Download Secondary Treatment of Cellulitis Abscess

Skin and Soft Tissue
Infections
 Cellulitis
 Impetigo
 Erysipelas
 Abscess
 Animal bite
 Human bite
 Surgical site infection
 Necrotizing fasciitis
Skin and Soft Tissue
Infections
 Increasing ER visits and hospitalizations
 29% increase in admissions, 2000 to 2004
 Primarily in age <65
 Presume secondary to community MRSA
 50% cellulitis and cutaneous abscesses
 Estimated $10 billion SSTI 2010
IDSA Guidelines
MUSC Antibiotic Stewardship &
Anti-Infective Subcommittee
“Practice guidelines are systematically developed
statements to assist practitioners and patients in
making decisions about appropriate health care
for specific clinical circumstances.”
Guidelines
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Reduce emergence of resistant organisms
Reduce hospital days
Reduce costs:
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Blood cultures
Consultations
Imaging
Hospital days
2011-Implementation of treatment guidelines
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Decreased use of blood cx
Decreased advanced imaging
Decreased consultations
Shorter durations of therapy
Decreased use of anti-pseudomonal
Decreased use of broader spectrum abx
Decreased costs
No change in adverse outcomes
Inpatient Hospitalization
 Systemic illness
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HR >100 and
Temp >38oC or <36oC and
Systolic bp <90 or decrease of 20 mmHg < baseline
CRP>13
Marked left shift
Elevated creatinine
Low serum bicarbonate
CPK 2 x the upper limit of normal
Inpatient Hospitalization
 Abnormally rapid progression of cellulitis
 Worsening infection despite appropriate
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antibiotics
Tissue necrosis
Severe pain
Altered mental status
Respiratory, renal or hepatic failure
Co-morbidities: immune compromise,
neutropenia, asplenia, preexisting edema,
cirrhosis, cardiac failure, renal insufficiency
Objectives
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Classification
Skin anatomy
Infection caused By SA
Infection caused By Streptococcus
Necrotizing fascitis
Bites ( human and animal)
MSSA/MRSA updates
what’s new in therapy?
CID,2005, 41:1373-1406
What is Localized skin infection?
 Localized SSSIs include lesions such as
furuncles, carbuncles, and abscesses, which
would generally be treated by incision and
debridement with drainage.
When to consider it complicated ?
 Surrounding cellulitis, immunocompromised, or
the presence of potentially infectable prostheses,
such as cardiac valves, orthopedic devises or
vascular grafts, mandates antibiotic use and
might well mean that the infection would be
classed as complicated
 In particular, there are a number of underlying
comorbidities that should be sought and
excluded as being particularly relevant to the
patient with an SSSI.
Diabetes
 Vascular insufficiency in the area of the infection
 Chronic renal or hepatic disease
 Potentially infectable prostheses
 Immunosuppression
 Debilitation or advanced age
 Recent antimicrobial therapy
 Recent surgery; and
 Recent hospitalization
cSSSI Definition
Abscess
Cellulitis
Ulcer
Skin/skin structure infections that:
• Involve deep, soft tissue
• Require surgical intervention
• Are associated with significant underlying disease
that complicate the response to treatment
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Epidemiology and Microbiology
 Colonized with Gram-positive organisms :
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Staphylococcus epidermidis;
Corynebacterium spp;
Micrococcus spp;
Diphtheroids;
Propionibacterium spp; and
Anaerobic cocci
 While the moist intertriginous areas have a wider
spectrum of colonizations:
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Escherichia coli;
Proteus spp
Enterobacter spp; and
Other organism (including fungi)
Anatomy of the skin
Clinical presentations of SSTIs
Surgical site
infection
Necrotising
SSTI
Cellulitis
Skin and soft tissue
infections
Diabetic foot
infection
Infected
wound
Abscess
Infected
ulcer
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~0.1% of adult population requires hospital treatment for SSTIs each year1
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SSTIs may become complicated if require hospitalisation, surgery, involve
