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PubMed2004

Hyperbaric oxygen treatment and survival from necrotizing soft tissue infection.

HYPOTHESIS: Necrotizing soft tissue infection (NSTI) refers to a spectrum of infective diseases characterized by necrosis of the deep soft tissues. Features of manifestation and medical management have been analyzed for association with outcome. The use of hyperbaric oxygen (HBO(2)) therapy has been recommended as an adjunctive treatment but remains controversial. DESIGN: Retrospective cohort study. SETTING: A major tertiary hospital. PATIENTS: All patients admitted with a diagnosis of NSTI across a 5-year period. INTERVENTION: Features of manifestation and medical management were analyzed for their association with survival to hospital discharge. Long-term survival was analyzed for the intervention of HBO(2) therapy. MAIN OUTCOME MEASURES: Primary outcome was survival to hospital discharge. Secondary outcomes were limb salvage and long-term survival after hospital discharge. RESULTS: Forty-four patients were reviewed, with 6 deaths (14%). Survival was less likely in those with increased age, renal dysfunction, and idiopathic etiology of infection and in those not receiving HBO(2) therapy. Logistic regression determined the strongest association with survival was the intervention of HBO(2) therapy (P = .02). Hyperbaric oxygen therapy increased survival with an odds ratio of 8.9 (95% confidence interval, 1.3-58.0) and a number needed to treat of 3. For NSTI involving an extremity, HBO(2) therapy significantly reduced the incidence of amputation (P = .05). Survival analysis revealed an improved long-term outcome for the HBO(2) group (P = .002). CONCLUSION: Hyperbaric oxygen therapy was associated with improved survival and limb salvage and should be considered in the setting of NSTI.

Adult↗
PubMed2005

Linezolid versus vancomycin in treatment of complicated skin and soft tissue infections.

Skin and soft tissue infections (SSTIs) are a common cause of morbidity in both the community and the hospital. An SSTI is classified as complicated if the infection has spread to the deeper soft tissues, if surgical intervention is necessary, or if the patient has a comorbid condition hindering treatment response (e.g., diabetes mellitus or human immunodeficiency virus). The purpose of this study was to compare linezolid to vancomycin in the treatment of suspected or proven methicillin-resistant gram-positive complicated SSTIs (CSSTIs) requiring hospitalization. This was a randomized, open-label, comparator-controlled, multicenter, multinational study that included patients with suspected or proven methicillin-resistant Staphylococcus aureus (MRSA) infections that involved substantial areas of skin or deeper soft tissues, such as cellulitis, abscesses, infected ulcers, or burns (<10% of total body surface area). Patients were randomized (1:1) to receive linezolid (600 mg) every 12 h either intravenously (i.v.) or orally or vancomycin (1 g) every 12 h i.v. In the intent-to-treat population, 92.2% and 88.5% of patients treated with linezolid and vancomycin, respectively, were clinically cured at the test-of-cure (TOC) visit (P=0.057). Linezolid outcomes (124/140 patients or 88.6%) were superior to vancomycin outcomes (97/145 patients or 66.9%) at the TOC visit for patients with MRSA infections (P<0.001). Drug-related adverse events were reported in similar numbers in both the linezolid and the vancomycin arms of the trial. The results of this study demonstrate that linezolid therapy is well tolerated, equivalent to vancomycin in treating CSSTIs, and superior to vancomycin in the treatment of CSSTIs due to MRSA.

Acetamides↗
PubMed2002

The Role of Fluoroquinolones in the Treatment of Skin and Soft Tissue Infection.

