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Thera VII > 23 Skin and Soft Tissue Infections Minejima > Flashcards

23 Skin and Soft Tissue Infections Minejima Flashcards

1
Q

What is Impetigo?

A

Highly contagious infection of epidermis. Typically transmitted through direct contact. Occurs in children ages 2-5 years old. Spontaneous resolution without scarring usually occurs within several weeks if left untreated

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2
Q

What are the two types of Impetigo?

A

Nonbullous (~70% of cases). Bullous

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3
Q

What is Nonbullous Impetigo?

A

Single red macule/papule that rapidly develops into a vesicle that ruptures easily to form an erosion and contents dry to form characteristic gold-colored crusts that may be pruritic

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4
Q

What is Bullous Impetigo?

A

Superficial vesicles develop to form rapidly enlarging, flaccid bullae with sharp margins and no surrounding erythema. Usually affects neonates

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5
Q

What often causes Bullous Impetigo?

A

Caused by toxin-producing S. aureus. Localized form of staphylococcal scalded skin syndrome

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6
Q

What are the predisposing factors of Impetigo?

A

Group A Strep skin colonization (10 days before appearance of impetigo) or S. aureus nasal colonization. Hot, humid summer weather. Areas with poor hygiene and in crowded living conditions. Minor trauma (insect bite, abrasion)

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7
Q

What are the causative organisms of Impetigo?

A

Staphylococcus aureus. Group A Strep/Streptococcus pyogenes

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8
Q

What does the treatment of Impetigo depend on?

A

Number of lesions, their location (face, eyelid, mouth) and the need to limit spread of infection to others

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9
Q

What are the treatment options for Impetigo?

A

Topical therapy (Mupirocin apply to lesions TID). If numerous lesions or not responding to Mupirocin: PO antibiotics active against both S. pyogenes and Staph aureus

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10
Q

What are the PO antibiotics active against both S. pyogenes and Staph aureus often used for Impetigo?

A

Dicloxacillin 250mg po QID. Cephalexin 250mg po QID, Augmentin 875/125mg po BID. B-lactam allergy: Erythromycin 250mg po QID, Clindamycin 300-400mg po TID

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11
Q

What is Folliculitis?

A

Pyoderma located within hair follicles and apocrine regions. Small (2-5mm), erythematous (sometimes pruritic papules) usually covered by central pustule

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12
Q

What are the causative organisms of Folliculitis?

A

S. aureus (most common), P. aeruginosa (swimming pools, hot tubs, whirlpools), Candida spp (prolonged antibiotics or corticosteroids)

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13
Q

What is the treatment for Folliculitis?

A

Saline compresses (promotes drainage), topical therapy with antibacterials or antifungals sufficient

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14
Q

What are Furuncles (Boils)?

A

Deep inflammatory nodule that typically develops from preceding folliculitis. Occurs in skin areas subject to friction, perspiration, and contain hair follicles (neck, face, axillae, buttocks)

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15
Q

What is the treatment for Furuncles?

A

Application of moist heat to promote drainage

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16
Q

What are Carbuncles?

A

When infection extends to involve several adjacent follicles producing a coalescing inflammatory mass with pus draining from multiple follicular orifices. Typically found at nape of neck, back, or on thighs. Fever and malaise usually present

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17
Q

What are the predisposing factors for Furuncles and Carbuncles?

A

Diabetes, obesity. Inadequate personal hygiene. Close contact with others with furuncles. Anterior nares colonization with S. aureus (recurrent cases)

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18
Q

What is the causative organism of Furuncles and Carbuncles?

A

S. aureus

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19
Q

What is the treatment for Furuncles and Carbuncles?

A

Incision and drainage (I&D). Systemic antibiotics rarely required unless extensive surrounding cellulitis or fever occurs

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20
Q

What is Cellulitis?

A

Acute, spreading infection of skin that involves subcutaneous tissues. Edema, redness, heat +/- lymphagitis and inflammation of regional lymph nodes. Vesicles, bullae, and cutaneous hemorrhage in form of petechiae or ecchymoses may develop on inflamed skin

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21
Q

What are the systemic manifestations of Cellulitis?