deeper tissues, co-morbidities or systemic symptoms
1. Eron LJ, et al. J Antimicrob Chemother 2003; 52 Suppl1:i3–17.
Obtain Careful History
 Immune status
 Geographic locale
 Travel history
 Recent trauma or surgery
 Previous antimicrobial therapy
 Lifestyle - occupation
 Hobbies
 Animal exposure
 Bite exposure
Cultures
 Blood cultures positive <5%
 Needle aspiration 5-40%
 Punch biopsy 20-30%
Blood Cultures
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HR >100 , Temp >38oC and <36oC, Sys <90mmHg
Lymphedema
Immune compromise/neutropenia/malignancy
Pain out of proportion to exam
Infected mouth or eyes
Unresponsive to initial antibiotics
Water-associated cellulitis
Diabetes
Recurrent or persistent cellulitis
Concern for a cluster or outbreak
Needle Aspiration or Skin Biopsy
 HR >100 , Temp >38oC and <36oC, Sys<90mmHg
 CRP>13
Marked left shift
 Elevated creatinine
Low serum bicarb
 CPK 2 x upper limit of normal
 Immune compromise/neutropenia/malignancy
 Diabetes
 Animal or human bite wounds
Broaden Antibiotics
 If no improvement in systemic signs in 48
hours
 If no improvement in skin in 72 hours
 As antibiotics kill organisms, released toxins
may cause a worsening of skin findings in first
48 hours
Deescalation
 Acute skin findings resolving
 Afebrile
 No signs of systemic illness
 Should see systemic signs improvement by 48
hours
 Should see skin improvement 3-5 days by at
the latest
What are the four main organisms?
 FIRST :S. aureus
 Is the commonest
 Two potent and clinically relevant exotoxins
from S. aureus are the enterotoxins (responsible
for food poisoning) and toxic shock syndrome
toxin (TSST-1)
 SECOND :Group A streptococci ( GAS)
 (S. pyogenes), much like S. aureus can produce a variety of
virulence factors. Group A streptococci secrete an array of
soluble exotoxins some of which are extremely potent
causing systemic toxicity known as streptococcal toxic
shock syndrome 9STSS) and necrotizing fascitis.
 THIRD :Clostridium perfringens is the most
frequently isolated, although isolates of C. septicum,
C. histolyticum, C. bifermentans, and C. novyii can
be equally pathogenics.
Cellulitis
 65% relative increase since 1999
 600,000 admissions annually
Risk Factors for Cellulitis
 Obesity
 Edema
 Venous insufficiency
 Lymphatic obstruction
 Fissured toe webs
 Maceration
 Fungal infection
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Inflammatory dermatoses – eczema
Repeated cellulitis
Subcutaneous injection or illegal drugs
Previous cutaneous damage
 All lead to breaches in the skin for organism invasion
Post-Surgical Risk Factors
 Saphenous venectomy
 Axillary node dissection for breast cancer
 Gyn malignancy surgery with lymph node
dissection *** in conjuction with XRT
 Liposuction
Non-Purulent Cellulitis
 INTACT SKIN
 No purulent drainage, no exudate, no
associated abscess
 Beta hemolytic streptococci
 Antibiotic:
 Cefazolin
 Documented anaphylactic cephalosporin allergy -
Vancomycin
Non-Purulent Cellulitis
 Deescalation:
 Cephalexin
 Beta-lactam anaphylaxis - clindamycin
 5 days of treatment
Purulent/Complicated Cellulitis
 BROKEN SKIN
 Purulent drainage
 Exudate
 Absence of a drainable abscess
Purulent/Complicated Cellulitis
 Deescalation:
 Trimethoprim/sulfamethoxazole + cephalexin
 Beta lactam anaphylaxis – clindamycin
 Sulfa allergy – tetracycline or doxycycline
 If sulfa and beta lactam allergies - linezolid
 5 days of treatment
Empiric SSTI algorithm
*This algorithm does NOT include:
surgical site infections, diabetic foot
ulcers, decubitus ulcers, insect,
animal or human bites, or gangrene
**Please see order form for guidance
(including renal dosing adjustments)
If cephalosporin allergic: Vancomycin
can be substituted for cefazolin
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The preferred method of treatment is I&D
Clinical Pearl: Treatment should continue for
48 hours prior to determination of clinical
failure; SSTIs often appear worse during initial
treatment period
Antibiotic De-escalation Criteria
1.Culture susceptibilities
2.Clinical response
1. Clinically stable
2. Decreased erythema
3. Decreased edema
4. Decreased warmth
5. Resolving leukocytosis
6. Afebrile
Total course of antibiotics is 5 days (i.e. 2 days of IV cefazolin + 3 days of PO cephalexin)
Note: Renal dose adjustments are required for patients with CrCL less than 30 mL/min
If sulfa allergic: Either tetracycline or doxycycline can be substituted to replace TMP/SMX
If beta-lactam anaphylaxis: Clindamycin (non-severe infection) can be substituted to replace cephalexin, or
linezolid can be substituted to replace both TMP/SMX and cephalexin
Secondary Treatment of
Cellulitis
 Elevation of affected leg
 Compression stockings
 Treat underlying tinea pedis, eczema,
trauma
 Keep skin well hydrated
Abscess
Abscess
 ALWAYS, ALWAYS
 Incision and drainage
Drainable Abscess <3cm
 Incision and drainage
 No blood cultures
 No aspirate culture
 NO ANTIBIOTICS
Abscess –When to Add
Antibiotics
 Drainable abscess >3cm
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Undrainable
Multiple sites of infection
Rapid progression in presence of cellulitis
Systemic illness (fever, hypotension, tachycardia)
Immune compromise
Elderly
Difficult to drain area (hand, face, genitalia)
Lack of response to incision and drainage
Septic phlebitis - multiple lesions
Gangrene
Bacterial pathogens as causative agents of
SSTIs in hospitalised patients
Relative incidence (%)
35
30
Enterococcus spp
25
S. aureus
20
Coagulase-negative
Staphylococci
E. coli
15
10
P. aeruginosa
5
0
USA
France Germany
Italy
Spain
Data from clinical laboratories participating in The Surveillance Network (TSN), 2001.
