Skin and Soft Tissue Infections Flashcards

1
Q

What must you consider in skin/soft tissue infections?

A

Site

Organism

Host

Environment

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2
Q

What host factors can affect skin infections?

A

DM

Immunosuppression

Renal failure

Milroy’s disease

Predisposing skin conditions

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3
Q

What is Milroy’s disease?

A

Congenital lymphoedema of the legs

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4
Q

What are the layers of skin?

A

Epidermis

Dermis

Hair Follicle

Subcutaneous fat

Fascia

Muscle

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5
Q

Which infections affect the epidermis?

A

Impetigo

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6
Q

Which infections affect the dermis?

A

Folliculitis

Eryspipelas

Cellulitis

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7
Q

Which infections affect the Subcutaneous fat?

A

Cellulitis

Erysipelas

Necrotising Fasciitis

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8
Q

How does impetigo present?

A

Superficial skin infection

Multiple vesicular lesions on a red base

Golden crust

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9
Q

What are the most common pathogens in impetigo?

A

Staph aureus

Strep pyogenes

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10
Q

What is this?

A

Impetigo

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11
Q

What is the epidemiology of Impetigo?

A

Children 2-5y/o

Highly infectious

Exposed parts of the body

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12
Q

How is impetigo treated?

A

Small areas = Topical antibiotics

Large areas = oral flucloxacillin

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13
Q

What is Erysipelas?

A

Painful infection of upper dermis

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14
Q

How does Erysipelas present?

A

Painful red area with no central clearing

Fever

Regional lymphadenopathy

Lymphangitis

Distinct, elevated borders

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15
Q

What is the most common causative pathogen of Erysipelas?

A

strep pyogenes

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16
Q

What is this?

A

Erysipelas

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17
Q

Erysipelas typically affects which parts of the body?

A

70-80% lower limbs

5-20% face

Areas of pre-existing lymphoedema, venous stasis, obesity, paraparesis, DM

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18
Q

What is the recurrence rate of Erysipelas?

A

30% in 3 years

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19
Q

What is Cellulitis?

A

•Diffuse skin infection involving deep dermis and subcutaneous fat

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20
Q

How does Cellulitis present?

A

Spreading erythematous area with no distinct borders

Fever

Regional lymphadenopathy/lymphangitis

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21
Q

What are the most common causative pathogens in Cellulitis?

A

Strep pyogenes

Staph aureus

Gram -ves (diabetics, febrile neutropaenics)

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22
Q

Cellulitis can cause what?

A

Bacteraemia

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23
Q

What is this?

A

Cellulitis

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24
Q

How is Cellulitis investigated?

A

Investigate for predisposing factors:

