1. Presentation:
a. Purulent discharge from the surgical site and/or incision with or without associated erythema, tenderness, or fever.
b. Symptoms (local or regional pain or joint stiffness) which may be less obvious signs of infection.
c. Absence of radiologic evidence of bone healing after several months, with or without fixation failure, may also suggest infection.
d. Intermittent fevers, chills, sweats (particularly, night sweats in the setting of chronic infections), and general malaise are common symptoms.
e. An untreated infection may progress rapidly and threaten the limb, lead to septic shock, or even lead to death.
2. Physical exam findings at the surgical site:
a. Pain.
b. Erythema or overlying cellulitis (▶Fig. 6.1).
c. Drainage.
d. External appearance may be benign with deep space infection.
3. Host risk factors for developing infection:
a. Diabetes mellitus.
i. Perioperative hyperglycemia.
ii. Micro- and macrovascular disease.
iii. Immunologic dysfunction.
b. Peripheral vascular disease.
c. Malnutrition.
Fig. 6.1 Clinical photos demonstrating varied clinical presentation of deep infection (a, b). High suspicion is necessary for post-operative surgical sites with atypical findings or patient reporting increased pain.
d. Obesity.
e. Advanced age.
f. Immunocompromised (HIV).
g. Immunomodulating drugs:
i. Steroid treatment.
ii. Chemotherapy (cancer treatment).
iii. Disease-modifying anti-rheumatic drugs (DMARDs) for autoimmune disorders.
h. Polytrauma.
II. Anatomy of Infection
A. Superficial surgical site infection
1. Early fracture site colonization and proliferation.
2. Affects the incision but does not extend to the fracture site and remains superficial to the level of the fascia.
B. Deep surgical site infection
1. Infection that penetrates deep to fascia and involves the fracture site.
2. Surgical devices represent a substrate for microbial colonization and biofilm-associated infection.
a. Variety of organisms have been associated with indwelling implants, some of the most common are:
i. Staphylococcus (aureus, epidermidis).
ii. Streptococcus pyogenes.
iii. Klebsiella pneumoniae.
iv. Pseudomonas aeruginosa.
v. Acinetobacter baumannii.
vi. Escherichia coli.
3. Pathogenesis of biofilm includes following four stages (▶Fig. 6.2):
a. Planktonic—free-floating which represents the inoculation phase.
b. Sessile phase: bacteria settle and form a mature biofilm.
Fig. 6.2 Biofilm pathogenesis. 1. Planktonic bacteria attachment: reversible and bacteria susceptible to antibiotics and rinsing. 2. Micro-colonies develop: reversible and bacteria susceptible to antibiotics and rinsing. 3. Continued cell division: more adhesion sites, matrix formation, and biofilm maturation. 4. Detachment: liberate planktonic bacteria or small segments and plankontic bacterial may relocate and colonize other surfaces.
c. Persister cells: dormant, multidrug tolerant cells that live within mature biofilm and have the ability to repopulate the biofilm.
d. Quorum-sensing molecules: chemomodulators within a mature biofilm permitting intercellular communication to permit bacterial resistance.
III. Serologic Analysis
A. Subacute postoperative period
1. Markers of inflammation, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), are routinely elevated in response to traumatic and surgical events (low specificity for infection diagnosis).
2. The magnitude of inflammatory marker elevation may be valuable.
3. The change of CRP over time is helpful rather than the overall value.
B. Chronic infection
1. ESR and CRP are sensitive markers of infection and relatively nonspecific.
2. Twenty percent of patients undergoing nonunion repair with normal preoperative inflammatory markers may be culture-positive at the time of surgery.
IV. Imaging
A. Diagnostic imaging in the weeks immediately following operative care often fails to show changes that are commonly seen over the course of time.
B. Computed tomography or ultrasound may provide findings of an abscess or presence of air. Such findings may either guide percutaneous drainage with a needle or direct surgical debridement.
V. Classification
Infections are typically referred to as superficial or deep according to whether the infection has penetrated deep to the fascia.
VI. Treatment
A. Surgical debridement (▶Fig. 6.3)
1. Excision of all infected and nonviable tissue may require several operations.
2. Retention versus removal of implants with staged internal fixation after temporary fixation (typically external fixation).
3. Mechanical debridement of implant surfaces.
4. Local antibiotic delivery.
5. Soft tissue coverage as necessary.
B. Antibiotic therapy
1. Six weeks of intravenous (IV) antibiotics is a commonly employed regimen.
2. No conclusive evidence on the effectiveness of IV compared to PO regimens. Basic science and clinical series have not shown a clear benefit of IV antibiotics to date; although, both are routinely used in clinical practice.
C. Modifiable risk factors should be addressed to optimize treatment(s) as local host factors related to reduced host vascularity, neuropathy, trauma, and immunodeficiency increase the likelihood of infection.
D. Predictors of eradication of infection and limb salvage
1. Short-term implant.
2. Absence of a sinus tract.