Skin and soft tissue infections vary widely in their nature and severity, and their nomenclature is complex. Most are readily recognized and easily treated, but more severe infections may masquerade in forms similar to those of more innocent infections, causing delay in diagnosis and treatment that may result in loss of limb or life. Antimicrobial therapy is clearly beneficial for both recovery from these infections as well as preventing disease progression. The fluoroquinolones are potent broad-spectrum antimicrobial agents. The older fluoroquinolones mainly have excellent in vitro activity against gram-negative bacilli and borderline activity against clinically important gram-positive organisms, but newer fluoroquinolones were developed to have enhanced activity against both gram-positive and anaerobic organisms while retaining broad-spectrum anti-gram-negative activity. Several comparative trials using fluoroquinolones suggest that the efficacy of these agents is similar to that of b-lactam antimicrobial agents. Additional clinical trials are necessary to determine the overall role of newer fluoroquinolones as alternatives for skin and soft tissue infections.

Journal Article↗
PubMed1999

Hyperbaric oxygen in the treatment of life-threatening soft-tissue infections.

Necrotizing soft-tissue infections are rapidly spreading bacterial infections that account for a relatively small proportion of infections, but are aggressive in nature and nearly uniformly fatal if left untreated. Prompt recognition, antibiotic therapy, aggressive surgical debridement, and hyperbaric oxygen (HBO) therapy have reduced the mortality resulting from these infections. Oxygen, at increased pressures, augments tissue oxygen partial pressure, allowing increased bacterial killing by providing substrate for the formation of oxygen free radicals and augmenting respiratory burst. During the healing process, hyperoxia causes increased formation of capillaries for oxygen, nutrient, and antibiotic delivery, leading to increased efficacy of some antibiotics in the high oxygen environment, and possibly more rapid overall wound healing. Although there are no randomized trials of HBO in these infections, in vitro data and meta-analysis of clinical cases strongly support the use of HBO.

Combined Modality Therapy↗
PubMed1998

Aspergillus: a rare primary organism in soft-tissue infections.

Nonclostridial necrotizing soft-tissue infections are usually polymicrobial, with greater than 90 per cent involving beta-hemolytic streptococci or coagulase-positive staphylococci. The remaining 10 per cent are usually due to Gram-negative enteric pathogens. We describe the case of a 46-year-old woman with bilateral lower extremity fungal soft tissue infections. She underwent multiple surgical debridements of extensive gangrenous necrosis of the skin and subcutaneous fat associated with severe acute arteritis. Histopathological examination revealed Aspergillus niger as the sole initial pathogen. Despite aggressive surgical debridement, allografts, and intravenous amphotericin B, her condition clinically deteriorated and she ultimately died of overwhelming infection. Treatment for soft-tissue infections include surgical debridement and intravenous antibiotics. More specifically, Aspergillus can be treated with intravenous amphotericin B, 5-fluorocytosine, and rifampin. Despite these treatment modalities, necrotizing fascitis is associated with a 60 per cent mortality rate. Primary fungal pathogens should be included in the differential diagnosis of soft-tissue infections.

Aspergillosis↗
PubMed2004

Effect of a bacterial pheromone peptide on host chemokine degradation in group A streptococcal necrotising soft-tissue infections.

BACKGROUND: Necrotising soft-tissue infections due to group A streptococcus (GAS) are rare (about 0.2 cases per 100000 people). The disease progresses rapidly, causing severe necrosis and hydrolysis of soft tissues. Histopathological analysis of necrotic tissue debrided from two patients (one with necrotising fasciitis and one with myonecrosis) showed large quantities of bacteria but no infiltrating neutrophils. We aimed to investigate whether the poor neutrophil chemotaxis was linked with the ability of group A streptococcus (GAS) to degrade host chemokines. METHODS: We did RT-PCR, ELISA, and dot-blot assays to establish whether GAS induces synthesis of interleukin 8 mRNA, but subsequently degrades the released chemokine protein. Class-specific protease inhibitors were used to characterise the protease that degraded the chemokine. We used a mouse model of human soft-tissue infections to investigate the pathogenic relevance of GAS chemokine degradation, and to test the therapeutic effect of a GAS pheromone peptide (SilCR) that downregulates activity of chemokine protease. FINDINGS: The only isolates from the necrotic tissue were two beta-haemolytic GAS strains of an M14 serotype. A trypsin-like protease released by these strains degraded human interleukin 8 and its mouse homologue MIP2. When innoculated subcutaneously in mice, these strains produced a fatal necrotic soft-tissue infection that had reduced neutrophil recruitment to the site of injection. The M14 GAS strains have a missense mutation in the start codon of silCR, which encodes a predicted 17 aminoacid pheromone peptide, SilCR. Growth of the M14 strain in the presence of SilCR abrogated chemokine proteolysis. When SilCR was injected together with the bacteria, abundant neutrophils were recruited to the site of infection, bacteria were cleared without systemic spread, and the mice survived. The therapeutic effect of SilCR was also obtained in mice challenged with M1 and M3 GAS strains, a leading cause of invasive infections. INTERPRETATION: The unusual reduction in neutrophils in necrotic tissue of people with GAS soft-tissue infections is partly caused by a GAS protease that degrades interleukin 8. In mice, degradation can be controlled by administration of SilCR, which downregulates GAS chemokine protease activity. This downregulation increases neutrophil migration to the site of infection, preventing bacterial spread and development of a fulminant lethal systemic infection.