A

Fever, tachycardia, confusion, hypotension, leukocytosis

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22
Q

What are the predisposing factors for Cellulitis?

A

Previous trauma (laceration, puncture wound). Conditions that cause skin to be more fragile or local host defenses less effective (obesity, previous cutaneous damage, edema (from venous insufficiency or lymphatic obstruction), surgical procedures (saphenous venectomy, axillary node dissection for breast cancer, gynecologic malignancy operations))

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23
Q

What is the location of Cellulitis?

A

Commonly on lower legs

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24
Q

What is Cellulitis diagnosis like?

A

No routine diagnostic test. Given the low yield, tests are not useful unless patients with diabetes, malignancy, unusual predisposing factors such as immersion injury, animal bites, neutropenia, immunodeficiency

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25
Q

What is a common cause of Perifolliculitis capitis?

A

S. aureus

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26
Q

What is a common cause of Facial (cheek) Cellulitis?

A

Buccal cellulitis: H. influenzae

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27
Q

What is a common cause of Cellulitis of the hands?

A

Erysipeloid: Erysipelothrix rhusiopathiae

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28
Q

What is a common cause of Cellulitis of the extremities?

A

Diabetic foot. Erysipelas (cellulitis of upper dermis)

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29
Q

What is a common cause of Perianeum Cellulitis?

A

Perianal Streptococcal cellulitis: Group A Strep

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30
Q

What is the most common causative organism of Cellulitis?

A

Group A Strep

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31
Q

What do you need to think about when deciding to treat Cellulitis?

A

Diffused cellulitis not associated with a defined portal usually involves Streptococcus sp. Cellulitis associated with furuncles, carbuncles or abscesses usually involves Staph aureus

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32
Q

Who often gets Cellulitis caused by CA-MRSA?

A

Recurrent or persistent furuncles in at risk groups: jail inmates, IVDUs, contact sports teams, Native Americans, gay men, children

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33
Q

What is the treatment for Cellulitis caused by Strep & S. aureus (penicillinase-producing)?

A

B-lactam antibiotics (PO: dicloxacillin or cephalexin. IV: Oxacillin or cefazolin). If B-lactam allergic: Clindamycin, erythromycin (Strep resistance high in erythromycin)

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34
Q

What is the PO treatment for Cellulitis caused by CA-MRSA?

A

PO: TMP/SMX, doxycycline, clindamycin

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35
Q

What is the IV treatment for Cellulitis caused by CA-MRSA?

A

IV: Vancomycin, Linezolid, Daptomycin, Tigecycline, Telavancin, Ceftaroline

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36
Q

When is the IV route preferred for Cellulitis?

A

If lesion rapidly spreading. If systemic response prominent. Significant comorbidities (asplenia, neutropenia, immunocompromised, cirrhosis, cardiac or renal failure, or preexisting edema)

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37
Q

What is the Duration of treatment for Cellulitis?

A

5-14 days. Dependent on severity and response to therapy

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38
Q

What is the Non-Medication therapy for Cellulitis?

A

Elevation of affected area

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39
Q

What are the measures to decrease Cellulitis recurrences?

A

Treating interdigital maceration. Emollient use to avoid dryness/cracking. Reduce underlying edema (elevation of extremity, compressive stockings, pneumatic pressure pumps, diuretic therapy). Prophylactic antibiotic therapy if all other measures are unsuccessful

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40
Q

What are the prophylactic antibiotic medications for Cellulitis?

A

Penicillin V 1g PO BID or 1.2 MU IM Qmonth or Erythromycin 250mg PO BID

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41
Q

What is the definition of recurrent MRSA SSTI?

A

2 or more discrete SSTI episodes at different sites over 6 month period

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42
Q

What is the MRSA SSTI-Treatment?

A

Decolonization for recurrent SSTI despite optimizing wound care and hygiene measures. Mupirocin 2% nasal decolonization BID x 5-10 days. Topical body decolonization (i.e. chlorhexidine, bleach bath: 1 tsp per gallon of water) x 5-14 days. Oral abx for decolonization NOT routinely recommended

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43
Q

What is some general information about Bite Wounds?

