Acs0302 Soft Tissue Infection

© 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
3 BREAST, SKIN, AND SOFT TISSUE 2 Soft Tissue Infection — 1

2 SOFT TISSUE INFECTION
Mark A. Malangoni, M.D., F.A.C.S., and Christopher R. McHenry, M.D., F.A.C.S.

Approach to the Patient with Soft Tissue Infection
Soft tissue infections are a diverse group of diseases that involve factors that may have disrupted the normal skin barrier [see Table
the skin and underlying subcutaneous tissue, fascia, or muscle. 2], as well as about any host factors that may increase their sus-
Such infections may be localized to a small area or may involve a ceptibility to infection and limit their ability to contain it. It is par-
large portion of the body. They may affect any part of the body, ticularly important that they be questioned about specific clinical
though the lower extremities, the perineum, and the abdominal scenarios associated with unusual pathogens, such as an animal
wall are the most common sites of involvement. Some soft tissue bite (associated with Pasteurella multocida), a human bite (Eikenella
infections are relatively harmless if treated promptly and ade- corrodens), chronic skin diseases (Staphylococcus aureus), saltwater
quately; others can be life-threatening even when appropriately exposure or ingestion of raw seafood (Vibrio vulnificus), and brack-
treated. The symptoms and signs range from subtle or nonspecif- ish or freshwater exposure (Aeromonas hydrophila).
ic indicators (e.g., pain, localized tenderness, and edema without Physical examination usually reveals erythema, tenderness, and
fever) to obvious features (e.g., necrosis, blistering, and crepitus induration. Vesicular lesions and honey-colored crusted plaques
associated with systemic toxicity). are seen in patients with impetigo. Intense, sharply demarcated
Soft tissue infections were first defined as such more than a cen- erythema is characteristic of erysipelas. A tender, swollen erythe-
tury ago. In 1883, Fournier described a gangrenous infection of matous papule, often containing a visible hair shaft, is indicative of
the scrotum that continues to be associated with his name.1 In folliculitis. A single painful, tender, indurated, erythematous skin
1924, Meleney documented the pathogenic role of streptococci in nodule suggests a furuncle, and the presence of multiple inflam-
soft tissue infection.2 Shortly thereafter, Brewer and Meleney matory nodules with sinus tracts is consistent with a carbuncle.
described progressive polymicrobial postoperative infection of the Cellulitis in association with a decubitus ulcer or an ischemic leg
muscular fascia with necrosis3 (though the term necrotizing fasci- ulcer frequently signals a polymicrobial infection with gram-nega-
itis was not introduced until more than 25 years later4).The asso- tive organisms. An erythematous linear streak, characteristic of
ciation between toxic-shock syndrome and streptococcal soft tis- lymphangitis, usually indicates a superficial infection secondary to
sue infection was delineated as this disease reemerged in the Streptococcus pyogenes; associated lymphadenopathy may be pre-
1980s.5 sent as well.
Various classification systems and eponyms are used to describe Patients with necrotizing soft tissue infections often complain of
specific forms of soft tissue infection [see Discussion, Etiology and severe pain that is out of proportion to their physical findings.
Classification of Soft Tissue Infection, below]. In our view, howev- Compared with patients who have nonnecrotizing infections, they
er, it is more important to develop a common approach to the are more likely to have fever, bullae, or blebs [see Figure 1]; signs of
diagnosis and treatment of these conditions than to refine the systemic toxicity; hyponatremia; and leukocytosis with a shift in
minor details of classification. For therapeutic purposes, the pri- immature forms. Physical findings characteristic of a necrotizing
mary consideration is to distinguish between necrotizing soft tissue infection include tenderness beyond the area of erythema, crepi-
infections and nonnecrotizing infections. Nonnecrotizing soft tis- tus, cutaneous anesthesia, and cellulitis that is refractory to antibi-
sue infections involve one or both of the superficial layers of the otic therapy.6 Tenderness beyond the borders of the erythematous
skin (epidermis and dermis) and the subcutaneous tissue, and they
usually respond to antibiotic therapy alone. Necrotizing soft tissue
infections may involve not only the skin, the subcutaneous tissue,
and the superficial fascia but also the deep fascia and muscle, and Table 1 Common Soft Tissue Infections
they must be treated with urgent surgical debridement. At times,
it is difficult to distinguish between these two categories of infec-
Pyoderma
tion, especially when obvious clinical signs of necrotizing soft tis- Impetigo
sue infection are absent. Erysipelas
In this chapter, we review diagnosis and management of the Folliculitis
main soft tissue infections seen by surgeons, including both super- Furuncles and carbuncles
ficial infections (e.g., pyoderma, animal and human bites, and cel- Superficial infections Infections developing in damaged skin
lulitis) and necrotizing infections involving superficial and deep tis- Animal bites
sues [see Table 1]. Human bites
Cellulitis
Nonnecrotizing
Clinical Evaluation Necrotizing

The diagnosis of soft tissue infection is usually made on the Necrotizing fasciitis
basis of the history and the physical examination. Patients typical- Deep necrotizing Myonecrosis
cutaneous infections Gas gangrene
ly seek medical attention because of pain, tenderness, and erythe-
Metastatic gas gangrene
ma of recent onset. They should be asked about environmental


value of these findings was only 26%.10 The absence of these find-
Table 2 Environmental Factors That Disrupt ings in a patient without obvious clinical signs of a necrotizing soft
Skin and Alter Normal Barrier Function tissue infection had a negative predictive value of 99%. A normal
serum creatine kinase (CK) level rules out muscle necrosis.
Cuts, lacerations, or contusions In a 2004 report, one group of investigators described the devel-
Injections from contaminated needles opment and application of the Laboratory Risk Indicator for
Animal, human, or insect bites
NECrotizing fasciitis (LRINEC) score.11 This scoring system
assigns points for abnormalities in six independent variables:
Burns
serum C-reactive protein level (> 150 mg/L), WBC count (>
Skin diseases (e.g., atopic dermatitis, tinea pedis, eczema, scabies,
15,000/mm3), hemoglobin level (< 13.5 g/dl), serum sodium level
varicella infection, or angular cheilitis)
(< 135 mmol/L), serum creatinine level (> 1.6 mg/dl), and serum
Decubitus, venous stasis, or ischemic ulcers
glucose level (> 180 mg/dl).With a score of 8 or higher, there is a
Contaminated surgical incisions 75% risk of a necrotizing soft tissue infection. The authors of the
report recommended that the LRINEC score be used to deter-
mine which patients require further diagnostic testing, given that
area is an especially important clinical clue that develops as the the negative predictive value of this screening tool was 96%.
infection in the deeper cutaneous layers undermines the skin. A plain x-ray of the involved area demonstrates soft tissue gas in
Early in the course of a necrotizing soft tissue infection, skin only 15% to 30% of patients with necrotizing infections [see Figure
changes may be minimal despite extensive necrosis of the deeper 3].6 Computed tomography is more sensitive in identifying soft tis-
cutaneous layers. Bullae, blebs, cutaneous anesthesia, and skin sue gas, but other CT findings are seldom diagnostic.
necrosis occur as a result of thrombosis of the nutrient vessels and Magnetic resonance imaging is currently the preferred imaging
destruction of the cutaneous nerves of the skin, which typically study for documenting deep necrotizing infections [see Figure 4].
occur late in the course of infection. The presence of soft tissue gas on MRI is diagnostic of a necrotiz-
Clinicians should be mindful of certain diagnostic barriers that ing soft tissue infection.T2-weighted images demonstrate thicken-
may delay recognition and treatment of necrotizing soft tissue ing and increased signal intensity of the deep fascial planes.12,13
infections.7 In particular, these infections have a variable clinical Increased signal intensity in the subcutaneous tissue and edema of
presentation. Although most patients present with an acute, rapid- the adjacent muscle are also frequently present. High signal inten-
ly progressive illness and signs of systemic toxicity, a subset of sity on T2-weighted images and tissue enhancement after gadolin-
patients may present with a more indolent, slowly progressive ium administration are indicative of inflamed tissue and may also
infection. Patients with postoperative necrotizing infections often occur with certain nonnecrotizing soft tissue conditions (e.g., exer-
have a more indolent course. Moreover, in the early stages, under- tional muscle injury, lymphedema, dermatomyositis, polymyositis,
lying necrosis may be masked by normal-appearing overlying skin. eosinophilic fasciitis, and neoplastic disease).13-17 Low or absent
As many as 20% of necrotizing soft tissue infections are primary signal intensity on gadolinium-enhanced T1-weighted images is
(idiopathic) and occur in previously healthy patients who have no indicative of necrosis, a finding that is more specific for a necro-
predisposing factors and no known portal of entry for bacterial tizing soft tissue infection.18-20 The reported sensitivity of MRI for
inoculation. Finally, crepitus is noted in only 30% of patients with diagnosis of necrotizing soft tissue infection ranges from 89% to
necrotizing soft tissue infections. Overall, fewer than 40% of 100%, and its specificity ranges from 46% to 86%.18,20
patients exhibit the classic symptoms and signs described.8,9 A prospective study from 2000 evaluated the use of MRI to dif-
Accordingly, it is imperative to maintain a high index of suspicion ferentiate necrotizing from nonnecrotizing soft tissue infection in
for this disease in the appropriate setting. nine patients.20 The absence of gadolinium enhancement on T1-
weighted images was indicative of fascial necrosis in all six patients
Investigative Studies
Diagnostic studies have a low yield in patients with superficial
soft tissue infections. They are rarely necessary and are used only
in specific clinical circumstances. Either needle aspiration at the
advancing edge of erythema with Gram staining and culture or
full-thickness skin biopsy and culture may be helpful when celluli-
tis is refractory to antibiotic therapy or when an unusual causative
organism is suspected. Because of their low yield, blood cultures
are obtained only in patients with signs of systemic toxicity, those
with buccal or periorbital cellulitis, and those with infection sus-
pected of being secondary to saltwater or freshwater exposure;
these clinical situations are associated with a higher likelihood of a
positive culture.
When the characteristic clinical features of necrotizing soft tis-
sue infection are absent, diagnosis may be difficult. In this setting,
laboratory and imaging studies become important [see Figure 2].
In one study, logistic regression analysis showed that an elevated
white blood cell (WBC) count (≥ 15,400/mm3) and hyponatre-
mia (serum sodium level lower than 135 mmol/L) at the time of
hospital admission were highly sensitive for the presence of a Figure 1 Lower-extremity necrotizing fasciitis is characterized
necrotizing soft tissue infection; however, the positive predictive by bullae, blebs, and discolored skin.


