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3151 finals > SSTI > Flashcards

SSTI Flashcards

1
Q

name the anatomical sites for Bacterial skin and soft tissue infections (diverse grp of diseases)

A

epidermis

dermis

Hair follicles

Sc fat

Fascia

muscle

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2
Q

epidermis

A

Impetigo
* Superficial infection
* Pustules, vesicles –> crusting, bullae

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3
Q

dermis

A

Ecthyma
* Deeper than impetigo, pustules/ vesicles –> crusting, bullae
Erysipelas
* Superficial infection of skin (lymphatics)
* Tender, erythematous plaque with well-demarcated borders

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4
Q

Hair follicles

A

Furuncles
* Infection of hair follicle with associated small sc abscess
Carbuncles
* Cluster of furuncles

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5
Q

Sc fat

A

Cellulitis
Acute infection of skin (deep dermis and sc)

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6
Q

Fascia

A

Necrotising fasciitis
* Aggressive infection of sc tissue, spreads along fascial planes
- flesh eating bact, fast

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7
Q

muscle

A

Myositis (pyomyositis)
- bone
* Purulent infection of skeletal muscles
* Often with abscess formation

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8
Q

Skin as protective barrier

A

physical
chemical
immunological

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9
Q

Physical barrier

A

Physical assault (injury, UV)
Microbial assault (bact, fungi, virus)
Chemical assault (irritant, allergens)

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10
Q

Chemical barrier

A

pH of 4-5 (acidic)
□ Produce FA from phospholipids
□ Acidic environ (keep bact, Candida low)
- Regulates desquamation (transient & resident bact low)

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11
Q

Immunological barrier

A

i. Anti-microbial peptides (AMPs), cytokines and cells w/ pattern-recognition receptors (PRR)
ii. When inflammation:
□ Directly kill pathogens
□ Influence cellular processes, promote wound healing. Initiate adaptive immune resp

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12
Q

Immunological barrier

A

i. Anti-microbial peptides (AMPs), cytokines and cells w/ pattern-recognition receptors (PRR)
ii. When inflammation:
□ Directly kill pathogens
□ Influence cellular processes, promote wound healing. Initiate adaptive immune resp

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13
Q

factors that impair skin barrier function

A

age
infection
physical damage
physical environment (humidity, moisture)
ischaemia (lack of perfusion)
diseases (DM)
drugs (immunosupp, SGLT2i)
pH
excessive soap, detergent use

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14
Q

Pathophysiology of SSTI

A

a. Normal skin function as protective barrier –> primary defense mechanism against infections
b. Other protective mechanisms:
i. Continuous renewal of epidermis layer (shed keratocytes and skin microbiota)
ii. Sebaceous secretions inhibits growth of many bact, fungi (pH)
iii. Normal skin commensal microbiome. balance
1) Prevent colonisation, overgrowth of more pathogenic strains

c. *** defense = intact skin
d. Majority of SSTIs: results from disrupt of normal host defense (overgrowth, invasion of skin, soft tissues) <—- PATHOGENIC microorg

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15
Q

Risk factors of SSTI

A

§ Traumatic
□ Laceration, recent surgery, burns, abrasion, crush injury, open fracture, inj drug use, human & animal & insect bites
§ Non-traumatic
□ Ulcers, tinea pedis, dermatitis, toe web intertrigo, chem irritants
§ Impaired venous, lymphatic drainage (decr blood flow)
□ Saphenous venectomy
□ Obesity
□ Chronic venous insufficiency
§ Peripheral artery disease
§ medical conditions that predispose….
§ Hist of cellulitis

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16
Q

Conditions predispose of SSTI

A

§ DM
§ Cirrhosis
§ Neutropenia
§ HIV
§ Transplant, immunosupp medications

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17
Q

Prevention of SSTIs

A

a. Prevention: manage predisposing risk factors
b. Good care, maintain skin integrity
i. Good wound care
ii. Treat tinea pedis
iii. Prevent dry, cracked skin
iv. Good foot care for DM pt (prevent wound and ulcers)

c. Predisposing factors (identified, treated at diagnosis, decr risk for recurrence)
d. Acute traumatic wounds
i. Copiously irrigated (wash)
ii. Foreign objects removed
iii.Devitalized tissues debrided