A

Most bites are due to dogs or cats. Cat bite wounds are usually more severe and have higher proportion of osteomyelitis and septic arthritis. Human bite wounds are typically more serious than animal bites. Anaerobes present > 60% of cases

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44
Q

What are the predominant pathogens in bite wounds?

A

Normal oral flora of biting organism. Human skin organisms. Secondary invaders (ex. S. aureus and S. pyogenes)

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45
Q

What are the complications caused by bite wounds?

A

Septic arthritis, osteomyelitis, subcutaneous abscess formation, tendonitis, bacteremia (rarely)

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46
Q

What is the bacteriology of Dog/Cat bite wounds?

A

Pasteurella (50% dog bites, 75% cat bites). Staph, Strep. Capnocytophaga canimorsus (causes bacteremia and fatal sepsis especially in asplenia or underlying hepatic disease patients), etc.

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47
Q

What is the bacteriology of Human bite wounds?

A

Strep (esp. viridans). Staph. Haemophilus. Eikenella corrodens. Fusobacterium (esp: F. nucleatum), etc

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48
Q

What are the treatment options for Bite Wounds?

A

Beta-Lactamase Inhibitor agents (Augmentin (PO), Unasyn (IV), Pip/Tazo (Zosyn) (IV)). Alternatives (B-Lactam Allergic): Doxycycline, Cefuroxime + Metronidazole, FQ + Metronidazole, Bactrim + Metronidazole. Treatment duration: 5-10 days

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49
Q

What should be avoided in the treatment of Bite Wounds?

A

1st generation CEPHs and Penicillinase-Resistant PCNs, Macrolides, Clindamycin d/t poor in vitro activity against P. multocida

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50
Q

What are some vaccines that can be used for Bite Wounds?

A

Tetanus. Rabies (for all feral, wild animal bites, areas with high prevalence of rabies)

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51
Q

What are Necrotizing Skin and Soft Tissue Infections?

A

Deeper and more devastating than milder, superficial infections. May involve fascial and/or muscle compartments. May cause major destruction of tissue and lead to mortality. Typically secondary infections that develop from an initial break in skin (trauma, surgery). Life threatening emergency

52
Q

What are the clinical features of Necrotizing Skin and Soft Tissue Infections?

A

Severe, constant pain. Bullae. Skin necrosis or ecchymosis (bruising). Gas in soft tissues. Edema. Cutaneous anesthesia. Systemic toxicity (fever, leukocytosis, delirium, renal failure). Rapid spread

53
Q

What are the two types of Infectious Gangrene?

A

Clostridial Gas Gangrene (Trauma-associated, Spontaneous gangrene) & Fournier Gangrene

54
Q

What is Trauma-Associated Clostridial Gas Gangrene?

A

C. perfringens most frequent cause. Skin initially pale –> bronze –> purplish red. Signs of systemic toxicity: tachycardia, fever, diaphoresis –> shock and multiple organ failure

55
Q

What is Spontaneous Clostridial Gas Gangrene?

A

C. septicum most frequent cause. Neutropenic and GI malignancy patients

56
Q

What do both forms of Clostridial Gas Gangrene require?

A

ICU care, supportive measures, aggressive surgical debridement, and appropriate antibiotics

57
Q

What is the antibiotic therapy for Clostridial Gas Gangrene?

A

PCN + Clindamycin (clincamycin for toxin-inhibitory effect). 5% of C. perfringens strains are clindamycin resistant

58
Q

What is Fournier Gangrene?

A

Perianal or retroperitoneal infection that spreads along fascial planes to genitalia. Progresses rapidly over 1-2 days with advancing skin necrosis. Most have significant underlying disease (diabetes). Typical microorganisms (mixed aerobic and anaerobic flora: Staph & Pseudomonas frequent)

59
Q

What is Synergistic Necrotizing Cellulitis?

A

Necrotizing soft-tissue infection that involves muscle groups in addition to superficial tissues and fascia

60
Q

What is the treatment of Fournier Gangrene and Synergistic Necrotizing Cellulitis like?

A

Treatment similar to other necrotizing infections

61
Q

What is Necrotizing Fasciitis?

