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PR3151 (cleefy) > IC14 PR3151 SSTI > Flashcards

IC14 PR3151 SSTI Flashcards

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1
Q

(Relate the anatomical site to the type of SSTI)
Epidermis

A

Impetigo

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2
Q

(Relate the anatomical site to the type of SSTI)
Dermis

A

Ecthyma, erysipelas

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3
Q

(Relate the anatomical site to the type of SSTI)
Hair follicles

A

Furuncles
Carbuncles (cluster of furuncles)

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4
Q

(Relate the anatomical site to the type of SSTI)
SubQ fat

A

Cellulitis

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5
Q

(Relate the anatomical site to the type of SSTI)
Fascia (surrounds blood vessels)

A

Necrotizing fasciitis

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6
Q

(Relate the anatomical site to the type of SSTI)
Muscle

A

Myositis

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7
Q

(Relate the anatomical site to the type of SSTI)
Skeletal muscle

A

Pyomyositis (purulent infection of skeletal muscle, often with abscess formation

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8
Q

Factors that impair skin barrier function (x9)

A

age (very young and old)
infection
phy dmg (pressure, friction, lacerations)
phy environment (contact w urine faeces sweat and chronic wound fluid)
ischaemia (lack of perfusion)
diseases (diabetes, etc)
drugs (immunosupps, SGLT2i, etc)
pH (unbalanced detergents, phy envi)
excess soap and detergent use

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9
Q

What are the protective mechanisms of the skin against SSTIs?

A

1) normal skin function acts as a protective barrier against infections.

2) continuous renewal of epidermal layer results in shedding of keratocytes and skin microbiota

3) sebaceous secretions inhibit growth of many bact and fungi

4) normal commensal skin microbiome prevents colonisation and overgrowth of more pathogenic strains.

5) others: pH (acidic environment of the skin), AMP anti-microbial peptides

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10
Q

What are the three risk factors for SSTIs?

A

1) disruption of the skin barrier

2) conditions that predispose to infection

3) history of cellulitis

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11
Q

how does a disruption of skin barrier become a risk factor for SSTI?

describe some of the conditions for the above^

A
  • traumatic
  • non-traumatic: ulcer, tinea pedis, dermatitis, toe web intertrigo, chemical irritants.
  • impaired venous and lymphatic drainage (poor flow preventing rescue agents from flowing there and fight invaders + retention and overgrowth of organism causing it to invade): saphenous venectomy, obesity, chronic venous insufficiency.
  • peripheral artery disease
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12
Q

what are the conditions (and drugs)that predispose to infection of sstis (risk factor)

A
  • diabetes, cirrhosis, neutropenia, hiv, transplantation and immunosuppressive meds
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13
Q

methods to prevent SSTIs?

A

1) good care to maintain skin integrity: good wound care, tx of tinea pedis, preventing dry cracked skin, good foot care for DM patients to prevent wounds and ulcers.

2) identify any predisposing factors and treat at same time of initial diagnosis to reduce risk for recurrence.

3) acute traumatic wounds irrigated, foreign objects removed, devitalised tissues debrided (source control).

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14
Q

what history taking should be done before diagnosis of SSTI?

A

underlying diseases

recent trauma, bites, burns, water exposure

animal exposure

travel history

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15
Q

HOW should culture sample be collected for SSTIs?

A

1) deep in the wound after cleansing surface
2) base of a closed abscess, where bact grow, rather than surface
3) curettage (debride top) instead of wound swab or irrigation

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16
Q

when to collect blood culture for ssti?

A

when there are marked systemic symptoms of infection or the patient is immunocompromised

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17
Q

when and what culture samples should not be collected for sstis?

A

mild and superfiical infections where the skin commensal bact may be taken instead

wound swabs because it may be difficult to obtain representative sample.

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18
Q

what is the clinical presentation of impetigo?

A

begins as erythematous papules that rapidly evolve into vesicles and pustules that rupture, with the dried discharge forming honey-colored crusts on an erythematous base.

Usually on exposed areas of body (face and extremities).

Lesions well localised, frequently
many, bullous or non bullous in appearance.

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19
Q

what is the clinical presentation of ecthyma?

A

ulcerative form of impetigo in which the lesions extend through the epidermis and deep into the dermis.

Pruritis is common, scratching may further spread
infection

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20
Q

what is the clinical presentation of furuncle?

A

an infection of the hair follicle in
which purulent material extends through the dermis into
the subcutaneous tissue, where a small abscess forms

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21
Q

what is the clinical presentation of carbuncle?

A

formed when furuncles coalesce and extent
into subcutaneous tissues.