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18
Q

Diagnosis

A

§ History taking and recognise risk factors
□ Underlying diseases
□ Recent trauma, bites, burns, water exposure
□ Animal exposure
□ Travel history
§ Physical examination
Clinical presentation
Lab results

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19
Q

§ Physical examination

A

□ Culture may not be required for MILD, SUEPRFICIAL infections

□ BLOOD Culture needed for severe cases, marked systemic symptoms// immunocompromised
- pus, exudates, tissue from wound
-Open, draining wounds
◊ Contaminated with potential PATHOGENIC org
- Wound swab avoided (not representative sample)
◊ Sample from deep in wound, after surface cleansed
◊ Base of closed abscess (bact grow)
◊ Curettage (cut away)

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20
Q

Lab results

A

□ Systemic signs of infection
- Complete blood count and differential
◊ Elevated WB, leuk
◊ Thrombocytopenia – severe infection
-Lactate
◊ Elevated – tissue, organ underperfusion (sepsis)/ necrosis)
-Creatine phosphokinase
◊ Elevated – myonecrosis (fasciitis)
- c-reactive protein
◊ Non-specific
- Gram stain, culture
◊Guide purulent infection therapy

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21
Q

radio

A

Radiography
CT with contrast
MRI
Ultrasonography

How deep is infection (identify drainable fluid/ abscess. Myositis reach bone?)

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22
Q

identify pathogens - Impetigo

A

Staphylococci/ streptococci
Bullous form caused by toxin- producing strains of S-aureus

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23
Q

impetigo Abx

A
  • Impetigo, mild limited lesions:
    Topical mupirocin BD 5days
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24
Q

Topical ABx

A
  • Controversial
    • Mild cases – self-limiting
    • Local wound care is impt
    • Not for SEVERE
    • Incr cost to treatment
      ○ Eg: mupirocin:
      § Effective against aerobic gram +ve cocci (S.aureus)
      □ Nasal staphylococcal carriage
      □ 2% ~bactericidal
      § Not for enterococci, gram -ve
      § Resistance in MRSA
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25
Q

ecthyma pathogen

A

Grp A streptococci (beta-hemolytic, complete)

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26
Q

ecthyma Abx

A
  • Impetigo, ecthyma:
    • Empiric
      ○ PO cephalexin, cloxacillin
      ○ (penicillin allergy) PO clindamycin
    • Culture directed
      ○ s.pyogene: PO penicillin V, amoxicillin
      ○ MSSA: PO cephalexin (moderate), cloxacillin (severe), clindamycin

PO 7 days

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27
Q

Purulent SSTIs — pathogen

Furuncles
Carbuncles
Cutaneous abscesses

Purulent cellulitis

A

S.aureus
Beta-hemolytic streptococcus

skin abscess in perioral/ perirectal/ vulvovag area
- Multiple org (gram neg. anaerobes)

CA-MRSA

28
Q

CA-MRSA

A

not common in SG
* Genetically distant from HA-MRSE (seen in SG)
* Susceptible to PO (non beta-lactam)
○ Clindamycin, co-trimoxazole, doxycycline
* Risk factors:
○ Contact (sports, military, IV drug abuse, prison)
* Overcrowded facilities, close contact, lack of sanitation

29
Q

purulent SSTI tx plan

A

1) Incision and drainage (I&D)
2) Adjunctive systemic Abx

Duration: 5-10days

30
Q

when to add Abx for purulent SSTI

A
  • Unable to drain completely
  • No response to I&D
  • Involve several sites
  • Extreme age
  • Immunosuppressed
  • Systemic illness
    a. Temp > 38// <36
    b. Heart rate > 90bpm
    c. RR: > 24 bpm
    d. WBC: > 12x10^9/L or <4x10^9/L
    e. CRP, procalcitonin
  • IV AB for severe disease
31
Q

mild, mod for purulent SSTI

A
  • MILD: I&D/ warm compress to promote drainage
  • MOD: I&D + PO AB
    - Cloxacillin, cephalexin, clindamycin (allergy)
32
Q

