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infec y3s1 > IC14 Skin & soft tissue Infections > Flashcards

IC14 Skin & soft tissue Infections Flashcards

1
Q

Classification: Anatomical sites

A
  1. epidermis
  2. dermis
  3. hair follicle
  4. SC fat
  5. fascia
  6. muscle
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2
Q

epidermis infections

A

impetigo
* Superficial skin infection
* Presence of pustules/ vesicles that progress to crusting or bullae

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3
Q

Dermis infections

A

ecthyma
* Deeper variant of impetigo
* Begins as vesicles/ pustules → evolves to ulcers

Erysipelas
* Superficial infection of skin; involves lymphatics
* Tender, erythematous plaque with well-demarcated borders

Cutaneous abscess
Localised collection of pus within dermis & deeper skin tissues

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4
Q

hair follicle infections

A

Furuncles
* Infection of hair follicle
* Associated with small SC abscess

Folliculitis
Superficial infection of hair follicle + purulence in epidermis
Carbuncles
Cluster of furuncles

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5
Q

SC tissue infection

A

Cellulitis
Acute infection involving deep dermis & subcutaneous fat

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6
Q

fascia infections

A

Necrotising factors
Aggressive infection of SC tissue; spreads along fascial planes

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7
Q

Muscles infection

A

Myositis

Pyomyositis
Purulent infection of skeletal muscle; often with abscess formation
Gas gangrene (clostridial myonecrosis)
Necrotising infection involving muscle

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8
Q

3 main protective barrier of skin

A

physical
immunological
chemical

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9
Q

derivation of SSTIs

A

disruption of normal host defences
Allows overgrowth & invasion of skin and soft tissues by pathogenic microorganisms

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10
Q

risks factors

A
  1. disruption of physical barrier of skin
  2. conditions predisposed to infection
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11
Q

RF: disruption of physical barrier of skin
traumatic

A

Lacerations, recent surgery, abrasions, crush injuries, open fractures, burns
Injection drug use
Human, animal & insect bites
Non-traumatic

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12
Q

RF: disruption of physical barrier of skin
non-traumatic

A

Ulcers, tinea pedis, dermatitis, toe-web intertrigo
Chemical irritants

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13
Q

RF: disruption of physical barrier of skin
impaired venous / lymphatic drainage

A

impaired BF
Saphenous venectomy, Obesity, Chronic venous insufficiency, peripheral artery disease

Impaired lymphatic drainage
Immune cells cannot reach site of infection quickly
Causes overgrowth of organism ⇒ invasion of tissues

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14
Q

RF: conditions predisposed to infection

A
  • suppression of immune system

DM, cirrhosis, neutropenia, HIV, transplantation & immunosuppressive medications
Hx of cellulitis

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15
Q

clinical presentation
impetigo

progression, location, appearance

A

Begins as erythematous papules
Rapidly evolve into lesions → vesicles (clear fluid) & pustules (pus) ⇒ rupture
Dried discharge forms honey-coloured crusts on erythematous base

Usually on exposed areas of body: face & extremities

Lesions well localised, frequently many bullous/ non-bullous appearance

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16
Q

clinical presentation furuncles

location of purulent material

A

Infection of hair follicle
Purulent material extends through dermis, into SC tissue ⇒ formation of abscess

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17
Q

clinical presentation of carbuncles

location

A

Furuncle coalesce & extend into SC tissues

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18
Q

clinical presentation
ecthyma

location, itch

A

Ulcerative form of impetigo
Lesions extend through epidermis & deep into dermis
Pruritus common; scratching may further spread infection

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19
Q

clinical presentation of cutaneous abscess

location, symptoms

A

Collection of pus within dermis & deeper skin tissue
May be painful, tender, fluctuant & erythematous nodules

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20
Q

clinical presentation of cellulitis

location, description of skin, onset, fever

A

Deeper & SC fats
Presents as acute, diffuse, spreading, non-elevated, poorly demarcated area of erythema
Relatively rapid onset/ progression
Mostly unilateral
Fever in 20-70% of patients
Normally on lower extremities

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21
Q

clinical presentation of erysipielas

location, description of skin

A

Affect upper dermis
Fiery red, tender, painful plaque (raised above surrounding skin) with well demarcated edges
Common on face & lower extremities

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22
Q

Culture to confirm infection

types, required individuals & how to obtain

A

Required for pus, exudates or tissues from wounds:
* Where sample should be collected
Deep in wound after cleaning surface
Base of closed abscess → where bacteria grow
By curettage → debriding top part, then remove tissue
* Problems (avoid taking sample from)
Open, draining wounds → often contaminated with potentially pathogenic organisms
Avoid wound swabs → difficult to obtain representative sample

Blood culture
For severe cases with marked systemic symptoms of infection
For immunocompromised patients

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23
Q

complications of SSTIs

A

Bacteremia
* can stick to heart valves (endocarditis), spine (osteomyelitis)
* Release of toxins (toxic shock → common in immunocompromised patients)

