Treat predisposing factors - Reduce recurrence risk
  4. Copious irrigation, removal of foreign objects & debridement of devitalized tissue for Acute Traumatic Wounds
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10
Q

What factors to confirm the presence of infections during diagnosis in history taking?

A
  1. Underlying diseases
  2. Recent trauma, bites, burns, water exposure
  3. Animal exposure
  4. Travel history
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11
Q

How and where should samples for cultures be collected from?

What should be avoided?

Why must it be done this way?

A

Collection:
1. From deep in wound after cleansing of surface
2. From base of a closed abscess
3. By curettage (Aspirate using needle)

Don’t do a wound swab or irrigation because it is difficult to obtain a representative sample

Contamination of open draining wounds with pus, exudates, tissues

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12
Q

What is the clinical presentation (appearance and location) of impetigo?

A
  • Erythematous papules
  • Rapidly evolve into vesicles/pustules that rupture
  • Dried discharge forms honey-colored crusts
  • Frequently many bullous/non-bullous in appearance
  • On exposed body areas (Face and extremities)
  • Well localized lesions
  • More common in children
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13
Q

What is the clinical presentation of ecthyma?

A
  • Ulcerative form of impetigo
  • Extend through epidermis and dermis
  • Pruritus
  • Scratching may spread
  • May coexist with impetigo
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14
Q

What is the clinical presentation of furuncles (“boil”)?

A
  • Hair follicle infection with purulence
  • Extend through dermis and subcutaneous tissue
  • Small abscess forms
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15
Q

What is the clinical presentation of carbuncles?

A
  • Multiple furuncles coalesce and extent into subcutaneous tissue
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16
Q

What is the clinical presentation of cutaneous abscesses?

A
  • Pus collection within dermis and deeper skin tissues
  • Manifest as painful, tender, fluctuant, erythematous nodules
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17
Q

What is the clinical presentation of cellulitis?

A
  • Deeper and subcutaneous fat
  • Acute, diffuse, spreading, non-elevated, poorly demarcated area of erythema
  • Rapid onset/progression
  • Unilateral lower extremities
  • Sometimes on any area of skin
  • Fever
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18
Q

What is the clinical presentation of erysipelas?

A
  • Upper dermis
  • Fiery red, tender, painful plaque (raised above surrounding skin)
  • Well demarcated edges
  • Face, lower extremities
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19
Q

When do you do lab tests or radiological tests for evaluating SSTI?

A

When you suspect deep layer infection

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20
Q

What are the likely pathogens for the different SSTIs?

A
  1. Impetigo - Staphylococci; Streptococci
  2. Ecthyma - GAS
  3. Nonpurulent (Cellulitis, Erysipelas) - Beta Hemolytic Streptococcus (Usually GAS); Other less common ones (S aureus, Aeromonas, Vibrio vulnificus, Pseudomonas with water exposure)
  4. Purulent (Furuncles, Carbuncles, Skin abscesses, Purulent cellulitis) - S aureus; Others (Some beta hemolytic Strep)
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21
Q

How is CA-MRSA genetically distinct from HA-MRSA?

A

Panton-Valentine Leucocidin (PVL)

SCCmec IV

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22
Q

What are risk factors for CA-MRSA?

A
  • Contact sports, Military personnel, IV drug abusers, Prison inmates (Close contact)
  • Crowded facilities, lack of sanitation
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23
Q

What is CA-MRSA susceptible to?

A

Oral Non-Beta Lactams (Clindamycin, Cotrimoxazole, Doxycycline)

24
Q

What should we note about CA-MRSA?

A

It is not common in Singapore

25
Q

What are some considerations for antimicrobial regimen?

A
  1. Need to treat with antibiotics?
  2. Regimen – choice, route, dose, duration
  3. Consider
    - Site of SSTI
    - Presence or absence of discharge (Purulent vs nonpurulent)
    - Microbiology
    - Severity or extent (Mild, moderate, severe)
26
Q

What antibiotic regimen can be given for impetigo with mild limited lesions?

A

Topical Mupirocin BID x 5 days

27
Q

What empiric therapy can be given for impetigo with ecthyma? Duration of therapy?

A
  • PO cephalexin or cloxacillin
  • PO clindamycin

7 days

28
Q

What culture-directed therapy can be given for impetigo with ecthyma?

A
  • S pyogenes: PO penicillin V, amoxicillin
  • MSSA: PO cephalexin or cloxacillin

7 days

29
Q

Why is topical mupirocin allowed for use? Why must the use of mupirocin be cautioned?

A

Superficial infection (Benefit outweighs risk of contagious spread for children with impetigo)

Highly effective against S aureus and aerobic Gram positive cocci but not against enterococci & Gram negatives - HENCE, MRSA resistance is a concern

30
Q

What is the treatment for purulent SSTI (Furuncles, Carbuncles, Skin abscesses, Purulent cellulitis)?