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22
Q

what is the clinical presentation of skin abscess?

A

collections of pus within the dermis and
deeper skin tissues. Skin abscesses manifest as painful, tender, fluctuant and erythematous nodules

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23
Q

what is the clinical presentation of erysipelas?

A

affects upper dermis; Fiery red, tender,painful plaque (raised above surrounding skin) with well‐demarcated edges.

Common on face, also lower extremities.

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24
Q

what is the clinical presentation of cellulitis ?

A

Involves deeper and subcutaneous fats.

Usually presents as an acute, diffuse, spreading, nonelevated, poorly demarcated area of erythema.

Relatively rapid onset/progression.

Almost always unilateral.

Fever in 20–70% of patients.

It is typically found on the lower extremities, although it can appear on any area of the skin.

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25
what are the complications of cellulitis and erysipelas
BET LONG Bacteremia, Endocarditis, Toxic shock, Lymphedema, Osteomyelitis, Necrotizing soft‐tissue infections, Glomerulonephritis
26
what are some cellulitis mimickers and how to manage?
deep venous thrombosis, calciphylaxis, stasis dermatitis, hematoma, erythema migrans, cellulitis just give a short course of narrow spectrum gram + and see whether patient improves. if no, explore further causes.
27
what are the likely pathogens for impetigo (non bullous)?
staphylococci and streptococci usually beta hemolytic strep (A-C, G)
28
what are the likely pathogens for impetigo (bullous)?
toxin-producing strains of s.aureus
29
what are the likely pathogens for ecthyma?
usually grp A strep (strep pyrogenes)
30
what are the likely pathogens for non-purulent SSTI (cellulitis and erysipelas)?
mainly beta haemolytic strep (grp A-C,G), but usually grp A (strep pyrogenes) S.aureus possible but less frequent. Others (not common): aeromonas, vibrio vulnificus, and pseudomonas with (water exposure).
31
what are the likely pathogens for purulent SSTI (furuncles, carbuncles, skin abscess, purulent cellulitis)?
mainly s.aureus sometimes beta haem strep (A-C,G)
32
what are some pathogenic characteristics of skin abscesses involving the peri oral, perirectal, vulvovaginal areas?
common to see isolation of multiple organisms including gram (-) and anaerobes.
33
CA-MRSA epidemiology?
Not common in SG, common in the US.
34
CA-MRSA virulence profile?
Presence of - panton valentine leucocidin (PVL) - SCCmecIV or staphylococcal chromosomal casette.
35
What are some risk factors for CA-MRSA?
contact sports, military personnel, IV drug abusers, prison inmates overcrowded facilities, close contact and lack of sanitation.
36
What is the susceptibility of CA-MRSA? | what drug works against CAMRSA
oral non-beta lactams - clindamycin - cotrimox - doxycycline
37
what is the definition of HA-MRSA?
this is an mrsa infection that occurs >48h following hospitalisation OR outside of the hospital within 12 months of exposure to healthcare
38
how does HA-MRSA spread in the healthcare setting?
MRSA able to form biofilm on devices
39
What are the risk factors of HA-MRSA
abx use, recent hosp or surgery, prolonged hosp, intensive care, hemodialysis, proximity to others with MRSA colonisation or infectoin
40
what abx to use for the treatment of impetigo (mild, limited lesions)?
topical mupirocin BD x 5days
41
what is the efficacy of mupirocin to pathogens (gram positive cocci vs enterococci vs gram neg vs MRSA)
highly effective against gram postive cocci esp s.aureus useful for erradication of nasal staphyloccal carriage not effective vs enterococci and gram negs MRSA resistance a concern
42
(culture directed) (MSSA)) what abx to use for the treatment of impetigo and ecthyma (multiple lesions)?
PO cephexin or cloxacillin x 7days
43
(empiric tx) what abx to use for the treatment of impetigo and ecthyma (multiple lesions)? | include length of treatment
NO penicillin allergy: - PO Ceph or cloxacillin x 7days penicillin allergy: - PO clindamycin x 7days
44
(culture directed) (s pyrogenes) what abx to use for the treatment of impetigo and ecthyma (multiple lesions)? | include length of treatment
PO penicillin V or amoxicillin x 7days
45
what is the mainstay of treatment for purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
incision and drainage (I&D)
46
when do you use adjunctive systemic abx for purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
when - unable to drain completely - lack of response to I & D - extensive disease involving several sites - extremes of age - immune suppressed - signs of systemic illness (SIRS ≥2 pts)
47
What is the SIRS criteria for purulent SSTI
