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Skin and Soft Tissue Infections – Top Ten Myths in Adults

Skin and Soft Tissue Infections – Top Ten Myths in Adults - Clinical Hub, UW Health Clinical Tool Search, UW Health Clinical Tool Search, Clinical Practice Guidelines, Infection and Isolation, Related


Last reviewed/revised: 01/2016
Skin, Skin Structure, and Soft Tissue Infection – Adult - Inpatient/Ambulatory Clinical Practice Guideline
Appendix A. Diagnosis and Treatment of Gram Positive Bacterial Skin and Soft Tissue
Infections – Top Ten Myths
Authors: Lucas Schulz, PharmD; Robert Hoffman, MD; Jeffrey Pothof, MD; Barry Fox, MD
Myth 1: Skin that is red and swollen is definitely cellulitis
Truth 1: Local presentation of edema, erythema, heat, “orange peel” appearance, vesicles, bullae,
petechiae, and pain should lead to a diagnosis of skin and skin structure infection.2,3,9,10
a. Diagnoses of deep venous thrombosis, venous stasis dermatitis, venous insufficiency,
lymphedema, contact dermatitis, gout, herpes zoster, acute lipodermatosclerosis, non-
infectious phlebitis and fixed drug reaction should be excluded.
b. All inflammatory responses include hyperemia, warmth, swelling, and usually pain
c. A simple physical exam skill that can help differentiate true cellulitis from other etiologies of
erythema of the lower extremity is to have the patient lie horizontally on exam table/bed,
manually elevate leg at 45 degree angle or higher, and hold it there for 1-2 minutes while
observing whether the erythema abates. Cellulitis erythema will persist upon elevation
whereas erythema due to other etiologies often disappears with elevation.
Myth 2: Bilateral leg swelling and redness always means bilateral leg cellulitis
Truth 2: Bilateral leg swelling is usually due to other disease states and does not mean that the patient
has developed bilateral cellulitis.40,53 Statistical probability would also make this occurrence exceedingly
rare.
a. Risk factors for developing erysipelas or cellulitis include obesity, previous cutaneous
damage (from trauma, preexisting skin infections, ulceration, and other causes), and edema
from venous insufficiency or lymphatic obstruction or disruption of lymphatic drainage, such
as following lymph node dissection.
1. Of 99 patients with bilateral leg swelling, 17 patients (17%) were found to have acute
deep vein thrombosis by venous duplex ultrasound. 2
b. Patients should elevate the affected area in order to hasten improvement by promoting
gravity drainage of the edema and inflammatory substances.
c. If edematous, apply ACE wrap from toes to thighs every 8 hours for lower extremity infections
to assist in reduction of lymphedema.
Myth 3: Patients with no risk factors for community acquired- methicillin-resistant
Staphylococcus aureus (CA-MRSA) cannot get MRSA
Truth 3: Any patient may develop cellulitis caused by CA-MRSA. The likelihood is increased if the
patient has risk factors for MRSA.
a. Between 2006 and 2009, a microbiologic study of skin and soft-tissue infections examined
the etiology of skin and soft tissue infections (SSTI) in a general population. A culture was
obtained in 23% (149,200/ 648699) of SSTI episodes, and a pathogen was identified in 58%
(87,839/149,200) of the cultures. Staphylococcus aureus was the pathogen in 80% of the
positive cultures 70,026/87,839), with 50% (35,180/70,026) of the Staphylococcus aureus
isolates being MRSA.54
b. Risk factors for community-acquired MRSA (CA-MRSA) include:29
ξ History of MRSA infection or colonization in patient or close contact
ξ High prevalence of CA-MRSA in local community or patient population
ξ Recurrent skin disease
ξ Crowded living conditions (e.g. homeless shelters, military barracks)
ξ History of incarceration
ξ Participation in contact sports
ξ Skin or soft tissue infection with poor response to beta-lactam antibiotics
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Skin, Skin Structure, and Soft Tissue Infection – Adult - Inpatient/Ambulatory Clinical Practice Guideline
ξ Recent and/or frequent antibiotic use
ξ Injection drug use
ξ Member of Native American, Pacific Island, Alaskan Native populations
ξ Male with history of having sex with men
ξ Shaving of body hair
c. Risk factors for hospital-acquired MRSA (HA-MRSA) include:30
ξ Nasal colonization
ξ Presence of indwelling devices such as catheters, tracheostomies, and nasogastric tubes
ξ Hospital admission within past 90 days
ξ Prolonged hospitalization
ξ Residence in long-term care facility
ξ Antibiotic therapy in past 90 days
ξ Diabetes mellitus
ξ Hemodialysis
ξ HIV infection/immunosuppression
d. In the absence of cultured abscess samples, MRSA nasal AND pooled axilla/groin PCR or
culture should be obtained for inpatients with risk factors for MRSA or to determine the
likelihood that infection is caused by MRSA31-34,55
1. If MRSA PCRs or cultures are negative, medications covering for MRSA may
potentially be de-escalated to beta-lactam antibiotics.55
Myth 4: All cellulitis needs to be treated with antibiotics
Truth 4: Not all cellulitis needs to be treated with antibiotics.