Jones M, et al. Int J Antimicrob Agents 2003; 22:406–419.
What sort of skin structure infections
are usually caused by staphylococci?
 It is often helpful to remember that localized
SSSIs above the belt are more likely to be
caused by S. aureus than those below the
belt, which are more likely to be associated
with mixed flora
 Furunculosis
 Cellulitis
 Abscesses
Staphylococcal Toxic Shock Syndrome
STSS
 It occurs in menstruating young females, but, at
present, most staphylococcal toxic shock
syndrome results from skin abscesses,
intravascular catheter infections, and S. aureus
pneumonia complicating influenza.
 Provable cases =microbiological criteria +4 of
the five clinical criteria.
 Confirmed cases =microbiological criteria + all
five of the clinical criteria.
Diagnostic Criteria for the Diagnosis of
Staphylococcal Toxic Shock Syndrome
Clinical Criteria
Fever
 38.9oC
Rash
Diffuse macular erythroderma rash
Desquamation
Desquamation of rash 1-2 weeks after onset of illness, especially on palms and soles
Hypotension
Systolic blood pressure  90 mmHg (for adults), <5th percentile by age for children under 16 years
Orthostatic drop in diastolic blood pressure  mmHg from lying to sitting, orthostatic syncope or
orthostatic dizziness.
Multiple organ failure
At least three of:
•Gastrointestinal involvement – vomiting or diarrhea at onset, hyperemic mucosa
•Muscular involvement – severe myalgia or creatinine phosphokinase at least twice the upper limit of
normal
• renal involvement – urea at least twice the upper limit of normal, or urinary sediment with pyuria
( 5 leukocytes per hpf) in the absence of urinary tract infection
•Hepatic involvement – total bilirubin, alanine aminotransferase, or aspartate aminotransferase
twice the upper limit of normal
•Hematological involvement – platelets <100 x 109/liter
•Neurological involvement – disorientation or reduced consciousness without focal neurological signs
when fever and hypotension are absent
•Mucous membrane involvement – vaginal, oropharyngeal, or conjuctival hyperemia
Microbiological Criteria (if Specimens Obtained)
Negative Results
Blood culture, throat culture, cerebrospinal fluid culture.
Anti-MRSA (other than vancomycin)
 Treatment failures with clindamycin have been
reported
 Clindamycin resistance is due to methylation of
the 235 portion of the ribosomal target
preventing the attachment of clindamycin to its
target
 Detection of inducible MLSb resistance in
staphylococci can easily be performed in the
microbiology laboratory by use of the D-test
Anti-MRSA (other than vancomycin)
 The overall cure rates with TMP-SMZ and
vancomycin were 85% and 98% (p=0.014. It is
interesting to note that all infections (endocarditis,
SSSIs, and others) due to MRSA were cured.
Rifampin should not be used as single agent
 Against S. aureus both doxycycline and minocycline
are more potent than tetracycline and a recent
study indicated that 95% or more of all MRSA and
MSSA isolates were susceptible to doxycyline.
What infections are caused by
sterptococci?
 Impetigo
 Cellulitis
 Erysipelas
 STSS
 Necrotizing fascitis
Streptococcal Cellulitis
 Erysipelas is a type of cellulitis most commonly
caused by group A streptococci, although in rare
cases other types of streptococci or S. aureus are
implicated.