A

Relatively rare subcutaneous infection that tracks along fascial planes and extends well beyond superficial signs of infection. Extension from skin lesion occurs in 80% of cases

62
Q

What is the initial presentation of Necrotizing Fasciitis?

A

Cellulitis. Progression leads to systemic toxicity: disorientation, lethargy, high temperatures

63
Q

What is the distinguishing feature of Necrotizing Fasciitis?

A

Wooden-hard feel of subcutaneous tissues

64
Q

What are the two types of Necrotizing Fasciitis?

A

Type I: Polymicrobial form. Type II: Monomicrobial form (Streptococcal gangrene)

65
Q

What are the associated settings of Type I Nectrotizing Fasciitis?

A

Surgery involving bowel/penetrating abdominal trauma. Decubitus ulcer or a perianal abscess. IVDU. Minor vulvovaginal infection

66
Q

What is Type II Necrotizing Fasciitis?

A

Monomicrobial form (streptococcal gangrene). Most community acquired. Present in limbs. Often an underlying cause (diabetes, arteriosclerotic vascular disease, or venous insufficiency with edema). Cases that arise after varicella or trivial injuries like scratches or insect bites are almost always due to S. pyogenes

67
Q

What is the Bacteriology of Type I Necrotizing Fasciitis?

A

Average of 5 pathogens. Most originate from bowel flora (coliforms and anaerobic bacteria)

68
Q

What is the bacteriology of Type II Necrotizing Fasciitis?

A

S. pyogenes (cases that arise after varicella or trivial injuries almost always d/t S. pyogenes). S. aureus, V. vulnificus, A. hydrophila, Anaerobic streptococci (Peptostreptococcus)

69
Q

What are the characteristics of necrotizing fasciitis caused by S. pyogenes?

A

Pathogenesis of severe Strep tissue infections is multifactorial. Invades and persists in human cells (epithelial cells, neutrophils, macrophages). Presence of virulence factors. Heavy filtration of inflammatory cells and mediators. Use of immune modulators as adjunctive therapy may be warranted for severe infections

70
Q

What is the treatment for Necrotizing Fasciitis?

A

Immediate surgical intervention: operative drainage and/or debridement (surgery generally required daily until no further debridement necessary)

71
Q

What is needed to treat Necrotizing Fasciitis caused by a polymicrobial infection?

A

B-Lactam/Lactamase combination + Clindamycin or 3rd gen ceph + clindamycin or carbapenem

72
Q

What is needed to treat Necrotizing Fasciitis caused by a Strep infection?

A

PCN + Clindamycin (Clindamycin: toxin suppression and modulation of cytokine production)

73
Q

What is needed to treat Necrotizing Fasciitis caused by a Staph infection?

A

1st gen ceph or oxacillin. Vancomycin: resistant strains

74
Q

What are the general characteristics of Diabetic Foot Infections?

A

Inframalleolar infection in DM (paronychia, cellulitis, myositis, abscesses, necrotizing fasciitis, septic arthritis, tendonitis, osteomyelitis). Infected diabetic foot ulcer: most common and classical lesion

75
Q

What are the predisposing factors for Diabetic Foot Injections?

A

Peripheral neuropathy-central role (sensory, motor, autonomic). Peripheral vascular disease. Neuro-osteoarthropathic deformities or limited joint mobility. Hyperglycemia. Older age/disabilities. Maladaptive patient behaviors

76
Q

What is the diagnosis for Diabetic Foot Infections?

A

Clinical assessment. Infection defined as presence of: Purulent secretions (pus) or At least 2 signs or symptoms of inflammation (redness, warmth, swelling or induration, and pain or tenderness), Secondary signs (nonpurulent secretions, discolored granulation tissue, foul odor), Laboratory (Leukocytosis, elevated erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), or procalcitonin

77
Q

What organisms cause the acute infections (typically monomicrobial) in diabetic foot infections?

A

S. aureus, B-hemolytic strep (Group A, B, C, G)

78
Q

What organisms cause necrotic tissue colonization in diabetic foot infections?

A

CoNS. Corynebacterium spp

79
Q

What organisms cause chronic wounds (typically polymicrobial) in diabetic foot infections?