a. For simple abscesses and boils (less than 5 cm in diameter of erythema and abscess),
incision and drainage alone is likely adequate as sole treatment and no treatment with
antibiotics are necessary2,3,9,29
b. For patients with abscesses/erythema (combination diameter) greater than 5 cm, multiple
lesions, cutaneous gangrene, signs of systemic infection, rapid progression of cellulitis, areas
that are difficult to drain (face, hand, genitalia), and/or risk factors for reduced ability to heal,
such as diabetes or immunosuppression, treatment with antibiotic therapy should be
considered29
Myth 5: All hospitalized patients need to be treated as though they have MRSA infection
Truth 5: Hospitalized patients should be treated with antibiotics to cover organisms based on individual
characteristics of the infection and risk factors for organisms.
a. Of 322 hospitalized patients with SSTIs, 47% (150/322) had a positive culture result and of
those with result, 43% (64/150) grew MRSA.5
b. Impetigo, erysipelas, and cellulitis that is diffuse or unassociated with a defined portal,
erythematous, non-purulent with extensive lymphangitic spread is more commonly caused by
Group A or other beta-hemolytic Streptococcus than Staphylococcal species (but
Staphylococcus aureus may also be present)35,36
c. For cellulitis with abscess that is fluctuant, has penetrating trauma, shallow ulcer or blister
with surrounding erythema, Streptococcus spp. and Staphylococcus spp. should be targeted
with antimicrobial therapy (including MRSA). 2,3,9,10
1. Abscess material should be obtained for culture whenever possible.
2. MRSA nasal and pooled axilla/groin PCR or culture should be obtained in the absence
of culture material for patients with risk factors for MRSA or patients receiving anti-
MRSA therapy31-34
3. If MRSA PCR or culture are negative, medications covering for MRSA may potentially
be de-escalated to more narrow-spectrum antibiotics
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Last reviewed/revised: 01/2016
Skin, Skin Structure, and Soft Tissue Infection – Adult - Inpatient/Ambulatory Clinical Practice Guideline
d. Severity of illness and co-morbidities, as well as risk factors for MRSA plays a large role in
determining whether or not to empirically treat for MRSA.
Myth 6: If the redness extends beyond the drawn wound margin in a patient with cellulitis, the
patient is getting worse
Truth 6: Because of the sub-acute spread of redness, edema, and/or induration in some patients at the
time of presentation with SSTI, the lesion may continue to spread during a short period of time after
administration of the first doses of antibacterial drug therapy.56
a. The erythema may extend beyond pen margins within the first 24 to 36 hours without
representing treatment failure. The intensity of the erythema is often a more important
variable, with improving cases resulting in less intensely red inflammation.
b. If erythema and fever continue beyond 48 to 72 hours, this is usually considered treatment
failure and antimicrobial therapy should be reassessed. Exceptions may include beta
hemolytic streptococcal infections where lymphangitis and lymphadenopathy may continue to
evolve over multiple days.
Myth 7: All patients with tick bites and surrounding redness have cellulitis
Truth 7: Local tick bite reactions are predictable and do not indicate that a patient has cellulitis.57 These
are usually no more than a few cm in size.
a. Erythema surrounding a tick bite can be differentiated from streptococcal and staphylococcal
cellulitis based the characteristics of erythema. Erythema due to tick bites usually remains
localized with limited spread to the site of the bite, while bacterial cellulitis and erythema
migrans from Borellia will continue to extend several cm beyond the bite site.