SEVERE purulent SSTI

A

I&D + IV AB

Cloxacillin, cefazolin
Clindamycin, vancomycin (allergy)

33
Q

add-on empiric for purulent SSTI

A
  • MRSA:
    ○ CA-MRSA: co-trimoxazole, doxycycline, clindamycin, vanco
    § No beta-lactams (resistant)
    ○ (HA MRSA) *SG: vancomycin, daptomycin, linezolid
  • Gram neg, anaerobe:
    ○ amoxicillin-clavulanic
34
Q

HA-MRSA risk factors

A

MRSA infection/colonization in last 12 months
prolonged/repeated hospital stay in the last 12 months
hemodialysis.

35
Q

Non-purulent SSTI pathogen

Cellulitis
erysipelas

A

Beta-hemolytic streptococcus
Grp A strep

S.Aureus (less freq)

Less common pathogen based on exposure, risk factors:
Aeromonas, vibrio vulnificus, pseudomonas with water exposure

36
Q

Non-purulent SSTI Abx (MILD)

A
  • MILD (w/o systemic signs of infection ) - cover strep pyogenes
    • PO: penicillin V, cephalexin, cloxacillin
    • Clindamycin (allergy)

Duration: 5-10days, 14 days for immunocompromised

37
Q

Non-purulent SSTI Abx (MODERATE)

A
  • MODERATE: systemic signs of infection, purulence + MSSA cover
    IV: cefazolin, clindamycin (penicillin)

Duration: 5-10days, 14 days for immunocompromised

38
Q

Non-purulent SSTI Abx (SEVERE)

systemic/ failed PO therapy/ immunocompromised

A
  • Broader coverage, possibility of necrotising infections
    ○ Cover +, -ve, anaerobes
  • IV: meropenem, imipenem, piperacillin-tazo
    Cefepime (but low -ve, anaerobe cover)
    no cipro (no cover +, anaerobe)

MRSA risk: + IV vanco, daptomycin, linezolid

Duration: 5-10days, 14 days for immunocompromised

39
Q

non-pharm for SSTI

A

Rest, limb elevation (drainage for oedema, inflamm sub)
Treat UNDERLYING conditions
* Tinea pedis
* Skin dryness
Limb oedema

40
Q

Diabetic foot infection

A
  • Soft tissue or bone infection below malleolus
  • Areas:
    • Skin ulceration (peripheral neuropathy)
      Wound (trauma)
41
Q

DFI complication

A

Hospitalisation
Osteomyelitis –> amputation

42
Q

DFI pathophysiology

A

1) neuropathy
- peripheral (lack sensation, pain)
- motor (imbalance
- autonomic (incr dryness, cracks, fissures)
2) vasculopathy
- early atherosclerosis
- PVD
- hypergly, hyperlipid
3) immunopathy
- immune response, incr susp to infections
- hypergly

—> ulcer form/ wounds —-> bact colonise, penetrate, proliferate

43
Q

DFI clinical presentation

A

1) Superficial ulcer, mild erythema
2) Deep tissue infection, extensive erythema
3) Infect bone, fascia, purulent discharge
4) Localised gangrene

44
Q

DFI pathogen

A
  • Polymicrobial (open wound + feet)
    ○ Staphylococcus aureus, streptococcus spp.
    ○ Gram neg bacilli (chronic wounds, previous tx with AB)
    § e.coli, klebsiella spp, proteus spp
    § Psuedo less common
      ○ Anaerobes (ischemia, necrotising wound) 
            §Peptostreptococcus spp, veillonella spp, bacteriodes spp
45
Q

Cultures for DFI?

A

Not culture uninfected wounds
- Mild DFI: optional

  • Moderate —- severe DFI:
    Deep tissue culture (after cleanse, before start AB)
46
Q

not always infected! By = bacterial colonisation of ulcers, wounds
what is ifnection?