Adult↗
PubMed2005

The evolving characteristics and care of necrotizing soft-tissue infections.

BACKGROUND: Necrotizing soft-tissue infections such as necrotizing fasciitis and Fournier's gangrene are a source of high morbidity and mortality. These difficult cases are increasingly being referred to burn centers for specialized wound and critical care issues. In this study, we examine our institution's recent experience with a large series of necrotizing soft-tissue infections. STUDY DESIGN: A retrospective chart review was performed of 65 consecutive patients over a 5-year period with necrotizing soft-tissue infections that required radical surgical debridement. RESULTS: Overall survival was 83%, with an average length of stay of 32.4+/-3.32 days for survivors and for the entire group of 29.5+/-3 days. Time from onset of symptoms to initial presentation to our institution averaged 6.9+/-1.19 days. Patients averaged 2.9+/-0.22 surgical procedures, and 46% of patients required skin grafting with an average graft area of 1554+/-248 cm(2). Of the survivors, only 54% were able to return home, with 46% needing further hospitalization or transfer to an inpatient rehabilitation facility. CONCLUSIONS: There were frequent delays in diagnosis and referrals to and from within our institution, and progress can be made in educating the medical community to identify these patients. Advancements in wound care and critical care have made inroads into the treatment of patients with necrotizing soft-tissue infections. However, these infections continue to be a source of high morbidity and mortality and significant healthcare resource consumption. These challenging patients are best served with prompt diagnosis, immediate radical surgical debridement, and aggressive critical care management. Referral to a major burn center may help provide optimal surgical intervention, wound care, and critical care management.

Adult↗
PubMed1992

Soft tissue infections.

Infections in soft tissues present with one or more of the cardinal signs of infections; however, presence of these signs may indicate manifestation of a deep systemic infection or of a noninfectious process. One of the earliest determinations to be made is whether the problem is likely to require patient admission or referral to another specialty. Only then is the primary management clear.

Bacterial Infections↗
PubMed1996

Necrotizing soft-tissue infections.

Necrotizing soft-tissue infections may be rapidly fatal because of toxin-induced circulatory collapse. Because of the often nonspecific clinical presentation, prompt diagnosis may be difficult but is imperative as prompt treatment can be lifesaving. This article discusses necrotizing fasciitis and clostridial myonecrosis, and highlights pathogenesis, clinical presentation, diagnosis, and treatment.

Diagnosis, Differential↗
PubMed1992

Necrotizing soft-tissue infections.

Necrotizing soft-tissue infections have been widely recognized for over a century, but they remain a challenging problem in clinical infectious disease. Patterns of disease are clearly apparent, but most are polymicrobial and derive increased virulence from synergy between bacteria. Early recognition and prompt surgical drainage are the keys to successful treatment. Edema extending beyond the area of erythema, skin vesicles, crepitus or air in the subcutaneous tissues, and absence of lymphangitis and lymphadenitis are markers of necrotizing infections, particularly when they occur in patients with serious underlying disease. Empiric broad-spectrum antibiotics, prophylactic heparin, and nutritional therapy are important adjuncts to aggressive "stepwise" surgical debridement. A knowledge of patterns of disease can aid in fine-tuning treatment to decrease morbidity.