Necrotizing soft tissue infection is suspected

Patient has one or more obvious clinical Patient has no obvious signs of
signs of necrotizing soft tissue infection necrotizing soft tissue infection

Initiate operative exploration.

Patient has WBC count > 15,000/mm3, Patient has WBC count ≤ 15,000/mm3
disproportionate pain, bullae or blebs, and does not have disproportionate pain,
or refractory cellulitis bullae or blebs, or refractory cellulitis

Perform MRI.

Initiate antibiotic therapy.

Soft tissue gas is seen on MRI No soft tissue gas is seen
on MRI
Initiate operative exploration. Antibiotic therapy is Antibiotic therapy fails
successful
Perform full-thickness
No further action is biopsy and frozen-
necessary. section examination, and
Edema, inflammation, or Edema, inflammation, and obtain cultures.
gadolinium enhancement gadolinium enhancement
of deep soft tissues is of deep soft tissues are
present absent

Perform biopsy and frozen-
section examination. Diagnostic studies Diagnostic studies
yield positive results yield negative results

Perform operative Reassess antibiotic
debridement. therapy.
Biopsy and frozen-section Biopsy and frozen-section
examination are positive examination are negative
Figure 2 Algorithm outlines diagnostic evaluation of
Perform operative
debridement. patients with soft tissue infection.6

who underwent operative debridement.20 Operation was avoided nose or rule out soft tissue infection [see Figure 2]. This procedure
in two patients who showed no evidence of necrosis on MRI. A may be performed at the bedside with local anesthesia.The obser-
third patient without MRI evidence of necrosis underwent opera- vation of necrotic or infected tissue through the biopsy incision
tive exploration because of a high degree of clinical suspicion and indicates that immediate debridement is needed.
was diagnosed as having nonnecrotizing cellulitis. In a prospective
study from 1998, the investigators successfully employed MRI to
differentiate necrotizing from nonnecrotizing infections in 16 of 17 General Management of Nonnecrotizing and Necrotizing
patients (11 of 11 patients with necrotizing fasciitis and five of six Soft Tissue Infection
patients with nonnecrotizing cellulites).19
NONNECROTIZING INFECTION
The finding of soft tissue gas on diagnostic imaging warrants
immediate operative exploration and debridement. Because of the Antibiotic therapy is the cornerstone of treatment for patients
high sensitivity of MRI, necrotizing infection can be excluded with nonnecrotizing infections. Such patients usually require
when no involvement of the superficial fascia, subcutaneous tissue, antibiotics that are effective against group A streptococci or S.
or the deeper cutaneous layers is demonstrated. However, the aureus. The prevalence of community-acquired methicillin-resis-
inflammatory changes seen on MRI when necrotizing soft tissue tant S. aureus (MRSA) strains has increased significantly. These
infection is present may also be seen in patients with nonnecrotiz- strains now outnumber methicillin-sensitive strains by a two-to-
ing infections, as well as in those with other inflammatory condi- one margin.21 This development has necessitated a change in the
tions affecting the deep soft tissues. Because of the relatively low empirical treatment of these infections. Topical, oral, or intra-
specificity of this study, biopsy of the deeper cutaneous layers, with venous preparations may be employed, depending on the nature
frozen-section examination and culture, may be needed to diag- and severity of the disease process [see Management of Specific


Nonoperative Measures

Patients with necrotizing soft tissue infections frequently present
with tachycardia and hypotension, reflecting depleted intravascular
volume and possible septic shock. Such patients often exhibit
extensive extracellular fluid sequestration within the affected area,
as well as more generalized sequestration resulting from sepsis. A
balanced isotonic electrolyte solution, such as lactated Ringer solu-
tion (or 0.9% normal saline, for patients with renal dysfunction),
is administered to replace these fluid deficits. The adequacy of
intravascular volume repletion is often assessed by monitoring vital
signs and urinary output; however, it sometimes proves necessary
to use a central venous catheter to monitor central venous or pul-
monary arterial pressure in patients with associated myocardial
dysfunction, septic shock, chronic pulmonary disease, renal insuf-
ficiency, or other severe chronic illnesses.
Hyponatremia is usually corrected by infusing isotonic fluids.
Hypocalcemia, which can result from calcium precipitation in
Figure 3 Upper-extremity x-ray of a patient with necrotizing patients with extensive fat necrosis, is usually corrected by admin-
soft tissue infection demonstrates soft tissue gas outlining the istering I.V. calcium gluconate. Hyperglycemia is corrected with
muscles. insulin, given either via subcutaneous injection or, for patients with
more severe abnormalities, via I.V. infusion. Lactic acidosis gener-
ally responds to fluid administration. Renal function is assessed by
measuring blood urea nitrogen (BUN) and serum creatinine con-
centrations. CK levels should be monitored and a qualitative eval-
uation of urine myoglobin done if muscle necrosis is suspected or
renal failure is present. Myoglobinuria and elevated CK levels are

Patient requires treatment for necrotizing
soft tissue infection

Replace fluid deficits with lactated Ringer
solution or 0.9% NS.
If patient is anemic, give RBCs.
Initiate broad-spectrum antibiotic therapy.

Figure 4 Lower-extremity MRI of a patient with necrotizing
fasciitis of the left leg demonstrates inflammatory changes typical
of necrosis.
Hypotension persists Hypotension resolves

Insert central venous or
Soft Tissue Infections, below]. If polymicrobial infection is suspect- pulmonary arterial catheter.
ed, broad-spectrum antimicrobial agents should be given, either
alone or in combination.
NECROTIZING INFECTION

Management of necrotizing soft tissue infections is predicated Patient shows evidence Patient shows no
on early recognition of symptoms and signs and on emergency of septic shock evidence of septic
shock
operative debridement. Once the diagnosis of necrotizing soft tis-
sue infection is established, patient survival and limb salvage are Administer vasoactive agents:
• Dopamine, 5–10 μg/kg/min, or
best achieved by means of prompt operation; precise identification
• Norepinephrine, 0.02–0.08
of the causative bacteria and correct assignment of the patient to a μg/kg/min, or
specific clinical syndrome are unnecessary.The delay between hos- • Vasopressin, 0.1–0.4 IU/min
pital admission and initial debridement is the most critical factor
influencing morbidity and mortality: a number of reports have
demonstrated a strong correlation between survival and the inter-
val between onset of symptoms and initial operation.9,22-24
The components of treatment of necrotizing soft tissue infection Perform operative debridement.
are (1) resuscitation and correction of fluid and electrolyte disor-
ders, (2) physiologic support, (3) broad-spectrum antimicrobial
therapy, (4) urgent and thorough debridement of necrotic tissue, Figure 5 Algorithm outlines treatment of necrotizing soft tissue
and (5) supportive care [see Figure 5]. infection.