A

Enterococcus, Enterobacteriaceae, Obligate anaerobes, Pseudomonas aeruginosa, other nonfermenting GNRs, MRSA, VRE

80
Q

When looking at the severity of diabetic foot infections, what does PEDIS stand for?

A

Perfusion, Extent/size, Depth/tissue loss, Infection, Sensation. Depth (which tissues involved) and if wound complicated by either ischemia or infection are key

81
Q

What is PEDIS Grade 1?

A

No symptoms. Uninfected

82
Q

What is PEDIS Grade 2?

A

Involvement of skin and SQ tissue only. Mild severity

83
Q

What is PEDIS Grade 3?

A

Extensive cellulitis or deeper infection. Moderate severity

84
Q

What is PEDIS Grade 4?

A

Presence of systemic inflammatory response syndrome (SIRS). Severe, potentially life-threatening, severity

85
Q

What should be done for uninfected diabetic foot ulcers?

A

Avoid antibiotic use (antibiotic use increases risk of antimicrobial resistance, financial cost, and may cause drug-related adverse effects)

86
Q

What should be done for mild-moderate diabetic foot infections?

A

Relatively narrow spectrum agent (cover aerobic GPC). Oral agent may be appropriate (especially with high BA)

87
Q

What should be done for severe chronic diabetic food infections?

A

Cover GPC (including MRSA), GNR, and anaerobes. Give parenteral therapy

88
Q

What should the duration of treatment be for diabetic foot infections?

A

Continue until evidence that infection has resolved. Mild infection: 1-2 weeks. Moderate and severe infections: 2-3 weeks

89
Q

What is wound care for diabetic foot infections?

A

Dressed in a manner that allows daily inspection and encourages a moist wound-healing environment. Removal of pressure from foot wound is necessary for healing. Accuzyme: topical debriding agent

90
Q

When is there a need for surgery with diabetic foot infections?

A

I/D of necrotic tissue. Revascularization of lower extremity. Urgent amputation for extensive necrosis or life-threatening infection

91
Q

What is Osteomyelitis?

A

Inflammation of bone that occurs secondary to open injury to bone or surrounding soft tissue. Progressive destruction of bone and formation of sequestra. Due to contiguous spread from adjacent soft tissues and joints, hematogenous seeding, or direction inoculation of microorganism into bone as a result of trauma surgery. Nonspecific pain with absence of systemic s/sxs normal. Infrequently present with fever, chills, local swelling, and erythema

92
Q

What are the 2 major classification systems for Osteomyelitis?

A

Cierny and Mader. Less and Waldvogel

93
Q

What is the Lee and Waldvogel classification of Osteomyelitis?

A

Based on duration of disease (acute vs. chronic) and route of infection (hematogenous vs. contiguous) and presence of vascular insufficiency. Doesn’t lend to what type of therapy patient should be on

94
Q

What is the Cierny and Mader classification of Osteomyelitis?

A

Based on affected portion of bone, physiologic status of host, local environment

95
Q

What is Cierny and Mader Stage 1?

A

Medullary osteo. Antimicrobial therapy alone

96
Q

What is Cierny and Mader Stage 2?

A

Superficial osteo. Antimicrobials after superficial debridement and soft tissue coverage

97
Q

What is Cierny and Mader Stage 3?

A

Localized osteo. Aggressive surgical debridement, antimicrobial thearpy, delayed ortho reconstruction

98
Q

What is Cierny and Mader Stage 4?

A

Diffuse osteo. Aggressive surgical debridement, antimicrobial thearpy, delayed ortho reconstruction

99
Q

How is Osteomyelitis diagnosed?

A

Confirmation by imaging studies +/- growth of microorganism from bone biopsy or surgical sampling

100
Q

What labs are abnormal in Osteomyelitis?

A

ESR and CRP elevated

101
Q

What imaging studies are done for Osteomyelitis?

A

X-ray (inexpensive): abnormalities typically seen 10-14 days post onset of infection). Nuclear bone scans: sensitive, but expensive and sometimes nonspecific. Magnetic resonance imaging (MRI): standard of care, sensitive and specific - provide anatomic delineation of infectious process and resolution of surrounding soft tissue

102
Q

What is the age of onset like for Contiguous Osteomyelitis?

