Complications in Canine Cranial Cruciate Ligament Surgery. Ron Ben-Amotz

identified from an aseptically collected sampleIncision is reopened with purpose and organisms are identified from an aseptically collected sample AND the patient exhibits localized swelling, pain, erythema, or heatDiagnosed as an SSI by a physician Deep SSI MUST:Occur within 30 days (no implant) or 90 days (implant)Involves tissues deep to the subcutaneous tissuesMust have AT LEAST one of the following:Purulent discharge from the incisionIncision spontaneously dehisces or is reopened with purpose AND organisms are identified from an aseptically collected sample AND the patient exhibits localized pain or pyrexiaLocal abscess formation Organ/space MUST:Occur within 30 days (no implant) or 90 days (implant)Involves any tissues deep to the fascia/muscle that was opened during surgeryMust have AT LEAST one of the following:Purulent discharge from a drain within the organ/spaceOrganisms are identified from an aseptically collected sample from fluid or tissue within the organ/spaceLocal abscess formation

3.3 Addressing Surgical Site Infections

      The vast majority of SSIs occur secondary to contamination of the surgical site by commensal or pathogenic organisms arising from the patient's own microbiome [8]. The most common microorganism identified in SSIs is Staphylococcus pseudintermedius. Other common microorganisms identified include Streptococcus spp., Pseudomonas aeruginosa, and Escherichia coli. Staphylococcus pseudintermedius is an opportunistic pathogen with an ability to create a biofilm, leading to its increased virulence [9]. The ability to create a biofilm is important as it makes eradication of these SSIs more challenging. Additionally, resistance of S. pseudintermedius is on the rise, creating an even greater challenge for management of patients with SSIs [9].

      Following the diagnosis of a SSI, several factors must be considered prior to determining a treatment protocol. These include the patient's overall clinical status, category of SSI (superficial, deep, organ/space), susceptibility of inciting microorganisms, presence of biofilm formation, stage of healing, availability of treatment options, and client considerations such as emotional and financial strain associated with treatment.

      The vast majority of SSIs reported by category in the veterinary literature are limited to superficial or deep tissue layers, with an organ/space SSI occurring in <1% of infections [4, 10].

For superficial incisional SSIs, topical or systemic antimicrobial therapy may be sufficient. Topical therapies may include antiseptic agents such as chlorhexidine or povidone‐iodine or antimicrobial therapies such as medical‐grade honey or silver compounds. When the SSI is relatively focal or has minimal purulent discharge, topical antiseptic solutions may be used to clean the site several times daily and may result in resolution of the SSI. However, when a large portion of the wound appears to be affected or when there are large volumes of purulent discharge, topical antimicrobial therapies are best employed if the wound is reopened and explored. This allows for greater source control by lavaging the wound and removing the large microbial burden and allows topical therapies to be in direct contact with the affected tissues. Medical‐grade honey and silver ointments are often used in these scenarios. There is no evidence for antimicrobial resistance for honey, but resistance may exist for silver compounds [11]. This resistance has been demonstrated in vitro and may not be clinically applicable.

      Regardless of the potential for resistance, response to topical therapy should be monitored and treatments altered if there is a lack of response. Ideally, a bacterial culture should be submitted from the onset of clinical signs, so that an appropriate systemic antimicrobial can be added to the treatment regime, should topical therapy fail to resolve the SSI.

      Systemic antimicrobial therapies should be employed in the face of an intact incision and direct identification of microorganisms. Initially, systemic antimicrobials will be chosen empirically until the results of culture and susceptibility testing are available to guide specific therapy. It is important to collect and submit a bacterial culture when an SSI is suspected, to ensure appropriate antimicrobial stewardship is followed and reduce the risk of potentiating antimicrobial resistance.

      Initial empirical recommendations will vary based on hospital known infectious agents and their resistance patterns. Appropriate duration of therapy is a topic of debate and varies between prescribers, with reported treatment lengths ranging from 1 to 6 weeks of antimicrobial therapy [12, 13]. While extended durations of antimicrobial therapy are reported, these prolonged courses of antimicrobials are not likely required unless implanted materials are involved. Most uncomplicated, superficial SSIs will resolve with a systemic course of antimicrobials for 3–5 days. Ultimately, when antimicrobial therapy is discontinued and there is recurrence of clinical signs, involvement of implanted materials should be considered and prolonged antimicrobial therapy based on culture and susceptibility results will be required until implanted materials can be removed or local therapies can be employed [12].

Deep SSIs involving implanted materials can be more challenging to manage, due to the risk for biofilm formation. A biofilm is a community of sessile bacteria embedded in a self‐produced matrix that has adhered to a surface (Figure 3.4) [14]. The most commonly implicated bacterium in veterinary SSIs is S. pseudintermedius which has a propensity for biofilm formation and multidrug resistance [9, 15, 16]. The self‐produced matrix protects the bacteria from antimicrobial penetration and makes treatment more complex as minimum inhibitory concentrations are much higher for bacteria in a biofilm than planktonic bacteria [17].

Because of this increased challenge of eradicating a biofilm‐associated infection, implant removal is often recommended. However, if the SSI is identified early postoperatively and insufficient healing has occurred, methods other than implant removal must be considered. Antimicrobials are often used in situations like this to try to control the SSI, with a realization that the goal is most likely to allow for bone healing, at which point implant removal would be indicated. In the face of a completely healed osteotomy or adequately stabilized extracapsular repair, implant removal, and thus biofilm eradication, are often recommended. Several studies have reported implant removal rates for TPLO, tibial tuberosity advancement (TTA), cranial closing wedge osteotomy, triple tibial osteotomy, and lateral fabellar suture extracapsular repairs [12, 13,18–23]. Explant rates for management of an SSI ranged from 1.3% to 71%, with TPLO and lateral fabellar sutures being the highest rate of explanted materials [12, 13,18–20, 22, 23].

Figure 3.4 Scanning electron microscopy image of a biofilm.

      Source: Adapted from Singh et al. [9].

      Additional approaches to biofilm infections are currently limited. Two enzymes have been identified as being able to prevent biofilm formation; deoxyribonuclease I and dispersin B. While both are capable of inhibiting biofilm formation, only dispersin B has been proven to be able to disrupt an established biofilm [24]. A recent in vitro study has identified that the combination of dispersin B and amikacin in a biodegradable gel allows for rapid elution of dispersin B with a gradual reduction in concentrations over a period of 10 days [25]. While this is a promising avenue, clinical application has not yet been assessed.

When implant removal cannot yet be performed, local antimicrobial therapies (Table 3.3) may be employed. The main goal of these therapies is to allow higher antimicrobial concentrations to be achieved locally than could be tolerated systemically, with limited systemic exposure [26]. Alternative local therapies may include antimicrobial‐eluting bone cement,