Table 3 I.V. Antibiotic Dosages for Adult Pathogenesis of Soft Tissue Infections, below], improved leukocyte
Patients with Necrotizing Soft Tissue Infection function, and attainment of tissue oxygen levels that are bacterici-
dal for Clostridium perfringens and bacteriostatic for other anaerobic
and Normal Renal Function bacteria. Hyperbaric oxygen does not, however, neutralize exotox-
in that has already been released.25 At present, except for some
Ampicillin-sulbactam 3 g q. 6 hr data from retrospective studies, there is little evidence supporting
Imipenem-cilastatin 500–750 mg q. 6 hr the benefits of hyperbaric oxygen therapy. Such therapy has not
Single agents Meropenem 1–2 g q. 8 hr been demonstrated to improve survival or to bring about earlier
Piperacillin-tazobactam 3.375 g q. 6 hr resolution of necrotizing soft tissue infection, and it has been asso-
Ticarcillin-clavulanate 3.1 g q. 6 hr
ciated with barotrauma, pneumothorax, and oxygen toxicity.
Aerobic/facultative coverage Accordingly, we believe that operative debridement should not be
Ampicillin 2 g q. 6 hr delayed to accommodate hyperbaric oxygen therapy and that such
Cefotaxime 1–2 g q. 8 hr therapy should not be considered a substitute for complete
Ceftazidime 1 g q. 8 hr
Cefuroxime 1.5 g q. 8 hr debridement of infected nonviable tissues.
Ciprofloxacin 400 mg q. 12 hr I.V. antimicrobial therapy is indicated in all patients with necro-
Agents used in
Daptomycin 4 mg/kg q. 24 hr tizing soft tissue infections [see Table 3]. Such therapy is important,
combination Gentamicin 1.7 mg/kg q. 8 hr or but it is not a substitute for prompt and adequate operative
regimens 5.1 mg/kg q. 24 hr
Linezolid 600 mg q. 12 hr debridement. Necrotizing soft tissue infections are most often
Moxifloxacin 400 mg q. 24 hr caused by a mixed polymicrobial bacterial flora [see Table 4].
Tigecycline 100 mg initially; then Approximately 25% to 30% of necrotizing soft tissue infections are
50 mg q. 12 hr monomicrobial. Although S. pyogenes is the bacterium most fre-
Vancomycin 1 g q. 12 hr
Anaerobic coverage quently involved, the microbiology of the infections often cannot
Clindamycin 600–900 mg q. 8 hr be accurately predicted before final identification of organisms on
Metronidazole 500 mg q. 6 hr culture. Thus, the empirical antibiotic regimen chosen should be
effective against a diverse group of potential pathogens.26 In addi-
tion, because these patients have a high incidence of associated
suggestive of myonecrosis. Anemia is treated with packed red nosocomial infections and even of metastatic infections, it is
blood cell transfusions. important to ensure that the dosage is high enough to achieve ade-
Patients whose hypotension does not resolve with appropriate quate serum concentrations.9,23 Once the results of intraoperative
intravascular fluid resuscitation often experience septic shock. In culture and antimicrobial sensitivity testing become available,
these circumstances, low dosages of I.V. dopamine (5 to 10 antibiotic therapy is adjusted accordingly. This adjustment can be
μg/kg/min), vasopressin (0.1 to 0.4 IU/min), or norepinephrine challenging, in that all of the pathogens identified must be treated.
(0.02 to 0.08 μg/kg/min) are useful for raising blood pressure and I.V. antimicrobial therapy is continued until operative debride-
improving myocardial function. ment is complete, there is no further evidence of infection in the
Patients with traumatic wounds or other contaminated sites involved tissues, and signs of systemic toxicity have resolved.
should receive tetanus toxoid or human tetanus immunoglobulin, Topical antiseptic agents (e.g., Dakin solution and Burrow solu-
depending on their immunization status. tion) may help control infection that progresses despite adequate
Hyperbaric oxygen has been advocated as adjunctive therapy for debridement and I.V. antibiotics.Topical application of mycostatin
extensive necrotizing infections, particularly those caused by powder may help control progressive fungal infection. When
clostridia.25 The beneficial properties of hyperbaric oxygen include patients are able to resume oral intake, they can often be switched
inhibition of bacterial exotoxin production [see Discussion, from I.V. to oral antimicrobial therapy. Antimicrobial therapy
should not, however, be prolonged merely because oral agents are
available.
Table 4 Organisms Causing Necrotizing
Soft Tissue Infection Operative Treatment
The most critical factors for reducing mortality from necrotiz-
Gram-positive ing soft tissue infections are early recognition and urgent operative
Group A Streptococcus debridement.9,22,24,27 The extent of debridement depends on intra-
Enterococcus species operative findings and cannot be accurately predicted before oper-
Staphylococcus aureus ation. Operative intervention helps limit tissue damage by remov-
Group B Streptococcus ing necrotic tissue, which serves as a nidus for infection.
Bacillus species Thorough exploration is necessary to confirm the diagnosis of
Gram-negative necrotizing soft tissue infection and determine the degree of
Aerobes
Escherichia coli involvement. Aggressive, widespread debridement of all apparent
Pseudomonas aeruginosa
necrotic, infected tissue is essential; antibiotics will not penetrate
Enterobacter cloacae
Klebsiella species
dead tissues.The underlying necrosis of subcutaneous tissues, fas-
Serratia species cia, and muscle typically extends beyond the obvious limits of cuta-
Acinetobacter calcoaceticus neous involvement. Operative debridement should therefore be
Vibrio vulnificus continued until viable tissue is reached. In most instances, the
involved tissues are easily separated from their surrounding struc-
Bacteroides species
tures.The presence of “dishwater pus” and noncontracting muscle
Anaerobes Clostridium species
Peptostreptococcus species
are additional indicators of necrotizing infection. The presence of
arterial bleeding generally indicates that tissues are viable; in the