  • DM
  • Tinea pedis
  • Lymphoedema
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25
How is cellulitis and erysipelas managed?
Anti-staphylococcal and anti-streptococcal antibiotics Potentially admission and IV antiB for severe disease
26
What are the most common hair-associated infections?
* Folliculitis * Furunculosis * Carbuncles
27
What is folliculitis?
Circumscribed, pustular infection of a hair follicle
28
How does Folliculitis present?
* Up to 5mm in diameter * Present as small red papules * Central area of purulence that may rupture and drain Typically on Head, back, buttocks and extremities
29
What is the most common causative pathogen of Folliculitis?
Staph aureus
30
What is Furunculosis?
Boils - single hair follicle associated inflammatory nodule Extension into dermis and subcutaneous tissue
31
Furunculosis typically affects which parts of the body?
Moist, hairy, friction prone areas
32
What is this?
Furunculosis
33
What is the most common causative pathogen of Furunculosis?
Staph aureus
34
What are the risk factors for Furunculosis?
–Obesity –Diabetes mellitus –Atopic dermatitis –Chronic kidney disease –Corticosteroid use
35
What is a Carbuncle?
Infection spreading to involve multiple furuncles Multi-septated abscesses Purulent material expressed from multiple sites
36
How does a Carbuncle present?
Back of neck, posterior trunk, thigh Constitutional symptoms
37
What is this?
Carbuncle
38
How is furunculosis treated?
Oral antibiotics if not improving by itself
39
How are Carbuncles treated?
Surgery Intravenous antibiotics
40
What are the predisposing conditions of Necrotising fasciitis?
–Diabetes mellitus –Surgery –Trauma –Peripheral vascular disease –Skin popping -- IVDA
41
What are the main types of Necrotising fasciitis?
Type 1 - mixed aerobic/anaerobic Type 2 - monomicrobial
42
What organisms are involved with type 1 Necrotising fasciitis?
–Streptococci –Staphylococci –Enterococci –Gram negative bacilli –Clostridium
43
What organisms are involved with type 2 Necrotising fasciitis?
Strep pyogenes
44
What is this?
Type 2 necrotising fasciitis
45
How does type 2 necrotising fasciitis present?
Cellulitis with extreme pain - opiates Haemorrhagic bullae
46
What is implied by a haemorrhagic bullae?
Necrotising fasciitis or Cellulitis with ANTICOAGULANTS
47
How does Necrotising fasciitis present?
Rapid onset Sequential erythema, oedema, severe pain Haemorrhagic bullae Skin necrosis Fever, hypotension, tachycardia, multiorgan failure
48
How is Necrotising fasciitis assessed?
Surgical review - see if NF has penetrated the fascia
49
How is Necrotising fasciitis treated?
Broad spec. antibiotics –Flucloxacillin –Gentamicin –Clindamycin
50
What mortality is associated with Necrotising fasciitis?
17-40%
51
What is pyomyositis?
Purulent deep infection in striated muscle - abscess Multiple sites
52
What sites are commonly effected by Pyomyositis?
–Thigh –Calf –Arms –Gluteal region –Chest wall –Psoas muscle
53
How does Pyomyositis present?
Fever, pain, induration of affected muscle
54
What complications are associated with untreated Pyomyositis?
Septic shock Death
55
What predisposing factors are associated with Pyomyositis?
–Diabetes mellitus –HIV/immunocompromised –Intravenous drug use –Rheumatological diseases –Malignancy –Liver cirrhosis
56
What is the most common pathogen in Pyomyositis?
Staph aureus Gram+ve/-ves TB Fungi
57
How is Pyomyositis investigated?
CT/MRI
58
How is Pyomyositis managed?
Drainage Antibiotics (depending on stain)
59
What are Bursae?
Small sac-like cavities that contain fluid in synovial membrane Reduce friction in joints
60
What are the most common sites of septic bursitis?
Patellar Olecranon
61
What is the cause of Septic bursitis?
Infection from adjacent skin site
62
What are the predisposing factors for Septic bursitis?
–Rheumatoid arthritis –Alcoholism –Diabetes mellitus –Intravenous drug abuse –Immunosuppression –Renal insufficiency
63
How does Septic bursitis present?
Peribursal cellulitis Swelling Warmth Fever Pain on movement
64
How is Septic bursitis diagnosed?
Aspiration of fluid
65
What are the most common organisms in Septic bursitis?
**Staph aureus** Gram -ves Myocbacterium Brucella
66
What is Infectious tenosynovitis?
Infection of synovial sheaths surrounding tendons
67
Which tendons are most commonly associated with Infectious tenosynovitis?
Flexor muscle associated tendons Tendon sheaths around hand
68
What is the most common cause of Infectious tenosynovitis?
Penetrating trauma
69
Which pathogens are most commonly responsible for Infectious tenosynovitis?
**Staph aureus** **Streptcocci**
70
What are the most common causes of chronic Infectious tenosynovitis?
Mycobacteria Fungi Disseminated gonoccal infection
71
How does Infectious tenosynovitis present?