Temperature >38 or <36 HR >90 RR > 34 WBC > 12x10^9 or <4x10^9
48
what is the (empiric) general treatment for mild infection of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
I and D or warm compress
49
what is the (empiric) general treatment for moderate infection (w systemic symptoms) of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
I&D plus oral abx - PO cloxacillin, cephalexin OR - PO clindamycin (penicillin allergy)
50
what is the severity classification for purulent SSTIs?
mild = no systemic infection moderate - severe = systemic symptoms (classification with the SIRS scale, ≥2 points qualifies) and other risk factors (recall)
51
what is the (empiric) general treatment for severe infection of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?
I&D plus IV abx - IV cloxacillin or cefazolin or clindamycin or vancomycin
52
what is the (empiric) (MRSA) treatment of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)? IF GOT MRSA RISK FACTORS | include length of treatment
mild PO cotrimox, doxy, clindamycin x5-10 days mod-severe IV Vanco, dapto, linezolid reserve dapto and linezolid is VRE or allergy
53
what is the (empiric) (including gram neg anaerobic) treatment of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)? Recall AND state when you treat for gram neg and anaerobe (simple)
PO amoxiclav x5-10 days - recall that this is better for skin abscess near the perioral, perirectal, vulvovaginal...
54
(long hospital stay and high resistance risk) Recall AND state when you treat for gram neg and anaerobe SEVERE PURULENT SSTI
piptazo
55
what is the (empiric) (including gram neg anaerobic) treatment of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)? Recall AND state when you treat for gram neg and anaerobe (very sick, i.e., severe illness)
carbapenem to cover for ESBL, amp c producing
56
what is the (empiric) treatment of mild, non-purulent SSTIs (cellulitis, erysipelas)? i.e., no systemic signs of infection
ORAL abx penicillin V, cephalexin, cloxacillin x5-10days penicillin allergy clindamycin x5-10days
57
what is the (empiric) treatment of moderate, non-purulent SSTIs (cellulitis, erysipelas)? i.e., systemic signs with some purulence | consider additional....
IV abx cefazolin, cloxacillin x5-10days penicillin allergy clindamycin x5-10days add cipro if water exposure
58
when there is moderate non purulent SSTI with water exposure, what are the extra organisms to cover for and what abx to add on for empiric tx?
vibrio, aeromonas, pseudomonas x5-10days include ciprofloxacin
59
what is the (empiric) treatment of severe, non-purulent SSTIs (cellulitis, erysipelas)? include additional therapy for MRSA risk factor coverage | add reason for change in reigmen
IV antibiotics: piptazo, cefepime, merepenem x5-10days (increase to 14 immunocompromised) add vancomycin, daptomycin, linezolid if MRSA risk factor. | to broaden coverage and include risk for necrotizing infections
60
what are the signs/factors for severe non purulent sstis?
systemic signs of infection, failed oral therapy, immunocompromised.
61
what are the non-phx measrues for nonpurulent SSTI?
rest and limb elevation (drainage of edema and inflammatory substances) Treat underlying conditions eg tinea pedis, skin dryness, limb edema
62
what are the goal and monitoring parameters for ssti?
1) resolution of s/sx - improvement 48-72h - no progression of lesion or development of complication - switch to oral once better - if no response 2-3 days, reassess condition + choice of abx 2) no need for repeat bact culture. 3) no ADR.
63
define DFIs in words
soft tissue or bone infections below the malleolus usually involving bacterial colonization of ulcers and wounds
64
what are the complications of DFIs?
hospitalisation osteomyelitis eventual amputation
65
what is the pathophysiology of DFIs?
1) Neuropathy Peripheral: ↓ pain sensation and altered pain response * Motor:muscle imbalance * Autonomic: ↑ dryness, cracks and fissures 2) Vasculopathy * Early atherosclerosis * Peripheral vascular * disease * Worsened by hyperglycemia and hyperlipidemia 3) Immunopathy * Impaired immune response * ↑ susceptibility to infections * Worsened by * hyperglycemia
66
what is the criteria for DFI?
purulent discharge OR ≥2 s/sx of inflammation: erythema, warm, tenderness, pain, induration
67
what is the clinical presentation and progression of DFIs?
Superficial ulcer, mild erythema --> Deep tissue infection, extensive erythema --> Infection of bone and fascia, purulent discharge --> Localized gangrene
68
what is the evolution of DFIs?
erythema (day 1), blisters (day 3), a necrotizing abscess (day 6), and wound infection requiring surgery (day 10).
69
what are the causative organisms for DFIs? include gram positive, gram negative, and anaerobes