absence of arterial bleeding, tissues are nonviable even if venous cera. Some have advocated using biologic materials or absorbable
bleeding is present.With deep necrotizing infections, debridement mesh for restoration of abdominal wall continuity; however, we
of the necrotic fascia and muscle may create large skin flaps that prefer to use permanent mesh in most circumstances, especially
are poorly perfused. It is best to preserve as much viable skin and when omentum is available for interposition between the mesh and
subcutaneous tissue as possible because these tissues can be essen- the small intestine.9
tial for later coverage of the wound. Nonviable skin, however, Mortality from necrotizing soft tissue infection ranges from 21%
should be resected. to 29%.9,22,24,27,28 Risk factors for mortality include age greater
Wound drainage or exudate should be submitted for Gram than 60 years, the presence of associated chronic illnesses, a rela-
staining, as well as for aerobic, anaerobic, and fungal cultures and tively high percentage of total body surface area involved, and,
antimicrobial sensitivity testing. Fasciotomy is rarely required.The most important, delays in recognition and treatment.9,22,24 Patients
presence of subcutaneous gas extending beyond areas of nonviable with truncal involvement or positive blood cultures also have a
tissue does not necessitate debridement if the surrounding tissues higher mortality.22,28
are viable. It is sometimes helpful to perform an exploratory inci-
sion over an area beyond the limits of debridement when it is
uncertain whether necrosis is undermining viable skin. If no necro- Management of Specific Soft Tissue Infections
tizing infection is found, the incision may be closed primarily. Normal skin functions as a protective barrier that prevents
Reexploration should be routinely performed within 24 to 48 microorganisms from causing soft tissue infection.The skin is made
hours to ensure that all necrotic tissue has been debrided. up of two layers, the epidermis and the dermis [see Figure 6]. The
Debridement is repeated as necessary until the infection is con- epidermis, the outer avascular epithelial layer, functions as a per-
trolled. If repeated debridement does not control infection, if there meability barrier for the rest of the body. The dermis, the inner
are persistent, fulminant infections of the extremities, or if an layer, contains blood vessels, lymphatic vessels, sweat and seba-
extremity remains nonfunctional after debridement has been com- ceous glands, and hair follicles. The subcutaneous tissue separates
pleted, amputation can be lifesaving. Amputation is most often the skin from the deep fascia, muscle, and bone.Typically, soft tis-
required for patients with clostridial myonecrosis and for diabetic sue infections result from disruption of the skin by some exogenous
patients with necrotizing infections.24 In two large series of patients factor; less commonly, they result from extension of a subjacent
with necrotizing soft tissue infections, the incidence of amputation infection or hematogenous spread from a distant site of infection.
was approximately 15% to 25%.9,22
SUPERFICIAL INFECTIONS
Patients with necrotizing soft tissue infections involving the per-
ineum and perirectal areas may need a diverting colostomy to pre- Superficial infections constitute the majority of soft tissue infec-
vent tissue contamination resulting from defecation and to control tions. They primarily involve the epidermis or dermis (pyoderma)
local infection. Overall, this measure is required in fewer than 25%
of cases.9
After debridement, the exposed areas should be treated with
0.9% normal saline wet-to-dry dressings. Once the initial infection
has been controlled and debridement is no longer necessary, dress-
ing changes can often be performed at the bedside after sufficient
analgesics have been given to achieve adequate pain management.
Patient-controlled analgesia is frequently useful early in the course
of treatment. Propofol or ketamine can be given in the intensive
care unit to facilitate pain control during dressing changes. Epidermis
Early enteral or parenteral nutritional support should be insti-
tuted to optimize recovery. Nutritional support should begin once
resuscitation is complete, the infection is adequately controlled, Papillary
and the signs of sepsis have resolved. Because it frequently proves Dermis
necessary to return the patient to the operating room, enteral feed-
ing tubes should be placed beyond the pylorus so that enteral Dermis
nutrition can be provided without interruption. Alternatively, par-
enteral nutrition may be employed.
Reticular
Once the localized infection is under control and the patient is Dermis
recovering, the exposed soft tissues should be covered.This is most
commonly done with split-thickness skin grafting, though other
reconstructive procedures (e.g., rotational flaps) [see 3:7 Surface Superficial
Fascia
Reconstruction Procedures] can be effective in this setting as well.
Subcutaneous
Vacuum-assisted closure devices can reduce the exposed surface
Tissue
area and lessen the need for skin graft coverage. Exposed tendons, Deep
nerves, or bone often should be covered with full-thickness skin to Fascia
prevent desiccation and preserve limb function. Premature closure Muscle
of highly contaminated or persistently infected sites usually fails and
leads to recurrence of infection and a greater likelihood of death.
When the abdominal or chest wall has been excised to control
infection, reconstruction is necessary. Prosthetic mesh is useful for
restoring continuity of the abdomen or the chest wall, and overly- Figure 6 Depicted is the normal anatomy of the skin and the
ing moist dressings can help prevent desiccation of underlying vis- deeper cutaneous layers.6


The diagnosis is established by Gram stain and culture of the
Table 5 Topical and Oral Antibiotic Agents vesicular fluid or the crusted plaque. The skin lesions usually
Used for Superficial Soft Tissue Infections* resolve spontaneously within 2 to 3 weeks.31 Antibiotic therapy
accelerates the resolution of these lesions. Mupirocin ointment
Mupirocin ointment (2%), applied to affected area t.i.d.† (2%) is applied topically three times a day until the lesions clear.
Erythromycin ointment (2%), applied to affected area b.i.d.† This agent possesses excellent in vitro activity against both staphy-
Clindamycin gel or lotion (1%), applied to affected area b.i.d.† lococci and streptococci and achieves high rates of cure in patients
Gentamicin cream or ointment (0.1%), applied to affected area t.i.d. with localized disease. Erythromycin and clindamycin ointments
or q.i.d. are acceptable alternatives [see Table 5]. For patients who have dis-
Penicillin V, 250–500 mg q.i.d. (pediatric: 25–50 mg/kg in divided
doses q.i.d.) seminated impetigo or impetigo of the scalp or mouth and those in
Amoxicillin, 250–500 mg t.i.d. (pediatric: 20–30 mg/kg/day p.o. in whom topical therapy fails, an oral antibiotic (e.g., dicloxacillin,
divided doses t.i.d.) cephalexin, cefadroxil, erythromycin, or clindamycin) may be used
Dicloxacillin, 250–500 mg q.i.d. (pediatric: 12.5–25.0 mg/kg/day in [see Table 5]. A 7-day course of oral antibiotic therapy is usually
divided doses q.i.d.)
sufficient.31
Cephalexin, 250–500 mg q.i.d. (pediatric: 25–100 mg/kg/day in
divided doses q.i.d.)
Cefadroxil, 500–1,000 mg b.i.d. (pediatric: 30 mg/kg/day in divided Erysipelas Erysipelas is an acute bacterial infection that prin-
doses b.i.d.) cipally involves the dermis. It is almost invariably caused by S. pyo-
Erythromycin, 250–500 mg q. 6 hr (pediatric: erythromycin ethyl genes. Most cases are preceded by influenzalike symptoms.
succinate, 40 mg/kg in divided doses q.i.d.)
Clindamycin, 150–450 mg q.i.d. (pediatric: 20 mg/kg/day in divided
Infection extends through the dermal lymphatic vessels and is typ-
doses t.i.d. or q.i.d.) ically manifested by a tender, pruritic, intensely erythematous,
Trimethoprim-sulfamethoxazole, 160/800 mg b.i.d. sharply demarcated, and raised plaque. Patients complain of pain,
Amoxicillin-clavulanate, 500 mg t.i.d. (pediatric: 40 mg/kg/day in often in conjunction with high fever, increased skin warmth, and
divided doses t.i.d.) leukocytosis. Lymphangitis and lymphadenopathy are sometimes
Ciprofloxacin, 500 mg p.o., b.i.d.
present as well. The leg is the most common site of involvement,
*All dosages are for patients with normal renal function.
but erysipelas may also occur on the face, the arms, and the upper
†Adult dosage and pediatric dosage are the same. thighs.
The factors predisposing to the development of erysipelas of the
extremity include local conditions such as tinea pedis (athlete’s
foot), leg ulcers, and venous stasis dermatitis.32 Erysipelas tends to
or the subcutaneous tissue (cellulitis) and secondarily occur in skin be more common in the presence of associated conditions such as
damaged by animal or human bites. Nonnecrotizing superficial lymphedema, diabetes mellitus, alcoholism, immunocompromise,
soft tissue infections are principally treated with antibiotics. and obesity,30,32 and it is more likely to recur in patients with these
Necrosis is rare but may develop in superficial infections that are associated diseases and in those whose underlying skin conditions
inadequately treated or neglected. are inadequately treated. Erysipelas recurs in 10% of patients with-
in 6 months of their first episode and in 30% within 3 years.32
Pyoderma The standard antibiotic treatment for uncomplicated erysipelas
Pyoderma is a general term referring to a bacterial infection of is penicillin, which is effective in at least 80% of cases. Oral and
the skin. It may be divided into several subcategories, including intravenous antibiotic regimens are equally efficacious. Amoxicillin
impetigo, erysipelas, folliculitis, and furuncles and carbuncles. appears to work as well as penicillin. Patients with erysipelas of the
lower extremity should be placed on bed rest, and the involved leg
Impetigo Impetigo is a highly contagious bacterial infection should be elevated to reduce edema and pain. Once the patient is
that is confined to the epidermis and that usually involves the face able to resume normal activities, he or she should be fitted with
or the extremities. It is most common in infants and preschool chil- elastic stockings, which help reduce the occurrence of edema and
dren and is seen more frequently in patients with preexisting skin lower the risk of lymphedema. For patients with tinea pedis, a top-
conditions (e.g., eczema, atopic dermatitis, varicella infection, ical antifungal agent is used to treat the infection and prevent
angular cheilitis, and scabies).Warm and humid weather, crowded recurrence.
living conditions, and poor hygiene can all contribute to the devel-
opment of impetigo.29 The dominant pathogen is S. aureus, which Folliculitis Folliculitis is an infection of the hair follicle that is
causes either a bullous or a nonbullous form of the disease; a less typically caused by S. aureus. It is characterized by a painful, ten-
common pathogen is S. pyogenes, which causes a nonbullous der, erythematous papule with a central pustule. A shaft of hair is
form.30 often seen in the center of the pustule. Shaving, plucking, waxing,
Impetigo usually occurs in areas of skin breakdown, though S. heat and humidity, the use of corticosteroids or antibiotics,
aureus may give rise to de novo infection in normal skin. Bullous immunosuppression, and occlusion of the skin by clothing, adhe-
impetigo is manifested by numerous blisters or bullae that rapidly sives, or plastics may predispose to folliculitis.29 Single or multiple
become pustules, then rupture within 1 to 2 days to form a thick, lesions may occur in the skin of any hair-bearing area. If the pus-
honey-colored, crusted plaque that remains for days to weeks. tule ruptures, superficial erosion often ensues. Infection that prin-
Nonbullous impetigo is characterized by erythema and tiny, less cipally involves the deeper part of the hair follicle is characterized
prominent vesicles that progress to crusted erosions in the skin. by a tender, swollen papule without an associated pustule at the
The skin lesions are intensely pruritic, and local spread may occur skin surface.
as a result of scratching and release of infected fluid from the blis- In rare cases, folliculitis is caused by pathogens other than S.
ters, bullae, or vesicles. Associated regional lymphadenopathy is aureus, such as Pseudomonas aeruginosa, Klebsiella species,
common. Glomerulonephritis may complicate streptococcal- Enterobacter species, Proteus species, yeasts, and fungi. Pseudomonas
induced impetigo.30,31 folliculitis usually results from exposure to inadequately chlorinat-