Myth 8: Patients should never have another infection if they are taking antibiotic prophylaxis for
recurrent infections,
Truth 8: Antibiotic prophylaxis may suppress infection, but recurrence may occur despite adherence to
therapy. Treatment of causes of infection and optimization of treatment of other disease states may
decrease the risk of recurrence.50-52
a. Of 398 patients, 40% (158/398) of patients reported cellulitis recurrence despite prophylactic
treatment of benzathine penicillin58
b. Causes of infection such as tinea pedis should be treated to prevent recurrence49,59
c. The management of other disease states, such as diabetes mellitus and especially
lymphedema, should be optimized in order to decrease the risk of recurrence.58
d. Skin should be kept well hydrated with emollients to avoid dryness and cracking
e. Underlying edema should be reduced by elevating the infected extremity and by the use of
compression stockings59
f. Reconfirmation of the diagnosis of cellulitis, appropriateness of antibiotic, dosing, timing, and
adherence should also be assessed60
Myth 9: Since one cannot tell whether cellulitis is caused by Streptococcus, Staphylococcus, or
CA-MRSA, each patient need two types of anti-infectives
Truth 9: Antimicrobial therapy should be selected based on characteristics of the infection and patient-
specific risk factors for different organisms, and the severity of the patients illness. Most uncomplicated
cellulitis will not need combination therapy with a beta- lactam and anti- MRSA anti-infective5,61
a. Cellulitis that is diffuse or unassociated with a defined portal, erythematous, and non-purulent
with extensive lymphangitic spread is most commonly caused by Streptococcal species35
b. Cellulitis with abscess that is fluctuant, has penetrating trauma, and/or open ulcer with
surrounding erythema is more likely caused by Staphylococcus than by Streptococcus
species 28
c. Dicloxacillin and cephalexin exhibit antimicrobial activity against MSSA and Streptococcus
2,3,9,10
Copyright © 201� University of Wisconsin Hospital s and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 01/2016CCKM@uwhealth.org

Last reviewed/revised: 01/2016
Skin, Skin Structure, and Soft Tissue Infection – Adult - Inpatient/Ambulatory Clinical Practice Guideline
d. For patients with risk factors for MRSA, trimethoprim-sulfamethoxazole has activity against
most MRSA strains; however, activity against Streptococcal spp. is variable. One recent
study found it very active for beta- hemolytic strep.62 Alternative agents (including
combination therapy) should be considered for the treatment of possible Streptococcal
infection.2,3,9,10 Doxycycline is not active for beta- hemolytic streptococci.
e. Clindamycin has activity against Streptococcus, MSSA, and some strains of MRSA, although
the sensitivity to MRSA is declining (see myth 10).2,3,9,10
Myth 10: Clindamycin is the most effective empiric antibiotic for CA-MRSA
Truth 10: Clindamycin may exhibit inducible resistance to MRSA, and caution should be used when
prescribing this agent for CA-MRSA. Microbiology labs are now routinely testing for this induceability, and
will report clindamycin as resistant. Resistance rates to clindamycin of greater than 35% have been
reported for CA-MRSA, and 100% of H-MRSA are resistant. Trimethoprim-sulfamethoxazole and
doxycycline resistance rates remain at less than 10% in most communities. 2,3,9,10,63,64 Clindamycin also
has the highest odds ratio for the development of Clostridium difficile.
References for Appendix A
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4. Bailey E, Kroshinsky D. Cellulitis: diagnosis and management. Dermatol Ther. Mar-Apr 2011;24(2):229-239.
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6. Glover JL, Bendick PJ. Appropriate indications for venous duplex ultrasonographic examinations. Surgery. Oct
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Copyright © 201� University of Wisconsin Hospital s and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 01/2016CCKM@uwhealth.org

Last reviewed/revised: 01/2016
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24. Semel JD, Goldin H. Association of athlete's foot with cellulitis of the lower extremities. Clin Infect Dis. Nov 1996;23(5):1162-
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Copyright © 201� University of Wisconsin Hospital s and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 01/2016CCKM@uwhealth.org