 Erysipelas involves more superficial layers of the skin
than cellulitis which is a deeper infection. There is
prominent involvement of the lymphatic vessels. The
more superficial nature of erysipelas accounts for its
predominant clinical feature, that of an area of
inflammation that is raised above the surrounding
normal skin and has an edematous, indurated
appearance.
 Vessels and lymphoedema
Diagnostic Criteria for the Diagnosis of
Streptococcal Toxic Shock Syndrome
Clinical Criteria
Hypotension
Multiple organ
failure
Clinical Criteria
Systolic blood pressure  90 mmHg (for adults), < 5th percentile by age for
children under 16 years
At least two of:
•Renal involvement – creatinine  mol/liter for adults, more than twice the
upper limit of normal by age for children; in pre-existing renal disease, more
than twice the baseline level
•Hematological involvement – platelets <100x109/liter or disseminated
intravascular coagulation
•Hepatic involvement – total bilirubin, alanine aminotransferase or aspartate
aminotransferace twice the upper limit of normal for the patient’s age: in preexisting hepatic disease, more than twice the baseline level
•Respiratory involvement – acute respiratory distress syndrome
•Rash – generalized erythematous macular rash, which may desquamate
•Soft-tissue necrosis, including necrotizing fasciitis or myositis, or gangrene
Microbiological Criteria
Isolation of group A streptococci
Necrotizing Fascitis
 Necrotizing fascitis is a fulminating inflammation
of the fascia that results in thrombosis of the
subcutaneous blood vessels and necrosis of the
underlying tissue
 Necrotizing fascitis itself is generally divided into
two broad
 Type I, caused by mixed aerobic/anaerobic
bacteria, including enterococci and non-group A
streptococci (usually C or G); and
 Type 2, caused by group A streptococci, either
alone or in combination with other organisms
What are the Clinical Features of
Necrotizing Fasciitis?
 The most common site of infection is the distal
lower limb, although fascial extension up the leg
is common. The progression is often
alarmingly rapid from a silent or apparently
minor process to a fulminant condition with
clinical features of systemic toxicity, extensive
destruction with threat to the affected limb, and
even imminent death.
 The first clue may be unexplained and
rapidly worsening pain
 By the time the bullae have appeared, there is
usually already extensive necrosis.
How to diagnose Necrotizing
Fascitis?
 Ncrotizing Facitis is LIMB + LIFE threatening
 Immediate extensive surgical debridement
must be done ASAP
 CLINDAMYCIN must be give , it also has
antitoxin action
Clostridial Infections
 Clostridia are large, anaerobic Gram-
positive, spore-forming bacilli.
 Clostridial infection can cause myonecrosis, or
gas gangrene, which can be divided into
three major groups
 Post-traumatic;
 post-operative or non-traumatic; and
 spontaneous
Infectious Gangren and
gangrenous cellulitis
Clostridial Infections
 Clostridial myonecrosis is often associated with a
traumatic event
 It can also develop in pre-existing wounds or
infections such as skin ulcers and rhinocerebral or
orbital mucormycosis. C. perfringens is the most
frequent cause of clostridial myonecrosis but less
frequent causes include C. septicum, C. novyii, C.