ed water in swimming pools, hot tubs, or whirlpools. Patients with
this infection have multiple papular or pustular lesions on the back, Table 6 Risk Factors for Soft Tissue Infection
the buttocks, and the extremities, along with fever and malaise
Complicating Animal or Human Bite
appearing 6 hours to 3 days after exposure.31,33 Organisms may be
cultured either from the pustules or from the infected water.
Location on the hand or the foot Immunosuppression
Klebsiella, Enterobacter, and Proteus species can cause folliculitis in or over a major joint Chronic alcoholism
patients receiving long-term antibiotic therapy for acne vulgaris.30 Location on the scalp or the face Diabetes mellitus
Yeast folliculitis and fungal folliculitis tend to occur in immuno- of an infant
Corticosteroid use
compromised patients.30 Puncture wound
Preexisting edema in an
In most patients, folliculitis resolves spontaneously within 7 to Delay in treatment lasting longer affected extremity
than 12 hr
10 days.31 Topical therapy with clindamycin, erythromycin, or
mupirocin ointments or benzoyl peroxide in combination with
warm soaks may accelerate resolution [see Table 5]. Isotretinoin can
be used to treat gram-negative folliculitis. Gentamicin cream may An incision-and-drainage procedure is recommended when a
be helpful in drying out the pustular lesions in patients with fluctuant carbuncle is present. A thorough search for loculated
Pseudomonas folliculitis. areas should be undertaken to facilitate drainage of deeper accu-
In patients with refractory or disseminated follicular infections, mulations of pus and to ensure adequate treatment. Wide local
oral antibiotic therapy is indicated.When S.aureus is considered the excision of the involved skin and subcutaneous fat is often neces-
most likely pathogen, trimethoprim-sulfamethoxazole, a tetracy- sary to prevent recurrent disease. An oral antistaphylococcal agent
cline, or clindamycin should be given, in view of the high preva- should be given. All patients with hair follicle infections should
lence of MRSA21,34; an oral quinolone is indicated for the treatment cleanse the site with chlorhexidine or an iodine-containing solution.
of gram-negative folliculitis [see Table 5]. Elimination of predispos-
ing factors is important for reducing the likelihood of recurrence. Infections Developing in Damaged Skin
Damage to skin as a result of animal or human bites predispos-
Furuncles and carbuncles Furuncles and carbuncles are es patients to soft tissue infection. An estimated 50% of all
deeper infections of the hair follicle that extend beyond the follicle Americans will be bitten by an animal or by another human being
to involve the subcutaneous tissue. For both, S. aureus is the usual during their lifetime.35 Animal and human bites account for
causative organism. approximately 1% of all emergency department visits.35 Soft tissue
A furuncle, or boil, is a small abscess, manifested as a firm, ten- infection is the most common complication of such bites.The risk
der, erythematous nodule that tends to occur in skin areas exposed of infection depends on the type of bite, the site of injury, the time
to friction (e.g., the inner thighs and the axilla). Furuncles also may elapsed from the bite until presentation, host factors, and the man-
occur on the face, the neck, the upper back, and the buttocks. agement of the wound [see Table 6].
Possible predisposing factors include increased friction and perspi- Most animal and human bites produce minor injuries for which
ration (as seen in obese individuals or athletes), corticosteroid use, patients do not seek medical attention.The overall risk of infection
diabetes mellitus, and inherited or acquired defects in neutrophil after a bite is estimated to be 5% to 15%36; however, among the
function.29,31 subset of patients who seek medical attention, estimated infection
Initial treatment consists of applying warm compresses to help rates range from 2% to 20% for dog bites, from 30% to more than
promote drainage and administering an oral antimicrobial agent 50% for cat bites, and from 10% to 50% for human bites.37 Most
that is effective against S. aureus (e.g., dicloxacillin, cephalexin, patients with an infected bite can be managed on an outpatient
cefadroxil, erythromycin, or clindamycin for infections presumed basis with oral antibiotic therapy and elevation of the involved site.
to be caused by methicillin-sensitive strains; trimethoprim-sul-
famethoxazole, a tetracycline, or clindamycin for suspected MRSA Animal bites In the United States, dog bites account for
infections) [see Table 5].With time, the furuncle becomes fluctuant, 80% to 90% of all animal bites, cat bites for 3% to 15%.37,38
and the pus coalesces at the skin surface. An incision-and-drainage Nondomestic animals are responsible for only 1% to 2% of all ani-
procedure is necessary when these lesions do not drain sponta- mal bites. Patients with infections resulting from animal bites typ-
neously. This procedure should be performed with local anesthe- ically present with significant pain, soft tissue swelling, and tender-
sia, and care should be taken to open the abscess cavity complete- ness; they may also have associated injuries to nerves, tendons,
ly. Lesions that have drained spontaneously should be examined to bones, joints, or blood vessels. Bites involving the hand are associ-
confirm that the cavity has been opened sufficiently. Failure to ated with an increased risk of tenosynovitis, septic arthritis, and
drain these lesions adequately may result in recurrence, as well as abscess formation.37
in progression to a more serious infection. Infections that occur after a dog or cat bite are usually polymi-
A carbuncle is a deep cutaneous infection involving multiple crobial, involving a mixture of aerobes and anaerobes [see Table 7].
hair follicles that is characterized by destruction of fibrous tissue P multocida is the major pathogen, isolated from 50% to 80% of
.
septa and consequent formation of a series of interconnected infections related to cat bites and from 25% of those related to dog
abscesses. It is typically manifested by a painful, red, tender, bites.35,37 Infection with P multocida is characterized by the acute
.
indurated area of skin with multiple sinus tracts. Systemic mani- onset of severe pain, tenderness, and swelling, usually within 12 to
festations (e.g., fever and malaise) are common. Carbuncles occur 18 hours of the bite. In rare cases (usually involving immunocom-
most frequently on the nape of the neck, the upper part of the promised patients), Capnocytophaga canimorsus causes soft tissue
back, or the posterior thigh. The thickness of the overlying skin in infection after a dog or cat bite. C. canimorsus infection can be quite
these areas leads to lateral extension of the infection and locula- serious, leading to overwhelming sepsis; the associated mortality is
tion. Patients commonly present with relatively large skin lesions 25% to 30%.37-39
that represent a confluence of inflammatory nodules.These lesions Wounds resulting from animal bites should immediately be
are associated with chronic drainage, sinus tracts, and scarring. washed with soap and water.When seen early, dog bites should be