A

Adults > 40 years

103
Q

What is the age of onset like for Osteomyelitis due to vascular insufficiency?

A

Adults > 40 years

104
Q

What is the age of onset like for Hematogenous Osteomyelitis?

A

Mostly in children (age < 20 yrs), adults > 50 yrs

105
Q

What are the sites of infections for Contiguous Osteomyelitis?

A

Femur, tibia, skull, mandible

106
Q

What are the sites of infections for Osteomyelitis due to vascular insufficiency?

A

Feet

107
Q

What are the sites of infections for Hematogenous Osteomyelitis?

A

Long bones (tibia and femur) and vertebrae (spondylodiskitis)

108
Q

What are the risk factors for Contiguous Osteomyelitis?

A

Infection secondary to soft tissue or direct inoculation into bone. Trauma. Surgery. Insertion of joint prosthesis. Cellulitis

109
Q

What are the risk factors for Osteomyelitis due to vascular insufficiency?

A

DM > 10 yrs. Poor glucose control. Peripheral neuropathy. Peripheral vascular disease

110
Q

What are the risk factors for Hematogenous Osteomyelitis?

A

Minor trauma. Transient bacteremia

111
Q

What are the typical microorganisms that cause Contiguous Osteomyelitis?

A

S. aureus. Usually polymicrobial (GNB and anaerobes)

112
Q

What are the typical microorganisms that cause Osteomyelitis due to vascular insufficiency?

A

S. aureus. CoNS (S. epidermidis). Mostly polymicrobial (GNB, anaerobes)

113
Q

What are the typical microorganisms that cause Hematogenous Osteomyelitis?

A

Neonates: Group B Strep, E. coli. Children: S. aureus and S. pneumoniae. Adults: S. aureus and CoNS. IVDU: P. aeruginosa. Usually monobacterial

114
Q

What does osteomyelitis therapy typically require?

A

Medical + surgical therapy for successful eradication of infection

115
Q

What does surgical therapy for osteomyelitis involve?

A

Extensive debridement of necrotic bone and other poorly vascularized, infected material

116
Q

What is the medical therapy like for Osteomyelitis?

A

Optimal duration unknown d/t lack of studies. Radical resection of infected tissue of diabetic foot osteomyelitis: 2-5 days of antibiotics. Acute, hematogenous: recommend 4-6 weeks of IV antibiotics. Chronic: months (IV initially followed by PO). Bone penetration importance still unclear. Treat based on cultures and susceptibilities

117
Q

What is the treatment for Hematogenous osteomyelitis like?

A

S. aureus (cefazolin or oxacillin). MRSA or S. epidermidis (Vancomycin). GNB (3rd gen ceph)

118
Q

What is the treatment for Contiguous or vascular insufficiency osteomyelitis like?

A

Polymicrobial (Pip/tazo. 3rd gen ceph + metronidazole or clindamycin). Pseudomonas coverage (Pip/tazo. Ceftazidime or cefepime. Ciprofloxacin)

119
Q

What is the role of topical antimicrobial therapy on an “uncertain” infection wound status?

A

Consider short-term topical antiseptic therapy

120
Q

What is the role of topical antimicrobial therapy on an infected wound?

A

Systemic antibiotic therapy (with or without topical antiseptic)

121
Q

What specific circumstances could use topical antimicrobial therapy?

A

Burn wounds (blood vessels to skin often destroyed). Eradicating wound bacteria prior to skin grafting. Reducing odor associated with nonhealing, necrotic wounds. Infected ischemic wound who cannot undergo revascularization. Removal of biofilms (implicated in persistent infections). MDR organisms untreatable with most systemic agents

122
Q

What is an Antiseptic?

A

Disinfectants used on intact skin and some open wounds to kill/inhibit microorganisms

123
Q

What is an Antibiotic?

A

Chemicals produced either naturally or synthetically in dilute solution to inhibit/kill other microorganisms

124
Q

What are the disadvantages of Antiseptics?

A

Often toxic to host cells

125
Q

What are the disadvantages of Antibiotics?

A

More likely to lose effectiveness d/t resistance

Thera VII (37 decks)

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