histolyticum, and C. sordelli.ws
Animal Bites
Animal Bites
 Pasteurella – mc organism
 Antibiotics:
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Ampicillin/sulbactam
Piperacillin/tazobactan
Cefoxitin
Meropenem
Ertapenem (restricted to ID and Surgery)
 Tetanus toxoid (if not up to date)
Human Bites
Human Bite
 Antibiotics:
 Ampicillin/sulbactam
 Meropenem
 Ertapenem (restricted to ID and Surgery)
 Tetanus toxoid (if not up to date)
 Closed fist***
 Antibiotics:
 Cefoxitin
 Ampicillin/sulbactam
 Ertapenem(restricted to ID and Surgery)
 Tetanus toxoid (if not up to date)
 Hand surgery consult***
Human Bites
 Deescalation:
 Amoxicillin/clavulanate
 Moxifloxacin + clindamycin
 Trimethoprim/sulfamethoxazole + metronidazole
 Treatment duration:
 Discontinue abx 3 days after acute inflammation
disappears
 Usually 5-10 days of treatment if no joint or tendon
involvement
Surgical Site Infection
Surgical Site Infection
 Pain, swelling, erythema, purulent drainage
 Usually have no clinical manifestations for at
least 5 days after operation
 Most resolve without antibiotics
 Open all incisions that appear infected >48 hours
after surgery
 No antibiotics if temperature <38.5oC and HR
<100 bpm
Surgical Site Infection
 If temperature >38.5oC or HR >100 bpm:
 Trunk, head, neck, extremity
 Cefazolin
 Clindamycin
 Vancomycin if MRSA is suspected
 Perineum, gi tract, female gu tract
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Cefotetan
Ampicillin/sulbactam
Ceftriaxone + metronidazole or clindamycin
Fluoroquinolone + clindamycin
 Treatment duration:
 Usually 24-48 hours or for 3 days after acute inflammation resolves
Neutropenia and SSTI’s
Neutropenic Patients with
SSTI
 ALWAYS blood CULTURES
 Initial infection - <7 days neutropenia
 Antibiotics
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Carbapenems
Cefepime
Ceftazidine
Piperacillin/tazobactam
PLUS
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Vancomycin
Linezolid (restricted to ID)
Daptomycin (restricted to ID)
(discontinue if culture negative after 72-96 hours)
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Neutropenic Patients with
Subsequent
infection- >7days neutropenia (fungi, viruses, atypical bacteria)
SSTI
Treatment:
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Amphotericin B
Micafungin (may require higher dose and ID consult)
Voriconazole (restricted to ID, Heme/Onc, Critical Care, Pulmonary, and Transplant)
PLUS
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Carbapenems
Cefepime
Ceftazidine
Piperacillin/tazobactam
PLUS
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Vancomycin
Linezolid (restricted to ID)
Daptomycin (restricted to ID)
(discontinue if culture negative after 72-96 hours)
Neutropenic Patients with
SSTI
 Deescalation:
 Ciprofloxacin and amoxicillin/clavulanate
 Treatment duration:
 At least 7 days
Vascular-Access Devices in
Neutropenia
 Device predisposes to SSTI
 66% Gram positive
 Entry site infection
 Antibiotics
 Tunnel infection and vascular port-pocket
infection
 Device removal and antibiotics
Diabetic Foot Ulcers
Diabetic Foot Ulcers
 Not all diabetic foot ulcers are infected.
 Infection if at least 2 present:
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Purulent secretions
Redness
Warmth
Swelling/induration
Pain/tenderness
Diabetic Foot Ulcers
 Common, complex, costly
 Largest number of diabetes-related hospital
bed days
 Most common proximate, non-traumatic
cause of amputations
MRSA Risk Factors
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Recent hospitalization last 90 days
Residence in long term care facility
Antibiotics last 90 days
Injection drug use
Hemo- or peritoneal dialysis
Incarceration last 90 days
Home infusion therapy
History of MRSA colonization
Immunosupressive state/medications
Wound care in past 30 days
Pseudomonas Risk factors
 ICU stay in last 90 days
 Immunosuppressive state/medications
 Immunosuppressive states includes:
 HIV, solid organ transplants, BMT
 Immunosuppressive medications includes:
 Rejection medications, >20mg/d prednisone x2w
Mild Diabetic Foot Ulcer
 Cellulitis or erythema extends <2cm around ulcer, infection limited to
skin – no systemic indications
 Obtain foot xray – screen for osteomyelitis
 Antibiotics:
 No MRSA risk:
 Cephalexin
 Amoxicillin/clavulanate
 MRSA risk:
 Trimethoprim/sulfamethoxazole
 Doxycycline
 Treatment duration
 Usually 1-2 weeks treatment (can be as long as 4 weeks)
Moderate Diabetic Foot
Ulcers
 Erythema extends >2cm around ulcer or signs of abscess,
osteomyelitis, septic arthritis, fasciitis – no systemic signs
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Foot x-ray
Culture wound
Wound care
Assess need for debridement
general surgery
CRP
ESR
Bone biopsy for culture
MRI if ESR and CRP elevated
ID consult if osteomyelitis present
Severe Diabetic Foot Ulcers
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Erythema extends >2cm around ulcer and signs of systemic
infection(hypotension, hyperthermia, tachycardia)
Foot xray
Culture wound
Blood cultures
Wound care
Assess need for debridement
general surgery
CRP
ESR
Consider MRI if suspect abscess or uncertain if osteomyelitis or if the ESR
and CRP
 Bone biopsy
 ID consult if osteomyelitis
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Secondary Treatment of
Diabetic Foot Ulcers
 Wound care
 Debridement
 Glycemic control
 Evaluate vascular status