copiously irrigated, debrided, and, in most circumstances, closed. species are more common [see Table 7]. Unlike the anaerobic
Infected wounds, wounds older than 12 hours, cat bites, and bites pathogens in dog and cat bites, however, those involved in human-
on the hand should be left open. In all cases of infection related to bite infections often produce β-lactamases.37 The predominant
an animal bite, aerobic and anaerobic cultures should be obtained aerobic organisms in human-bite infections are S. aureus,
from the site of infection.Tetanus immune status should be deter- Staphylococcus epidermidis, α- and β-hemolytic streptococci,
mined, and immunization against tetanus should be provided Corynebacterium species, and E.corrodens.E.corrodens is a fastidious
when appropriate. In cases of bites from nondomestic carnivores facultative aerobic gram-negative rod that is cultured from approx-
(e.g., bats, skunks, raccoons, foxes, or coyotes), wounds should be imately 25% of clenched-fist injuries and frequently causes a
irrigated with povidone-iodine to reduce the transmission of chronic indolent infection.37 It typically is susceptible to amoxi-
rabies, and immunization against rabies should be provided. cillin-clavulanate, trimethoprim-sulfamethoxazole, doxycycline,
Patients with established soft tissue infection and patients with and ciprofloxacin but resistant to dicloxacillin, nafcillin, first-gen-
noninfected bites who have risk factors for infection should receive eration cephalosporins, clindamycin, and erythromycin. Other
antibiotic therapy [see Table 6]. A broad-spectrum antibiotic effec- pathogens may also be transmitted as a result of contact with blood
tive against aerobic and anaerobic organisms should be chosen [see or saliva, including hepatitis B and C viruses, Mycobacterium tuber-
Table 5]. Amoxicillin-clavulanate is the antibiotic of choice because culosis, and, possibly, HIV.
of its broad spectrum of activity against common pathogens; Management of human-bite wounds is similar to that of animal-
trimethoprim-sulfamethoxazole, doxycycline, and ciprofloxacin bite wounds. The wound must be thoroughly irrigated, preferably
are also used [see Table 5]. Infections secondary to P multocida
. with 1% povidone-iodine, which is both bactericidal and viricidal.
respond to oral treatment with penicillin V, amoxicillin, cefurox- Puncture bite wounds should be irrigated with a small catheter to
ime, or ciprofloxacin.37 Infections secondary to C. canimorsus achieve high-pressure irrigation. If the wound appears infected,
respond to penicillin, ampicillin, ciprofloxacin, erythromycin, or aerobic and anaerobic cultures are obtained. Devitalized tissue
doxycycline. Whether antibiotics are indicated for a fresh animal should be debrided, and the wound should be left open, whether
bite in a patient with a low risk of infection is controversial. infected or not. The injured extremity should be immobilized and
Because it is difficult to predict which bite wounds will become elevated.
infected, some experts advocate routine antibiotic treatment of all Because of the high degree of contamination and local tissue
dog bites for at least 3 to 5 days.35 damage associated with human-bite wounds to the hand, antimi-
crobial therapy is indicated for all such injuries. A prospective, ran-
Human bites Human bites may be classified as either occlu- domized study of 45 patients with human bites to the hand seen
sional bites (in which teeth puncture the skin) or clenched-fist within 24 hours after injury and without evidence of infection, ten-
injuries (in which the hand is injured after contact with teeth).37,39 don injury, or joint capsule penetration demonstrated that infec-
Occlusional bites carry roughly the same risk of infection as animal tion developed in 47% of the patients who did not receive antibi-
bites, except when they occur on the hand. Clenched-fist injuries otics but in none of those who did.40 Patients with an uncompli-
and all hand injuries are associated with a higher risk of infection. cated human bite to the hand should receive a broad-spectrum
Clenched-fist injuries typically occur at the third metacarpopha- oral antimicrobial agent, such as amoxicillin-clavulanate (or doxy-
langeal joint. Penetration of the metacarpophalangeal joint capsule cycline if they are allergic to penicillins).
may occur, with subsequent development of septic arthritis and Patients with human-bite wounds at sites other than the hand
osteomyelitis.35 who have risk factors for infection [see Table 6] should also receive
Soft tissue infections resulting from human bites are polymicro- antimicrobial therapy. However, minor bite wounds in patients
bial, involving a mixture of aerobes and anaerobes. On average, five who have no risk factors for infection do not call for antibiotic ther-
different microorganisms are isolated from a human-bite apy. As with animal-bite wounds, tetanus immunization status
wound37—significantly more than are usually isolated from an ani- should be determined, and tetanus toxoid, tetanus immunoglobin,
mal-bite wound. In addition, the concentration of bacteria in the or both should be administered as indicated.
oral cavity is higher in humans than in animals.The anaerobic bac- Patients with systemic manifestations of infection (e.g., fever or
teria isolated from human-bite wounds are similar to those that chills); severe cellulitis; compromised immune status; diabetes
cause infection after dog and cat bites, except that Bacteroides mellitus; significant bites to the hand; associated joint, nerve, bone,
or tendon involvement; or infection refractory to oral antibiotic
therapy should be admitted to the hospital for I.V. antibiotic ther-
Table 7 Organisms Most Frequently Isolated apy.37 Appropriate choices for I.V. treatment include cefoxitin,
cefotetan, and piperacillin-tazobactam. Tenosynovitis, joint infec-
from Dog- and Cat-Bite Wounds tions, and associated injuries to deep structures must also be treat-
ed if present.
Pasteurella multocida
Corynebacterium species Cellulitis
Aerobes Staphylococcus species Cellulitis is an acute bacterial infection of the dermis and the
Streptococcus species
subcutaneous tissue that primarily affects the lower extremities,
Capnocytophaga canimorsus (rare)
though it can affect other areas as well (e.g., the periorbital, buccal,
Bacteroides species and perianal regions; the areas around incisions; and sites of body
Prevotella species piercing).41 The most common causes of cellulitis are (1) soft tis-
Porphyromonas species sue trauma from injection of illicit drugs, puncture wounds from
Anaerobes Peptostreptococci foreign bodies or bites (animal, human, or insect), or burns; (2)
Fusobacterium species
surgical site infection; and (3) secondary infection of preexisting
Bacteroides fragilis
skin lesions (e.g., eczema; tinea pedis; and decubitus, venous sta-
Veillonella parvula
sis, or ischemic ulcers). Less common causes include extension of


a subjacent infection (e.g., osteomyelitis) and bacteremia from a Table 8 Suggested Parenteral Antibiotic Regimens
remote site of infection. Predisposing factors for the development for Treatment of Cellulitis in Adults
of cellulitis include lymphatic disruption or lymphedema, intersti-
tial edema, previous irradiation of soft tissue, diabetes mellitus,
immunocompromise, and peripheral vascular disease. Agent I.V. Dosage

