A 54-year old gentleman with a history of type 2 diabetes mellitus presents with several days of progressive left lower extremity redness, pain, swelling, and subjective fevers.
On physical examination the patient is afebrile and hemodynamically stable. The left lower extremity is swollen, warm, and tender to light palpation with an irregular area of erythema extending anteriorly from the ankle to just below the knee. There are no areas of purulence or fluctuance. Labs are notable for a mild leukocytosis of 11,500 cells/mcL. An ultrasound shows no evidence of deep vein thrombosis and the patient is started on vancomycin and ceftazidime and admitted for intravenous antibiotics.
Does the patient require hospital admission and continuation of intravenous antibiotics?
The clinical presentation of SSTIs can vary greatly. Consequently, the management of SSTIs can be as simple as a short course of outpatient oral antibiotics or escalate to as complicated as surgical intervention and/or prolonged courses of IV antibiotics. Given the frequency with which these infections result in hospital admission, it is essential for the practicing hospitalist to be able to appropriately triage and treat SSTIs in order to assure adequate therapy, while simultaneously reducing unnecessary hospital days and avoiding indiscriminate exposure to broad spectrum antibiotics.
Pathophysiology and clinical presentation
SSTIs represent a diverse range of presentations and severities from superficial impetigo to life-threatening necrotizing infections, with abscesses and cellulitis being most commonly diagnosed.1
All SSTIs emerge from microbial invasion of the layers of the skin and underlying soft tissues. The accepted minimal criteria for diagnosis of an SSTI are erythema, edema, and warmth and tenderness of the affected area. Comorbid conditions that impair skin integrity, such as lymphedema, chronic inflammation (for example, eczema), intertrigo, or venous insufficiency therefore increase the risk of infection. However, the strongest risk factor for development of an SSTI is disruption of the skin barrier via trauma (foreign body, bite wound), ulceration, laceration, fissures, or surgical wound.2,3
The hallmark features of SSTI are present in other noninfectious skin disorders, thus often yielding misdiagnosis. In a study of 259 patients hospitalized for lower extremity cellulitis, 79 patients (30.5%) were misdiagnosed.4 The most common mimic of SSTI is stasis dermatitis due to chronic venous insufficiency. Other conditions that are often misdiagnosed as SSTI include lymphedema, lipodermatosclerosis, contact dermatitis, papular urticaria and deep venous thrombosis. Differentiating between true SSTI and these “pseudo-cellulitic” conditions is essential to reducing unnecessary hospitalization and exposure to antibiotics, which contribute to nosocomial infection, iatrogenic injury (that is, Clostridium difficile infection, anaphylaxis) and avoidable health care costs.
In the majority of cases, the causative pathogen is not identified; superficial culture data is often confounded and positive results do not guarantee pathogenicity of the identified organism. However, the mechanism of bacterial entry, location of infection, and presence of underlying medical conditions also influence the infectious organism(s). For example, infections of the lower extremities may involve enteric organisms such as E. coli and Enterococcus due to fecal runoff. SSTIs due to cat and dog bites commonly involve Pasteurella multocida, while hot tub exposure and intravenous drug use increase the risk of infection with Pseudomonas aeruginosa. Patients with neutropenia are at increased risk for fungal and yeast infections. Consequently, an assessment for potential risk factors is essential in determining appropriate management. Common pathogens associated with various clinical presentations and risk factors are outlined in Table 2.
In addition to host risk factors, the type of SSTI may hint at the most likely organisms. Among purulent (“culturable”) SSTIs, up to 76% of infections are due to S. aureus, whereas in diffuse (“nonculturable”) cellulitis, the majority of cases are attributable to B-hemolytic streptococcus.7 The role of S. aureus in SSTIs is further complicated by the rise of methicillin-resistant S. aureus (MRSA), both nosocomial and community-acquired. It is estimated that between 25%-50% of all S. aureus isolates in the United States show methicillin resistance.6,8 Despite the rising prevalence of MRSA, reflexive treatment for MRSA should be avoided in the absence of high-risk presentations (for example, purulent SSTI) or patient risk factors for MRSA (Table 3).