Gangrene↗
PubMed1975

Needle aspiration in the diagnosis of soft tissue infections.

Diagnosis of soft tissue infections is often delayed or made incorrectly because of reliance on indirect means to determine the etiologic agent. A rapid, speific method is the needle aspiration of these lesions combined with Gram-stain and culture studies. More frequent use of this direct method should facilitate diagnosis and improve treatment. Seven case studies are present to illustrate the usefulness of this technique.

Abscess↗
PubMed1995

Identifying high risk patients for Staphylococcus aureus infections: skin and soft tissue infections.

Staphylococcus aureus is the causative organism for many skin and soft tissue (SST) infections. Some SST infections have severe systemic complications, such as bacteraemia and sepsis. S. aureus is the cause of 75% of primary pyodermas. Pre-existing conditions, like tissue injury (ulcers, wounds) or tissue inflammation (exudative dermatitis), and also underlying disorders (such as poorly controlled insulin-dependent diabetes mellitus or cancer) are some of the risk factors for secondary infection with S. aureus. In S. aureus-infected primary skin disorders (impetigo, recurrent eczema), 2% mupirocin ointment has proved effective in several clinical trials. S. aureus is responsible for 25% of all burn-wound infections, and burn units could be the point of entry and source of spread of methicillin-resistant S. aureus infection outbreaks. Mupirocin (2% ointment) has also proven effective for topical treatment of these infections. Pressure sores develop in 6% of all patients admitted to acute and chronic health care institutions. An average of three aerobic species (including S. aureus) plus one anaerobic species are isolated when infected. Infectious complications are responsible for 60-80% of all intravenous drug user (IVDU) hospital admissions, 5-20% being due to S. aureus infective endocarditis (IE). The origin of IE in IVDUs is probably the skin. Data from a Collaborative Spanish Study of IVDU infectious complications (including more than 10,000 episodes) are discussed.

Burns↗
PubMed1990

Pefloxacin versus ceftazidime in therapy of soft tissue infections in compromised patients.

Soft tissue infections in compromised patients are frequently caused by Gram-negative organisms and particularly by Pseudomonas aeruginosa. These pathogens are effectively eradicated by pefloxacin as well as by ceftazidime. The effectiveness and safety of these two agents were compared in a prospective randomized study in 67 patients with soft tissue infections. Underlying conditions included malignant diseases, diabetes mellitus and chronic renal failure. The infections included: post operative infection, septic foot, soft tissue abscess and cellulitis. Thirty-three patients were treated with intravenous ceftazidime for a mean duration of ten days. More than half the 34 patients given pefloxacin were treated only orally for a mean period of 13 days. The clinical and bacteriological outcomes were similar in both groups. There was clinical cure or improvement in 26 pefloxacin cases and in 23 ceftazidime cases, failure in six pefloxacin cases and in seven ceftazidime and relapse in two pefloxacin and in three ceftazidime patients. The bacteriological responses were eradication in 23 pefloxacin cases and in 22 ceftazidime cases, persistence in five pefloxacin cases and in six ceftazidime cases, relapse in one pefloxacin case and in none of the ceftazidime group, reinfection in four pefloxacin cases and in three ceftazidime cases and there was one unassessed patient in the pefloxacin group and two in the ceftazidime group. Nausea and vomiting occurred in three patients and elevation of liver enzymes in another patient; all side effects were observed only in the pefloxacin treated patients. These results suggest that oral pefloxacin could offer an alternative to intravenous ceftazidime in half the compromised patients with tissue infections. However, adverse reactions due to pefloxacin administration should be watched for during such therapy.

Administration, Oral↗
PubMed2003

A practical guide to the treatment of complicated skin and soft tissue infections.