Nafcillin 2 g q. 4 hr
Nonnecrotizing The overwhelming majority of patients with
cellulitis have a nonnecrotizing form of the disease. Patients typi- Cefazolin 1–2 g q. 8 hr
cally present for medical attention because of pain and soft tissue Clindamycin 600–900 mg q. 8 hr
erythema, and they often have constitutional symptoms (e.g.,
fever, chills, or malaise). Physical examination reveals erythema Vancomycin 1 g q. 8 hr
with advancing borders, increased skin warmth, tenderness, and Ampicillin-sulbactam 3 g q. 6 hr
edema. Lymphangitis may also be present, manifested as an ery-
thematous linear streak that often extends to a draining lymph
node basin; associated lymphadenopathy, fever, and leukocytosis Patients who are diabetic or immunocompromised and those
with a shift to immature forms may be apparent. who have high fever and chills, rapidly spreading cellulitis, or cel-
Cellulitis is usually caused by a single aerobic pathogen. The lulitis that is refractory to oral antibiotic therapy should be admit-
organisms most frequently responsible for cellulitis in otherwise ted to the hospital for I.V. antibiotic therapy [see Table 8]. Nafcillin
healthy adults are S. pyogenes and S. aureus. Of the two, S. pyogenes is the preferred I.V. agent. Cefazolin or piperacillin-tazobactam
is the more common and is the usual pathogen in patients with should be added if gram-negative organisms are suspected
associated lymphangitis. S.aureus is usually present in patients with pathogens, as when cellulitis complicates a decubitus or a diabetic
underlying chronic skin disease. Other microorganisms may cause foot ulcer.Vancomycin, tigecycline, linezolid, or gentamicin should
cellulitis on rare occasions but usually only in specific clinical cir- be given to patients with MRSA infections and those with serious
cumstances. Haemophilus influenzae sometimes causes cellulitis in penicillin allergies.
children or adults infected with HIV.42 Streptococcus pneumoniae
may cause this condition in patients with diabetes mellitus, alco- Necrotizing Necrotizing cellulitis is similar to nonnecrotizing
holism, nephrotic syndrome, systemic lupus erythematosus, or cellulitis in etiology and pathogenesis but is more serious and pro-
hematologic malignancies.43 P multocida may cause cellulitis as a
. gressive. Necrosis generally occurs when the infection is neglected
complication of dog or cat bites. S. epidermidis is a recognized cause or inadequately treated. The microbiology of necrotizing cellulitis
of cellulitis among immunocompromised patients, including those is also similar to that of nonnecrotizing cellulitis, except that C. per-
with HIV infection and those receiving organ transplants.44 V vul-. fringens and other clostridial species may be involved when necro-
nificus occasionally causes cellulitis in patients who have ingested sis is present. In addition to antimicrobial therapy [see Table 8],
raw seafood or who have experienced minor soft tissue trauma and urgent operative debridement is indicated. In other respects,
are exposed to sea water.41 A. hydrophila may cause cellulitis in necrotizing cellulitis is treated in much the same way as deep
patients with soft tissue trauma who are exposed to brackish or necrotizing infections are (see below). In some patients with necro-
fresh water, soil, or wood.41 Cellulitis that complicates decubitus or tizing fasciitis, the skin is involved secondarily.
other nonhealing ulcers is usually a mixed infection that includes
DEEP NECROTIZING INFECTIONS
gram-negative organisms.
In most situations, cellulitis is treated with empirical antibiotic Infections that involve the soft tissues deep to the skin tend to
regimens that include agents effective against S. pyogenes and S. become apparent after necrosis has developed. It is possible that
aureus. Attempts to isolate a causative pathogen are usually unsuc- deep necrotizing infections begin without necrosis but progress
cessful; needle aspiration and skin biopsy at an advancing margin rapidly as a result of intrinsic factors. Alternatively, such infections
of erythema are positive in only 15% and 40% of cases, respective- may develop as a result of delayed recognition attributable to the
ly.45 Bacteremia is uncommon, and as a result, blood cultures are tissue depth at which the process takes place and the lack of spe-
positive in only 2% to 4% of patients with cellulitis.41,46 Blood cul- cific early signs and symptoms.The relatively poor blood supply to
tures are obtained selectively when the patient has high fever and subcutaneous fat makes this tissue more susceptible to microbial
chills, preexisting lymphedema, or buccal or periorbital cellulitis or invasion. Contamination of the deep soft tissues occurs either
when a saltwater or freshwater source of infection is suspected. In through neglect or inadequate treatment of cutaneous or subcuta-
all of these clinical situations, the prevalence of bacteremia is high- neous infections or through hematogenous seeding of microorgan-
er.46 Radiologic examination should be reserved for patients in isms in an area of injury.
whom it is difficult to exclude a deep necrotizing infection. Most deep necrotizing soft tissue infections are polymicrobial
In an otherwise healthy adult, uncomplicated cellulitis without and occur on the extremities, the abdomen, and the per-
systemic manifestations can be treated with an oral antibiotic on an ineum.9,22,24 Necrotizing infections that involve only muscle are
outpatient basis. Because the vast majority of cellulitides are uncommon; therefore, necrotizing fasciitis can be considered the
caused either by S. pyogenes or by a penicillinase-producing S. paradigm for these infectious processes.
aureus, one of the following agents is usually given: dicloxacillin, The early signs and symptoms of deep necrotizing soft tissue
cephalexin, cefadroxil, erythromycin, or clindamycin. When infection are localized pain, tenderness, mild edema, and erythema
MRSA infection is suspected, trimethoprim-sulfamethoxazole, a of the overlying skin. These characteristics may be subtle, and this
tetracycline, or clindamycin should be administered [see Table 5]. diagnosis may not readily come to mind. Sometimes, there is a his-
The margins of the erythema should be marked with ink to facili- tory of previous injury to the area of suspected infection, which can
tate assessment of the response to treatment. For lower-extremity lead to confusion about the diagnosis. The more classic findings
cellulitis, reduced activity and elevation are important ancillary associated with these infections—skin discoloration, the formation
measures. Appropriate analgesic agents should be given. of bullae, and intense erythema—occur much later in the process.


It is important to understand this point so that an early diagnosis fect environment for clostridial proliferation. A rare form of this dis-
can be made and appropriate treatment promptly instituted. ease occurs in patients with colon cancer in whom myonecrosis
caused by Clostridium septicum develops in the absence of tissue
Necrotizing Fasciitis damage. Myonecrosis may also result from the spread of contigu-
Necrotizing fasciitis is characterized by angiothrombotic micro- ous fascial infections.
bial invasion and liquefactive necrosis.6 Progressive necrosis of the Clostridial myonecrosis has a notably short incubation period:
superficial fascia develops, and the deep dermis and fascia are infil- severe progressive disease can develop within 24 hours of contam-
trated by polymorphonuclear leukocytes, with thrombosis of nutri- ination. This condition is characterized by acute catastrophic pain
ent vessels and occasional suppuration of the veins and arteries in the area of infection, with minimal associated physical findings.
coursing through the fascia; bacteria then proliferate within the Systemic signs of toxicity (e.g., confusion, incontinence, and delir-
destroyed fascia. Initially, tissue invasion proceeds horizontally, but ium) often precede the physical signs of localized infection. The
as the condition progresses, ischemic necrosis of the skin develops, skin initially is pale, then gradually becomes yellowish or bronze.
along with gangrene of the subcutaneous fat and dermis (charac- Blebs, bullae, and skin necrosis do not appear until late in the
terized by progressive skin necrosis, the formation of bullae and course of the disease. Edema and tenderness occur early, and the
vesicles, and occasional ulceration [see Figure 1]). absence of erythema distinguishes clostridial infections from strep-
tococcal infection. A thin serosanguineous discharge is present in
Myonecrosis involved areas and may emanate from an involved incision. Gram
Myonecrosis is a rapidly progressive life-threatening infection of stain reveals gram-positive coccobacilli with few leukocytes.
skeletal muscle that is primarily caused by Clostridium species.The When clostridial myonecrosis is suspected or confirmed, peni-
classic example of myonecrosis is clostridial gas gangrene, a disease cillin G, 2 to 4 million U every 4 hours, should be given immedi-
that was common in World War I soldiers who sustained extremity ately; clindamycin, 900 mg every 8 hours, should be added.When
injuries that were contaminated with soil. Delays in definitive treat- C. septicum is identified on culture, a search for an occult GI tract
ment and the use of primary closure for these contaminated malignancy should be made. Clostridial myonecrosis is the one soft
wounds contributed to the severity and mortality of these infec- tissue infection for which hyperbaric oxygen is recommended,
tions.47 Clostridial myonecrosis may also occur as a deep surgical though as yet, there is little evidence that this modality improves
site infection after contaminated operations, particularly those outcomes. If hyperbaric oxygen therapy is to be used, it should not
involving the GI tract or the biliary tract. Devitalized tissue is a per- be given before operative debridement.