A

○ Purulent discharge
OR

○ >2 signs of inflamm
§ Erythema
§ Warmth
§ Tender
§ Pain
§ Induration
§ pus

○ Systemic (temp, HR, WBC, RR, BP)
= Severe DFI

47
Q

Abx for DFI depends on

A

1) Severity of infection
a. Infectious Disease Society of American (IDSA) classification
b. Extent of tissue involvement

2) Pt specific factors
a. Allergies
b. MRSA risk factor
c. Pseudomonal risk factors (warm climate, exposure to water)
- Empiric cover esp for severe infection// failure of Abx

48
Q

mild DFI definition

A

infection of skin and SC tissue
+
erythema <2cm around ulcer
+
no sign of systemic infection

49
Q

mild DFI org

A

Staphylococcus aureus (pus), streptococcus spp.

50
Q

mild DFI Abx

A

PO (cephalexin, cloxacillin, clindamycin)

MRSA risk factor: CMX, clindamycin, doxycyclin

51
Q

moderate DFI severity

A

infection of deeper tissue (bone, joint)
OR
erythema >2cm around ulcer
+
no sign of systemic infection

52
Q

moderate DFI org

A

Staphylococcus aureus (pus), streptococcus spp.

gram neg (pseudo)

anaerobes

53
Q

moderate DFI Abx

A

IV (amox-clav)
IV cefa/ metro
ceftriaxone/metro

MRSA risk factor: vanco, daptomycin, linezolid

54
Q

severe DFI defintion

A

infection of deeper tissue (bone, joint)
OR
erythema >2cm around ulcer

+ sign of systemic infection

55
Q

severe DFI org

A

Staphylococcus aureus (pus), streptococcus spp.

gram neg (pseudo)

anaerobes

56
Q

severe DFI abx

A

IV (pip-tazo)
IV meropenem
IV cefepime + metronidazole
IV cipro + clindamycin

MRSA risk factor: IV vanco, daptomycin, linezolid

57
Q

non pharm adjunctive measures:

A
  • Wound care
    ○ Debridement
    ○ Off-load
    ○ Apply dressings that promote healing environment
    § Control excess exudation
  • Foot care
    ○ Daily inspection
    ○ Prevent wounds and ulcers

*Optimal glycemic control

58
Q

duration of tx — no bone

A

no bone
(mild 1-2wk)
(mod 1-3 wk)
(severe 2-4wk)

59
Q

duration of tx — bone

A

amputate 2-5 days
residual soft tissue 1-3wk
residual viable bone 4-6wk

no surgery/ residual dead bone > 3mnths

60
Q

streamline Abx for DFI

A

not continue until complete wound heal
streamline choice based on culture, AST

switch to PO, when pt improves

61
Q

Decubitus ulcers/ bed sores 4 contributing factors

A

1) Moisture
2) Pressure (amt, duration)
3) Shearing force
4) Friction

62
Q

PU risk factors
(unable to feel/ turn themselves)

A
  • Reduced mobility
    ○ Spinal cord injuries, paraplegic
  • Debilitated by severe chronic diseases
    ○ Multiple sclerosis, stroke, cancer
  • Reduced consciousness
  • Sensory and autonomic impairment
    ○ continence (moisture)
  • Extreme age
    ○ Malnutrition
63
Q

Clinical progression of PU

A

Stage 1
○ Abrasion of epidermis
○ Irregular area of tissue swelling
○ NO OPEN WOUNDS
Stage 2
○ Extend through dermis
○ Open wound
Stage 3
○ Extend deep into sc fat
○ Open sore/ ulcer
Stage 4
○ Muscle, bone
○ Deep sore or ulcer

64
Q

Infected pressure ulcer = criteria for DFI

A

○ Purulent discharge
OR
○ >2 signs of inflamm
Erythema, warmth, tender, pain, induration

65
Q

micro + culture for PU?

A
  • Microbiology
    • Same as DFI
    • Polymicrobial (+ve, -ve, anaerobes)
  • Culture
    • Deep tissue culture/ biopsy specimens
      *Not skin swabs
66
Q

adjunct of PU

A
  1. Debridement of infected or necrotic tissue
    1. Local wound care
      a. Normal SALINE
      b. Avoid harsh chemicals
    2. Relief pressure
      a. Turn/ reposition every 2hrs
      b. ** prevention
      c. Specific dressing
      i. (off-load)
      ii. Control exudation

3151 finals (9 decks)

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