A
  1. Mainstay of treatment is incision and drainage
  2. Adjunctive systemic antibiotics
    - Unable to drain completely
    - Lack of response to I&D
    - Extensive disease involving several sites
    - Extremes of age
    - Immunosuppressed (e.g. chemotherapy, transplant)
    - Signs of systemic illness (SIRS criteria*: temperature > 380C or < 360C, heart rate > 90 bpm, respiratory rate > 24 bpm, WBC > 12 x 109/L or < 4 x 109/L)
    - IV antibiotics for severe disease

**SIRS: systemic inflammatory response syndrome (Not very used now because non-specific)

30
Q

What is the treatment for purulent SSTI (Furuncles, Carbuncles, Skin abscesses, Purulent cellulitis)?

A
  1. Mainstay of treatment is incision and drainage
  2. Adjunctive systemic antibiotics
    - Unable to drain completely
    - Lack of response to I&D
    - Extensive disease involving several sites
    - Extremes of age
    - Immunosuppressed (e.g. chemotherapy, transplant)
    - Signs of systemic illness (SIRS criteria*: temperature > 380C or < 360C, heart rate > 90 bpm, respiratory rate > 24 bpm, WBC > 12 x 109/L or < 4 x 109/L)
    - IV antibiotics for severe disease

**SIRS: systemic inflammatory response syndrome (Not very used now because non-specific)

31
Q

What is the treatment for mild, moderate and severe purulent SSTI?

A

Mild - I&D, warm compress

Moderate (With systemic symptoms) - Oral Abx (Cloxacillin, Cephalexin, Clindamycin)

Severe (Failed drainage, failed oral abx, systemic symptoms worsen) - IV Abx (Cloxacillin, cefazolin, clindamycin, vancomycin)

32
Q

What is the empiric therapy for MRSA or gram negative/anaerobic purulent SSTIs? Duration of treatment?

A

Empiric (MRSA):
* Co‐trimoxazole, doxycycline, clindamycin, vancomycin, daptomycin, linezolid

Empiric (gram‐neg, anaerobe):
* Amoxicillin‐clavulanate

5-10 days

33
Q

What is the treatment for mild, moderate and severe NON-purulent SSTI? Duration of therapy?

A

Mild (without systemic signs of infection), mainly only cover Strep pyogenes, use oral antibiotic:
 Penicillin V, cephalexin, cloxacillin
 Penicillin‐allergy – clindamycin

Moderate (with systemic signs of infection, some purulence), to include MSSA cover, may initiate IV:
 Cefazolin, Clindamycin (penicillin‐allergy)

Severe (with systemic signs of infection, failed oral therapy or immunocompromised), to include broader coverage and explore possibility of necrotizing infections
 IV Pip-Tazo, Cefepime, Meropenem
 If MRSA risk factor(s): Add IV vancomycin, daptomycin, linezolid

Duration: 5 ‐ 10 days; 14 days may be needed for immunocompromised

34
Q

Apart from Abx treatment, what other things to treat or ensure?

A
  • Ensure rest and limb elevation (drainage of edema and inflammatory substances)
  • Treat underlying conditions eg tinea pedis, skin dryness, limb edema
35
Q

What are the 3 goals of treatment and monitoring parameters?

A

1) Resolution of signs & symptoms

 Improvement or resolution by 24 to 72 hrs after initiation of effective antibiotics (But don’t need all the redness to go away)
 No progression of lesion or development of complication
 Switch to oral antibiotic when patient is better
 If the patient fails to respond clinically within 2 to 3 days, reassess indication and/or choice of antibiotics

2) Bacteriological clearance
 Repeat culture is not required for patients who responded

3) Absence of adverse drug reactions and allergies

36
Q

Where does diabetic foot infections occur? What are the clinical presentations?

A
  • Soft tissue or bone infections below the malleolus
  • Areas of DFIs
    – Skin ulceration (peripheral neuropathy)
    – Wound (trauma)
37
Q

What are some complications of DFIs?

A
  • Complications
    – Hospitalization
    – Osteomyelitis ➔amputation
  • Singapore: one the world’s highest rates of lower extremity
    amputation in diabetes patients
38
Q

What is the pathophysiology of DFI?

A
  1. Neuropathy - Autonomic (Dryness, cracks, fissures), Motor (Muscle imbalances), Peripheral (Pain sensation reduced)
  2. Vasculopathy - Atherosclerosis, PAD
  3. Immunopathy - Susceptibility to infections

All these lead to ulcer formations / wounds

Creating environment for bacterial colonization, penetration, proliferation leading to DFI

39
Q

What is the definition of DFI infection?

A

– Purulent discharge; or
– ≥ 2 signs or symptoms of inflammation
* Erythema
* Warmth
* Tenderness
* Pain
* Induration

40
Q

What is the evolution of DFI clinical presentation?