Erythematous fusiform swelling of finger Semiflexed position Tenderness overlength of tendon sheath Pain with extension
72
How is Infectious tenosynovitis treated?
Antibiotics Hand surgeon review
73
What are the most common causes of toxin-mediated syndromes?
Superantigens (pyrogenic exotoxins)
74
How do superantigens work?
Bypass APC and attach directly to T-cell receptors Massive burst in cytokine release Endothelial leakage, haemodynamic shock, multiorgan failure
75
Which strains of Staphyloccus aureus are responsible for Toxin-mediated syndromes?
TSST1 ETA ETB
76
Which strains of Streptococcus pyogenes are responsible for Toxin-mediated syndromes?
TSST1
77
What is the diagnostic criteria for Staphylococcal toxic shock syndrome?
Fever Hypotension * Fever * Hypotension * Diffuse macular rash * Three of the following organs involved (Liver, blood, renal, gatrointestinal, CNS, muscular) * Isolation of Staph aureus from mucosal or normally sterile sites * Production of TSST1 by isolate * Development of antibody to toxin during convalescence
78
What is streptococcal toxic shock syndrome associated with?
Deep seated infections: Erysipelas Necrotising fasciitis
79
What is the rate of mortality for Streptococcal TSS compared to Staphylococcal TSS?
Strep: 50% Staph: 5%
80
How are toxic shock syndromes treated?
Surgical debridement of infected tissues IV fluids Inotropes Antibiotics IV immunoglobulins
81
What is Staphylococcal scalded skin syndrome?
Infection due to Staph aureus strains producing exfoliative toxin A or B
82
How does Staphylococcal scalded skin syndrome present?
Widespread bullae Skin exfoliation Children
83
How is Staphylococcal scalded skin syndrome managed?
IV fluids Antimicrobials
84
What mortality is associated with Staphylococcal scalded skin syndrome?
3% children Higher in adults
85
What is Panton-Valentine leucocidin toxin?
Gamma haemolysin Transfers from one strain of Staph aureus to another
86
Panton-Valentine leucocidin toxin can cause what?
SSTI Haemorrhagic pneumonia
87
Panton-Valentine leucocidin toxin affects which patients?
Children/young adults
88
How does Panton-Valentine leucocidin toxin present?
Recurrent, difficult to treat boils
89
How is Panton-Valentine leucocidin toxin treated?
Antibiotics that reduce toxin production
90
How do Intravenous-catheter associated infections present?
Starts with SST inflammation, progresses to cellulitis then tissue necrosis Associated bacteraemia
91
What are the risk factors for Intravenous-catheter associated infections?
–Continuous infusion \>24 hours –Cannula in situ \>72 hours –Cannula in lower limb –Patients with neurological/neurosurgical problems
92
What organisms are associated with Intravenous-catheter associated infections?
Staph aureus (MSSA/MRSA)
93
How does the pathogen act in Intravenous-catheter associated infections?
Staph aureus forms a biofilm - spills into blood stream Can seed to other places
94
How is Intravenous-catheter associated infections diagnosed?
Blood cultures
95
How are Intravenous-catheter associated infections treated?
Remove cannula Express andy pus 14 days antibiotics Echocardiogram (**Prevention**)
96
How are Intravenous-catheter associated infections prevented?
–Do not leave unused cannula –Do not insert cannulae unless you are using them –Change cannulae every 72 hours –Monitor for thrombophlebitis –Use aseptic technique when inserting cannulae
97
What are the classes of surgical wounds?
Class 1-4 1. Clean wound 2. Clean-contaminated wound 3. Contaminated wound 4. Infected wound
98
What is a class 1 surgical wound?
Clean wound - resp/alimentary/genital/urinary system not entered
99
What is a class 2 surgical wound?
Clean-contaminated wound: respiratory, alimentary, genital or infected urinary systems entered but not contaminated
100
What is a class 3 surgical wound?
Contaminated wound - Open, fresh accidental wound or gross spillage from GIT
101
What is a class 4 surgical wound?
Infected wound - infection present before operation
102
Name 3 bacterial causes of surgical site infections?
* **Staph aureus** * Coagulase negative Staphylococci * Enterococcus * Escherichia coli * Pseudomonas aeruginosa * Enterobacter * Streptococci * Fungi * Anaerobes
103
What are the patient associated risk factors for surgical site infections?
–Diabetes –Smoking –Obesity –Malnutrition –Concurrent steroid use –Colonisation with Staph aureus
104
What are the procedural factor associated risk factors for surgical site infections?
–Shaving of site the night prior to procedure –Improper preoperative skin preparation –Improper antimicrobial prophylaxis –Break in sterile technique –Inadequate theatre ventilation –Perioperative hypoxia
105
How are surgical site infections diagnosed?
Send pus/infected tissue for culture - esp. when wound clean Avoid superficial swabs (go deep fam) Consider unlikely pathogen if sterile site Antibiotics