Complicated skin and soft tissue infections (SSTIs) remain a common reason for hospitalisation. Optimal management of complicated SSTIs begins with a physical examination, and obtaining the complete social and medical history of the patient. Empirical intravenous antibacterial therapy is guided by expected pathogens, patient factors and diagnostic procedure reports, such as the Gram-stained smear of discharge or exudates. The majority of community-acquired SSTIs are caused by Staphylococcus aureus and beta-haemolytic streptococci. On the basis of recent surveillance data, 80-90% of these pathogens remain susceptible to cefazolin or oxacillin. Consequently, a first generation cephalosporin or an antistaphylococcal penicillin remains the first line empirical therapy for community-acquired skin and soft tissue infections. Vancomycin may be an appropriate alternative when vancomycin-resistant S. aureus is highly suspected on the basis of patient history and co-morbid conditions. With the global emergence and spread of macrolide-resistant S. aureus and beta-haemolytic streptococci, clindamycin rather than a macrolide is the recommended agent for empirical antibacterial therapy of community-acquired SSTIs in penicillin-allergic patients. Nosocomial complicated SSTIs are predominantly caused by S. aureus, Pseudomonas aeruginosa, Enterococcus spp., Escherichia coli and other Enterobacteriaceae. Piperacillin/tazobactam with or without vancomycin is the preferred agent for empirical treatment depending on local resistance statistics. The newer fluoroquinolones may have a role in the treatment of complicated SSTIs, especially in penicillin-allergic patients. More clinical studies are needed before a formal recommendation can be made. Many of the newer antimicrobial agents such as the carbapenems, oxazolidinones and streptogramins have been shown to be effective for the treatment of complicated SSTIs. However, because of their proven activity against highly resistant organisms including methicillin-resistant S. aureus and vancomycin-resistant enterococci (oxazolidinones and streptogramins), and Gram-negative bacilli producing extended spectrum beta-lactamases (carbapenems), these antibacterials should be reserved for life-threatening situations and/or when resistant pathogens are suspected. Complicated skin and soft tissue infections are often associated with exudates, ulcerations, fluid collections or abscesses. Adequate debridement of devitalized tissues and drainage of abscesses and fluid collections in addition to systemic antibacterial therapy is an integral part of appropriate management.

Animals↗
PubMed2005

Can a pin-tract infection cause an acute generalized soft tissue infection and a compartment syndrome?

A patient who developed soft tissue infection and osteomyelitis secondary to pin tract infection after skeletal traction was evaluated. Tibial traction was performed on a patient who had exposed to a femoral pertrochanteric fracture after falling from a tree in a rural public hospital. On the first postoperative day shortly after development of soft tissue swelling, redness, and tenderness in the affected leg, compartment syndrome was noted with subsequent removal of the pin at the same health center. After arrival of the case in our center surgical decompression with an open faciatomy and proper antibiotherapy were instituted. Simultaneously hyperbaric oxygen was administered. After eradication of soft tissue infection we treated the fracture with a Richards compression screw-plate device. The patient was discharged with complete cure. This case presented how seriously a simple pin-tract infection can cause a grave clinical entity resulting in potential loss of an extremity.

Adult↗
PubMed1993

Intervention to discontinue parenteral antimicrobial therapy in hospitalized patients with urinary tract infection, skin and soft tissue infection, or no evident infection.