Discussion
Etiology and Classification of Soft Tissue Infection Primary (idiopathic) soft tissue infections occur in the absence
Soft tissue infection commonly results from inoculation of bac- of a known causative factor or portal of entry for bacteria. Such
teria through a defect in the epidermal layer of the skin, such as may infections are uncommon and are believed to result from
occur with injury, preexisting skin disease, or vascular compromise. hematogenous spread or bacterial invasion through small unrecog-
Less commonly, soft tissue infection may be a consequence of nized breaks in the epidermis.48,49 Soft tissue infection caused by V .
extension from a subjacent site of infection (e.g., osteomyelitis) or vulnificus is an example of a primary soft tissue infection: it is attrib-
of hematogenous spread from a distant site (e.g., diverticulitis or C. uted to bacteremia developing after the ingestion of contaminated
septicum infection in patients with colonic carcinoma). It may also raw seafood. Only 10% to 15% of all necrotizing soft tissue infec-
occur de novo in healthy patients with normal-appearing skin, often tions are idiopathic; the remaining 85% to 90% are secondary
as a result of virulent pathogenic organisms.48 infections, developing as a consequence of some insult to the skin
Conditions that disrupt the skin and alter its normal barrier that predisposes to infection. Secondary soft tissue infections may
function [see Table 2] predispose patients to bacterial contamina- be further categorized as posttraumatic, postoperative, or compli-
tion. Host factors may increase susceptibility to infection and limit cations of preexisting skin conditions.
the patient’s ability to contain the bacterial inoculum. Clinically Soft tissue infections are classified as monomicrobial when they
occult infection or inadequate treatment of other conditions may are caused by a single organism and as polymicrobial when they are
also lead to secondary development of soft tissue infection (as is caused by multiple organisms. Most superficial soft tissue infec-
sometimes seen in patients with diverticulitis; perirectal, pilonidal, tions are caused by a single aerobe, usually S. pyogenes or S. aureus.
or Bartholin’s cyst abscesses; strangulated hernias; or panniculitis). Exceptions to this general rule include infections caused by animal
Delayed or inadequate treatment of superficial infections (e.g., fol- or human bites, cellulitis associated with decubitus or other non-
liculitis, furuncles, carbuncles, cellulitis, and surgical site infections) healing ulcers, and infections in immunocompromised patients.
may lead to more severe necrotizing infections. These infections are typically polymicrobial, often involving aero-
Soft tissue infections may be classified as superficial or deep, as bic or facultative gram-negative organisms and anaerobes in addi-
nonnecrotizing or necrotizing, as primary (idiopathic) or section to aerobic gram-positive bacteria.
ondary, and as monomicrobial or polymicrobial. Superficial infec- Deep necrotizing soft tissue infections are polymicrobial 70% to
tions involve the epidermis, dermis, superficial fascia, or subcuta- 75% of the time.They are caused by the synergistic activity of fac-
neous tissue, whereas deep infections involve the deep fascia or ultative aerobes and anaerobes [see Figure 7].50,51 S. aureus, S. pyo-
muscle [see Figure 6]. Necrotizing soft tissue infections are distin- genes, and enterococci are the most common gram-positive aer-
guished by the presence of extensive, rapidly progressing necrosis obes. Escherichia coli is the most common gram-negative enteric
and high mortality. Such infections are termed necrotizing celluli- organism. Bacteroides species and peptostreptococci are the most
tis, necrotizing fasciitis, or myonecrosis according to whether the common anaerobes.9,27,51 The remaining 25% to 30% of deep
deepest tissue layer affected by necrosis is subcutaneous tissue, necrotizing infections are monomicrobial. Most primary necrotiz-
deep fascia, or muscle, respectively. ing soft tissue infections are monomicrobial.48 These infections are


patient factors predispose susceptible individuals to these infec-
tions. Chronic illnesses can contribute to a diminished immuno-
logic response. Peripheral vascular disease impairs the local blood
and oxygen supply. Diabetes mellitus inhibits WBC function.
Chronic pulmonary disease can result in systemic hypoxemia.
Patients with congestive heart failure or significant coronary artery
disease may be unable to increase their cardiac output in response
to infection. Malnutrition can result in a lack of nutrients and crit-
ical enzymatic cofactors involved in the normal cellular response to
infection. Each of these patient factors impairs the host response
and thereby increases the likelihood that infection will develop.
In the 1920s, Meleney demonstrated that injection of animals
with pathogens isolated from patients with infectious gangrene
reproduced the characteristics of infection.2 Decades later, the
importance of bacterial synergy and exotoxins was demonstrated
in experiments performed by Seal and Kingston,52 who showed
that a spreading infection developed in 12% of animals that
received an intradermal injection of group A β-hemolytic strepto-
Figure 7 Meleney’s ulcer is characterized by central necrosis, cocci.When S. aureus was coinjected with β-hemolytic streptococ-
erythema, and edema. ci, spreading infections developed in 50% of animals, and when the
α-lysin of S. aureus was coinjected with streptococci, spreading
infections developed in 75%.
more fulminant and are notable for their acute onset, rapid pro-
gression, and systemic toxicity. Their characteristic clinical mani-
festations are related to exotoxin production by the pathogen Streptococcal Toxic-Shock Syndrome
involved [see Table 9 and Pathogenesis of Soft Tissue Infections, Hemolytic streptococci were originally described by Meleney as
below]. S. pyogenes is the pathogen in more than half of monomi- the cause of a “synergistic gangrene.”2 The current resurgence of
crobial infections; S. aureus, C. perfringens,V vulnificus, and P aerug-
. . necrotizing soft tissue infections attributed to so-called flesh-eating
inosa are less common. bacteria probably represents an adaptation of group A streptococ-
ci to the contemporary environment.53 Streptococcal toxic-shock
syndrome (STSS) is defined as the isolation of group A strepto-
Pathogenesis of Soft Tissue Infections
cocci from a normally sterile body site in conjunction with
Soft tissue infections generally induce localized inflammatory hypotension and either renal impairment, acute respiratory distress
changes in the involved tissues, regardless of the species of bacte- syndrome, abnormal hepatic function, coagulopathy, extensive tis-
ria involved. As the infection progresses, tissue necrosis occurs as a sue necrosis, or an erythematous rash.45 STSS is considered the
result of (1) direct cellular injury from bacterial toxins, (2) signifi- probable diagnosis when these abnormalities occur in conjunction
cant inflammatory edema within a closed tissue compartment, (3) with isolation of group A streptococci from nonsterile body sites.
thrombosis of nutrient blood vessels, and (4) tissue ischemia. More than 60% of patients with STSS have bacteremia. STSS has
The exotoxins produced by gram-positive cocci and some been shown to be a major risk factor for mortality among patients
gram-negative bacteria are powerful proteolytic enzymes. S. pyo- with necrotizing soft tissue infections.54
genes produces hemolysins, fibrinolysins, hyaluronidases, and Population-based studies in North America and Europe docu-
streptolysins. S. aureus and P aeruginosa produce coagulases that
. mented a nearly fivefold increase in group A streptococcal infec-
result in local tissue damage and necrosis. C. perfringens produces tions between the late 1980s and 1995.55 The current incidence of
numerous exotoxins. The α-toxin, a lecithinase enzyme, is highly group A streptococcal infections in the population of Ontario,
lethal: it destroys cell membranes, causes hemolysis, and alters cap- Canada, is estimated to be 1.5 per 100,000.55 STSS develops in
illary permeability. Other clostridial toxins lyse red blood cells and
have direct cardiotoxic effects. These toxins also cause platelet
aggregation and fibrin deposition, with resultant vascular throm- Table 9 Major Exotoxins Associated with
bosis and necrosis. Production of the θ-toxin leads to intravascular
Organisms Causing Monomicrobial Necrotizing
leukostasis and inhibits diapedesis of white blood cells into infect-
ed tissue.This unique collection of bacterial toxins accounts for the Soft Tissue Infection
rapid progression of C. perfringens infection in a setting of minimal
inflammatory changes. Bacterium Exotoxins
That most necrotizing soft tissue infections involve multiple bac-
Pyrogenic exotoxins A and B, hemolysin,
terial species strongly suggests that bacterial synergy plays an Streptococcus pyogenes
fibrinolysin, hyaluronidase, streptokinase
important role in their pathogenesis.Toxin-induced cellular necro-
Hemolysins (intravascular hemolysis and
sis establishes an anaerobic environment that facilitates the growth Staphylococcus aureus
local tumor necrosis), coagulase
of both facultative and anaerobic bacteria.These anaerobes elabo-
rate additional enzymes and other by-products that facilitate tissue Collagenase (local tissue damage and
Pseudomonas aeruginosa
necrosis)
invasion and destruction.
Preexisting local tissue damage frequently serves as a nidus for α-Toxin (lecithinase causing tissue necrosis,
soft tissue infection.The reduced oxygen tension of this abnormal Clostridium perfringens intravascular hemolysis, hemoglobinemia,
and acute renal failure)
environment allows pathogens to proliferate. In addition, various

Acs0302 Soft Tissue Infection

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (20)

Similar to Acs0302 Soft Tissue Infection

Similar to Acs0302 Soft Tissue Infection (20)

More from medbookonline

More from medbookonline (20)

Acs0302 Soft Tissue Infection