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24
Q

likely pathogen: impetigo

A

Staphylococci OR streptococci
Bullous form → toxin-producing strains of S.aureus

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25
Q

likely pathogen: ecthyma

A

Group A streptococci

26
Q

likely pathogen: nonpurulent

Cellulitis, Erysipelas

A

B-hemolytic streptococcus (main)
Group A streptococci (Strep. Pyogenes)

Less common pathogens
S.aureus, Aeromonas, Vibrio Vulnificus
Pseudomonas with water exposure (or near to GI)

27
Q

likely pathogen: purulent

Furuncles, Carbuncles, Skin abscess, Purulent cellulitis

A

S.aureus (main)
B-hemolytic streptococcus (some)

28
Q

community acquired MRSA

RF, possible treatment

A

Possible treatments: PO non-beta lactam
Clindamycin, co-trimoxazole, doxycycline

Risk factors:
* participants of contact sports, military personnel, IV drug abusers (IVDA), prison inmates
* overcrowded facilities, close contact & lack of sanitation ⇒ contributes to spread

29
Q

hospital acquired MRSA

requirements/ classifications, RF

A

Requirements/ classifications
* >48 hours following hospitalisation
* Outside hospital within 12 months exposure to healthcare

Risk factors:
* AB use, recent hospitalisation/ surgery, prolonged hospitalisation, intensive care
* MRSA colonisation, close proximity to others with MRSA colonisation/ infection

30
Q

impetigo management
(mild, limited lesions)

A

Topical Mupirocin BD x 5 days
Effective against aerobic G+ (esp S.aureus)

31
Q

impetigo (multiple lesions) & ecthyma managment

duration of treatment, empiric & culture therapy

A

Duration of treatment: 7 days

Empiric
PO cephalexin or cloxacillin ⇒ can assume susceptible
PO clindamycin → for penicillin allergy

Culture-directed (definitive)
S.pyogenes: PO penicillin V, amoxicillin
MSSA: PO cephalexin or cloxacillin

32
Q

nonpurulent management: mild

classification & symptoms; therapy

A

(w/o systemic signs of infection)
Mainly cover Strep pyogenes
* PO penicillin V, cephalexin, cloxacillin
If have bacteremia, use IV penicillin G
No coverage for MSSA
* PO clindamycin → for penicillin allergy

33
Q

nonpurulent management
duration of treatment

A

5-10 days, 14 days for immunocompromised

34
Q

nonpurulent management: moderate

classification & symptoms; therapy

A

(w systemic signs of infection; some purulence)
Cover Strep pyogenes & MSSA
* IV cefazolin, cloxacillin
* IV Clindamycin → for penicillin allergy

35
Q

nonpurulent management: severe

classification & symptoms; therapy

A

(w systemic signs of infection, failed PO therapy/ immunocompromised)
Broader coverage: G+, G-, anaerobes + necrotising infections
* IV piperacillin-tazobactam, cefepime, meropenem
* MRSA RF → add IV vancomycin, daptomycin, linezolid

36
Q

nonpurulent management: Risk factors

A

Ensure rest & limb elevation
Drainage of edema & inflammatory substances
Treat underlying conditions

37
Q

purulent management: main therapy

A

Insertion & drainage

38
Q

purulent management:
when to consider systemic AB

A
  • Unable to drain completely; Lack of response to I&D
  • Extensive disease involving several sites; severe disease
  • Extremes of age
  • Immunosuppressed (ie: chemotherapy, transplant)
  • Signs of systemic illness
  • SIRS criteria: (any 2/4 met = systemic)
    Temperature > 38degC or < 36degC;
    HR > 90 bpm
    RR > 24 bpm
    WBC > 12 x 10^9/L or < 4 x 10^9/L
39
Q

purlent management: empiric

duration of treatment, MRSA, G-, Long hospitalisation, ICU

A

5-10 days

Empiric (MRSA): G+ & MRSA
Cotrimoxazole, doxycycline, clindamycin
Vancomycin
Daptomycin, linezolid → for vancomycin-resistant bacteria OR if have nephrotoxicity to vancomycin

Empiric (G-, anaerobe): G+ & G-
Usually near anal area, gut, rectal area
Amoxicillin-clavulanate

Resistant risks & long hospital stay: Piperacillin-tazobactam
ICU & septic shock: Carbapenem (To cover for ESBLs)

40
Q

purulent management: culture directed

mild, moderate, severe

A

Mild infection
I&D or warm compress to promote drainage

Moderate (with systemic symptoms)
I&D AND
PO cloxacillin or cephalexin
PO clindamycin → for penicillin allergy

Severe
I&D AND
IV cloxacillin or cefazolin
IV Clindamycin → for penicillin allergy
IV Vancomycin ⇒ if have allergy + Covers MRSA

41
Q

DFI: background

areas of DFI, complications

A

Soft tissue/ bone infections below malleolus
Areas of DFI
Skin ulceration → peripheral neuropathy
Wound → trauma
Complications
Hospitalisation
Osteomyelitis ⇒ deep infection requiring amputation