A
  1. Superficial ulcer, mild erythema
  2. Deep tissue infection, extensive erythema
  3. Infection of bone and fascia, purulent discharge
  4. Localized gangrene
41
Q

What are the causative organisms of microbiology for DFIs?

A

– Typically polymicrobial

– Staphylococcus aureus and Streptococcus spp. most common

– Gram‐negative bacilli
* Particularly in chronic wounds or previously treated with antibiotics
* E. coli, Klebsiella spp., Proteus spp., etc.
* Pseudomonas aeruginosa less common

– Anaerobes
* Particularly in ischemic or necrotic wounds
* Peptostreptococcus spp., Veillonella spp., Bacteroides spp.

42
Q

When is cultures needed in DFI?

A

– Mild DFIs = Optional
– Moderate - severe DFIs = Deep tissue cultures after cleansing and before starting antibiotics (if possible); Avoid skin swabs
– Do not culture uninfected wounds

43
Q

What does the antibiotic choice and route depend on for DFI treatment?

A
  1. Severity of infection - IDSA classification, SIRS criteria, Tissue involvement extent
  2. Patient factors - Allergy, MRSA risks, Pseudomonal risks (warm climate, water exposure)
44
Q

What is IDSA infection severity definition for DFI?

A

Mild - Skin & SC tissue + Erythema with ≤ 2cm around ulcer (Non-systemic infection)

Moderate - Deeper tissue (Bone, Joint) + Erythema with > 2cm (Non-systemic infection)

Severe - Deeper tissue (Bone, Joint) + Erythema > 2cm (Systemic infection)

45
Q

What organisms are present in Mild, Moderate, Severe DFI?

A

Mild - Streptococcus + S aureus

Moderate - Streptococcus + S aureus + Gram negatives + Anaerobes +/- Pseudomonas

Severe - Streptococcus + S aureus + Gram negatives + Anaerobes + Pseudomonas

46
Q

What antibiotic therapy will be given to mild, moderate, severe DFI?

A

Mild (PO)
* Cephalexin, Cloxacillin, Clindamycin
* If MRSA risk factor(s), Co‐trimoxazole, Clindamycin, Doxycycline

Moderate (IV)
* Amoxicillin/clavulanate
* Cefazolin/Ceftriaxone + Metronidazole
* If MRSA risk factor(s), Vancomycin, Daptomycin, Linezolid

Severe (IV)
* Piperacillin‐tazobactam
* Cefepime + Metronidazole
* Meropenem
* Ciprofloxacin + Clindamycin
* If MRSA risk factor(s), Vancomycin, Daptomycin, Linezolid

47
Q

What is the duration of DFI treatment?

A
  1. No Bone involved
    Mild = 1-2 wks
    Moderate = 1-3 wks
    Severe = 2-4 wks
  2. Bone involved
    Surgery – all infected bone/tissue removed (e.g. amputation) = 2-5 days
    Surgery – Residual infected soft tissue = 1-3 wks
    Surgery – Residual viable bone = 4-6 wks
    No surgery or Surgery – residual dead bone ≥ 3 months
48
Q

What are some adjunctive measures for DFI?

A
  • Wound care
    – Debridement
    – “Off‐loading”
    – Apply dressings that promote a healing environment and control excess exudation
  • Foot care
    – Daily inspection
    – Prevent wounds and ulcers
  • Optimal glycemic control
49
Q

Pressure ulcers involve synergistic interaction between which 4 factors?

A

– Moisture
– Pressure (amount and duration)
– Shearing force
– Friction

50
Q

What are some risk factors for pressure ulcers?

A
  • Reduced mobility – E.g. spinal cord injuries, paraplegic
  • Debilitated by severe chronic diseases – E.g. multiple sclerosis, stroke, cancer
  • Reduced consciousness
  • Sensory and autonomic impairment – Incontinence
  • Extremes of age
  • Malnutrition
51
Q

What are the 4 stages of pressure ulcer clinical presentation?

A

Stage 1
* Abrasion of epidermis
* Irregular area of tissue swelling
* No open wound

Stage 2
* Extends through the dermis
* Open wound

Stage 3
* Extends deep into subcutaneous fat
* Open sore or ulcer

Stage 4
* Involves muscle and bone
* Deep sore or ulcer

52
Q

What is the criteria for infected pressure ulcer?

A

Same as DFI criteria

53
Q

What are the causative organisms of pressure ulcers?

A

Same as DFIs and polymicrobial

54
Q

What is pressure ulcer treatment?

A
  • Antibiotic selection, route and treatment duration are identical to DFIs
  • Adjunctive measures
    – Debridement of infected or necrotic tissue
    – Local wound care
  • Normal saline preferred
  • Avoid harsh chemicals
    – Relief of pressure
  • Turn or reposition every 2 hours
  • Also important for prevention

PR3151 Finals (10 decks)

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