OBJECTIVES: In a previous study, we found that unsolicited recommendations to physicians of medically stable patients with pneumonia to suspend parenteral antimicrobials shortened hospital length of stay (LOS) significantly. In this study, we made similar recommendations to physicians treating patients with different indications for parenteral antimicrobials, to examine the effect on LOS. METHODS: A nurse-interventionist presented randomly assigned physicians with nonconfrontational suggestions to discontinue parenteral antimicrobials by substituting comparable oral antimicrobials or stopping treatment. Patients were being treated for urinary tract infection, skin infection, or no evident infection. Blinded observers evaluated in-hospital and 30-day postdischarge patient courses. Methodologies were identical to the previous study. RESULTS: There were 70 physician-patient episodes (49 intervened episodes, 21 control episodes). In 44 episodes (90%), compliant physicians discontinued parenteral antimicrobials. Compared to a median postrandomization LOS of 2.5 days (range, 0 to 40.5) for 21 patients of control physicians, the corresponding LOS for 44 patients of compliant physicians was two days (range, 0 to 8; P = 1.0), and for five patients of noncompliant physicians, five days (range, 3 to 11; P = 0.04). The combined occurrence of all adverse events detected in this and the previous study was 11% for patients of control physicians, compared to 14% for patients of compliant physicians (P = 0.2), and 19% for patients of noncompliant physicians (P < 0.05). CONCLUSIONS: For patients of compliant physicians hospitalized with urinary tract infection, skin and soft tissue infection, or no evident infection, cessation of parenteral antimicrobials did not significantly shorten LOS, due to brief LOS of patients of control physicians. Patients of noncompliant physicians experienced more adverse events and prolonged LOS. The appropriateness of routine continuous use of parenteral antimicrobials in medically stable inpatients is questioned.

Aged↗
PubMed1990

Topical liposomal delivery of antibiotics in soft tissue infection.

A new drug delivery system (lipid microcarriers) was studied in an experimental model of infected soft tissue wounds. Superficial, nonlethal infection was produced in the adult rat by injecting 1 ml containing 10(8) colony-forming units (CFU) of Pseudomonas aeruginosa under the superficial fascia of the paraspinus muscle of a 2-cm2 excised wound. All wounds were dressed with N-Terface, a nonadherent wound material, and covered with Kontor sponge, an open-cell polyurethane sponge containing either normal saline (group I), free tobramycin (groups III and V), liposome-entrapped tobramycin (groups II and IV), silver sulfadiazene (group VI), or liposome-entrapped silver sulfadiazene (group VII). At 24, 48, and 72 hr postinjection, animals were sacrificed and colony-forming units of P. aeruginosa per gram of muscle tissue were determined. Group I had significantly higher colony-forming units of P. aeruginosa per gram than groups II and III at 48 and 72 hr and than groups IV and V at all times. One single dose of liposome-encapsulated silver sulfadiazine significantly decreased bacterial counts compared to untreated controls and, to a similar extent, compared to multiple applications of free drug. Colony-forming units in all treatment groups (II and III, IV and V, VI and VII) were similar at all time periods within equivalent dosages. The ability of one application of liposomal-entrapped antibiotics to result in a therapeutic effect that requires multiple applications of topically applied free antibiotics offers potential clinical advantages.

Administration, Topical↗
PubMed1998

Molecular analysis of the role of the group A streptococcal cysteine protease, hyaluronic acid capsule, and M protein in a murine model of human invasive soft-tissue infection.

Human invasive soft-tissue infections caused by group A Streptococcus are associated with significant morbidity and mortality. To investigate the pathogenesis of these serious infections, we characterized the host response to bacterial challenge with an M-type 3 isolate recovered from a patient with necrotizing fasciitis, or with isogenic gene replacement mutants deficient in cysteine protease, hyaluronic acid capsule, or M protein in a murine model of human invasive soft-tissue infection. Animals challenged with the wild-type or cysteine protease-deficient strain developed spreading tissue necrosis at the site of inoculation, became bacteremic, and subsequently died. Histopathologic examination of the necrotic lesion revealed bacteria throughout inflamed subcutaneous tissue. Arterioles and venules in the subcutaneous layer were thrombosed and the overlying tissue was infarcted. In contrast, animals challenged with either an acapsular or M protein-deficient mutant developed a focal area of tissue swelling at the site of inoculation without necrosis or subsequent systemic disease. Histopathologic examination of the soft-tissue lesion demonstrated bacteria confined within a well-formed subcutaneous abscess. We conclude that the group A streptococcal hyaluronic acid capsule and M protein, but not the cysteine protease, are critical for the development of tissue necrosis, secondary bacteremia, and lethal infection in a murine model of human necrotizing fasciitis.

Abscess↗