42
Q

DFI: diagnosis

Criteria for infection

A

Bacterial colonisation of ulcers/ wounds
Criteria for infection
* Purulent discharge
* ≥ 2 signs or symptoms of inflammation:
Erythema, warmth, tenderness, pain, induration

43
Q

DFI: Pathophysiology & outcomes

A

(1) neuropathy (2) vasculopathy (3) immunopathy
formation of ulcers & wounds
bacteria colonisation, penetration & proliferation
leads to DFI

44
Q

DFI: Pathophysiology
neuropathy

A

Peripheral: reduced pain sensation & altered pain response
Motor: muscle imbalance
Autonomic: increased dryness, cracks & fissures

45
Q

DFI: Pathophysiology
immunopathy

A

Impaired immune response
Increased susceptibility to infections
Worsened by hyperglycemia

46
Q

DFI: Pathophysiology
vasculopathy

A

Early atherosclerosis
Peripheral vascular disease
Worsened by hyperglycemia & hyperlipidemia

47
Q

DFI clinical presentation

A
  • Superficial ulcer, mild erythema
  • Deep tissue infection, extensive erythema
  • Infection of bone & fascia; purulent discharge
  • Localised gangrene
48
Q

DFI & pressure wounds causative organisms

A

Common: Staphylococcus aureus & Streptococcus
Gram negative bacilli→ E.coli, Klebsiella, Proteus
* In chronic wounds/ previously treated with AB
* Less common for P.aeruginosa

Anaerobes → Peptostreptococcus spp., Veillonella spp., Bacteroides spp.
* In ischemic/ necrotic wounds (very deep)

49
Q

DFI culture requirements

A

Moderate-severe DFIs
Deep tissue culture after cleansing & before starting AB
* In order to opt for narrow spectrum

50
Q

treatment of DFI & pressure wounds
classification

A
  1. Infection of skin & SC tissue
    If erythema ≤ 2 cm around ulcer
    No signs of systemic infection
  2. Infection of deeper tissue (ie bone, joints) OR
    If erythema > 2 cm around ulcer
    No signs of systemic infection
  3. Infection of deeper tissue OR
    If erythema > 2 cm around ulcer
    Signs of systemic infection
51
Q

treatment of DFI & pressure wounds
organisms to cover

A
  1. Streptococcus spp & S. aureus
  2. Streptococcus spp, S. aureus, Gram negs (± P.aeruginosa), Anaerobes
  3. Streptococcus spp, S. aureus, Gram negs (P.aeruginosa), Anaerobes
52
Q

treatment of DFI & pressure wounds
therapy (No MRSA concern)

mild, mod, severe

A
  1. PO
    Cephalexin
    Cloxacillin
    Clindamycin (Penicillin resistance)
  2. Initial IV
    Amox/ clav
    Cefazolin/ ceftriaxone + metronidazole
  3. Initial IV
    Pip-tazo
    Cefepime + metronidazole
    Meropenem
    Ciprofloxacin + clindamycin
53
Q

treatment of DFI & pressure wounds
therapy (MRSA concern)

mild vs mod & severe

A

Mild (PO)
Co-trimoxaxzole
Clindamycin
Doxycycline

moderate & severe (IV)
Vancomycin
Daptomycin
Linezolid

54
Q

treatment of DFI & pressure wounds
duration of therapy

bone involved (surgery Vs no surgery)

A

Surgery
Amputation (removal of all infected bone & tissues)
⇒ 2-5 days
Residual infected soft tissue ⇒ 1-3 weeks
Residual viable bone ⇒ 4-6 weeks

no surgery
Residual dead bone ⇒ ≥ 3 months

55
Q

treatment of DFI & pressure wounds
duration of treatment

normal

A
  1. 1-2 weeks
  2. 1-3 weeks
  3. 2-4 weeks
56
Q

treatment of DFI adjunctive therapy

A

Wound care
Debridement
Off loading → avoid weight on infected foot
Apply dressings that promote healing environment & control excess exudation

Foot care
Daily inspection
Prevent wounds & ulcers

Optimal glycemic control

57
Q

factors causing pressure wound

SPFM

A

Moisture, pressure (amount & duration), shearing force, friction

58
Q

Adjunctive measures for pressure ulcers

A

Debridement of infected/ necrotic tissue
Local wound care
Use of normal saline
Avoid harsh chemicals
Relief of pressure
turn/ reposition every 2 hours
Use air/ water bed

59
Q

clinical presentation of pressure wounds (4 stages)

A
  1. Abrasion of epidermis
    Irregular area of tissue swelling
    No open wound
  2. Extension through dermis
    Open wound
  3. Extend deep into SC fat
    Open sore/ ulcer
  4. Involves muscle & bone
    Deep sore/ ulcer
60
Q

risk factors of pressure wounds

MMACCS

A

Reduced mobility (ie: spinal cord injuries, paraplegic)
* Reduced blood circulation at area of pressure ⇒ breakage of skin

Severe chronic diseases (ie: multiple sclerosis, stroke, cancer)
Reduced consciousness
Sensory & autonomic impairment → incontinence
Extremes of age
Malnutrition

infec y3s1 (7 decks)

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