usually polymicrobial gram positive most common: S.aureus and strep spp gram negative: EKP Pseudomonas less common anaerobes: peptostreptococcous, veillonella, bacteriodes
70
when would there be presence of gram negs in DFIs?
chronic wounds/wounds treated with abx
71
when would there be presence of anaerobes in DFIs?
ischaemic or necrotic wounds
72
cultures for DFIs? when and how? consider the different classifications
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
73
what are pseudomonal risk factors for DFIs
frequent water exposure, warm climate
74
when to cover for psuedomonas in DFIs?
risk factors severe infection or mod infection with risk factors?
75
what is the classification for MODERATE DFI?
Infection of deeper tissue (e.g. bone, joints); or If erythema: > 2 cm around ulcer No signs of systemic infection
76
what is the classification for MILD DFI?
Infection of skin and SC tissue + If erythema: ≤ 2 cm around ulcer + No signs of systemic infection
77
what is the classification for SEVERE DFI?
Infection of deeper tissue (e.g. bone, joints); or If erythema: > 2 cm around ulcer + Sign(s) of systemic infection
78
what are the organisms to cover for MILD DFI?
Streptococcus spp + S. aureus
79
what are the organisms to cover for MODERATE DFI?
Streptococcus spp + S. aureus + gram‐negatives (±P. aeruginosa) + anaerobes
80
what are the organisms to cover for SEVERE DFI?
Streptococcus spp + S. aureus + gram‐negatives (include P.aeruginosa) + anaerobes
81
what is the empiric tx for MILD DFI?
PO Antibiotics * Cephalexin * Cloxacillin * Clindamycin If MRSA risk factor(s), use PO: * Co‐trimoxazole * Clindamycin * Doxycycline
82
what is the empiric tx for MODERATE DFI?
Initial IV Antibiotics * Amoxicillin/clavulanate * Cefazolin (more ideal because 1st and 2nd gen)/Ceftriaxone + Metronidazole IfMRSA risk factor(s), addIV: * Vancomycin * Daptomycin * Linezolid
83
what is the empiric tx for SEVERE DFI? (need to expand the spectrum)
Initial IV Antibiotics * Piperacillin‐tazobactam * Cefepime + metronidazole * Meropenem * Ciprofloxacin + clindamycin IfMRSA risk factor(s), addIV: * Vancomycin * Daptomycin * Linezolid
84
what are some adjunctive measures to DFI
1) wound care - debridement - offloading - dressing that promotes wound healing and exudate removal 2) optimal glycaemic control 3) foot care - daily inspections - prevent wounds and ulcers
85
how to diagnose and confirm infection for SSTI
based on history and physical examination generally mild and superficial infections do not require any culture take wound culture only if it fulfills any of the three criteria take blood culture only if systemic symptoms or patient is immunocompromised
86
how to differentiate the severity non-purulent SSTIs? ie mild moderate severe
mild: no systemic symptoms moderate: systemic symptoms and some purulence severe: systemic symptoms with PO treatment failure, immunocompromised/suppressed
87
what are the addional pathogens to cover for the different severities of non-purulent SSTIs?
moderate: include MSSA coverage. severe: broader coverage and explore possibility of necrotising infections
88
89
what are the 4 synergistic factors to pressure ulcers
friction shearing pressure moisture
90
what are the risk factors for pressure ulcers
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
91
what is the criteria for pressure ulcer infection
1) purulent discharge OR 2) ≥2 of the following: - erythema - tenderness - pain - induration - warmth
92
what is the clincal presentation of pressure ulcer (4 stages)
stage 1: - epidermis abrasion - irregular area of tissue swelling - no open wound stage 2: - dermis - open wound stage 3: - subQ - open sore or ulcer stage 4: - deeper tissue (joints, muscle, bone) - deep sore or ulcer
93
what are the pathogens for pressure ulcer
similar to DFI polymicrobial
94
how to culture for pressure ulcers
deep tissue culture or biopsy specimens avoid skin swabs
95
adjunctive measures for pressure ulcers?
1) debridement of necrotic/infected tissue 2) local wound care - normal saline preferred - avoid harsh chemicals 3) relief of pressure - turn/reposition every 2h
96
what is the dosing for daptomycin
4-6mg/kg q24
97
what is the dosing for linezolid
600mg q12
98
how to classify the severity of non-purulent SSTIs?
mild: no systemic symptoms moderate: systemic symptoms with some purulence of the wound severe: systemic symptoms with failed oral treatment or immunocompromised/suppressed.
99
what is the reason for changing the drug regimen for severe (nonpurulent) SSTI?
broaden the spectrum of activity + potentially cover for necrotising infections (typically anaerobic bacteria)

PR3151 (cleefy) (12 decks)

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