A shoulder periprosthetic joint infection (PJI) is among the most significant complications a patient, a surgeon, or a health system can face. It is difficult to diagnose, difficult to eradicate, and disproportionately likely to be caused by Cutibacterium— an organism that lives in the pilosebaceous units of the normal dermis, beyond the reach of any antiseptic applied to the skin surface and that the host's immune system may not recognize as "foreign".
Cutibacterium can be isolated from healthy shoulders. So we need to consider an "infction" as "bacteria doing harm". Whether Cutibacterium are doing harm in a shoulder arthroplasty - a periprosthetic infection - depends primarily on the interaction between it and the host in the environment of the prosthetic joint.
Shoulder periprothetic infections can present in different ways.
An "obvious" presentation is one in which there is pain, swelling, erythema, draining sinus, intraarticular pus, elevated serum inflammatory markers, and cultures than rapidly turn positive. While obvious infections can be caused by Cutibacterium, methicillin resistant staphylococcus and methicillin sensitive staphylococcus are common offenders.
A "stealth" presentation is one in which the patient's expected post-arthroplasty course becomes complicated by otherwise unexplained pain and stiffness after a "honeymoon" recovery. Stealth infections are commonly associated with Cutibacterium.
Given the stakes, it is not surprising that a great deal of time, money, and effort is being spent on interventions that claim to reduce PJI risk. What is worth asking is what the supporting evidence actually shows.
It helps to distinguish two questions about any proposed intervention: (1) Does it reduce a surrogate for PJI — skin-surface colony counts, dermal culture positivity, intraoperative field culture positivity, or bacterial load on instruments? (2) Does it address the clinical outcome the patient cares about — periprosthetic infection, revision for infection, or poorer comfort and function?
The surrogate-to-outcome link is biologically plausible but unproven; there is direct evidence that intraoperative culture positivity at primary TSA does not predict clinical PJI or inferior patient-reported outcomes[reference 1].
Another confounding finding is that the Cutibacterium positive culture rate for a sterile swab or sponge exposed to the air in a shoulder OR is 5 to 15% [32],[34]. Thus a positive culture for a shoulder tissue specimen may be due to contamination of the specimen on its path from the patient to the OR environment to the lab. Surgeons should consider periodically testing the culture results for sterile samples in their ORs to guide the interpretation of their surgical specimen culture results.
Approaches to lowering infection risk
The one intervention with robust shoulder-specific outcome data: weight-based IV cefazolin
A single-institution review of 7,713 primary shoulder arthroplasties over two decades reported that cefazolin, compared with non-cefazolin alternatives (vancomycin, clindamycin), was associated with a 69% reduction in all-cause PJI and a 78% reduction in Cutibacterium PJI over 15-year follow-up [reference17]. The findings of this observational, retrospective analysis were congruent with a separate analysis of 139,032 primary shoulder arthroplasties[18] providing the strongest shoulder-specific outcome evidence in the entire infection-prevention literature. The mechanism is consistent with Cutibacterium's susceptibility to beta-lactams and with the tissue concentrations cefazolin achieves when given inside the guideline window.
When vancomycin is used (usually for self-reported penicillin allergy), the protective effect depends on complete infusion before incision: a fourfold increase in PJI risk has been reported when vancomycin infusion-to-incision was less than 30 minutes[19]. A large randomized trial in total joint arthroplasty found no benefit to adding IV vancomycin to cefazolin, and in the knee subgroup vancomycin addition was associated with a higher surgical site infection (SSI) rate; the shoulder subgroup (n = 30) was too small to support inference[30].
IV cefazolin reduces but does not eliminate deep-tissue inoculation. Cutibacterium is still recoverable from deep tissues at primary arthroplasty despite prophylaxis and standard skin preparation[5]. A 2024 prospective genomic study of 90 primary reverse shoulder arthroplasties showed that the Cutibacterium recovered from deep tissues after cefazolin and chlorhexidine gluconate (CHG) skin preparation was genotypically identical to the organism present on the skin, consistent with skin-to-deep-tissue inoculation[20]. Falconer and colleagues similarly documented surgical field contamination despite prophylaxis[21]. Adding doxycycline to cefazolin did not further reduce culture positivity in a randomized trial[22].
Patient-side risk factors with shoulder-specific supporting data
Glycemic control in patients with diabetes
A shoulder-specific analysis of patients with diabetes mellitus identified a perioperative HbA1c threshold of 8.0 as an inflection point above which wound-complication and deep-infection rates rise significantly[49]. The absolute infection rate remains low even above this threshold, and HbA1c alone has limited discrimination as a predictive test — but the data support preoperative HbA1c screening in patients with diabetes and consideration of glycemic optimization before elective surgery.
Timing of corticosteroid injection
Shoulder injection within 3 months of arthroplasty is associated with increased postoperative infection risk in a Medicare analysis[50]; a subsequent national-database study of reverse shoulder arthroplasty found the increased PJI risk concentrated in patients injected within 4 weeks of surgery[51]. Scheduling arthroplasty ≥4 weeks — and ideally ≥3 months — after any ipsilateral glenohumeral corticosteroid injection is a reasonable risk-reduction step.
Operative time
A 33,987-case NSQIP analysis showed an increasing odds of SSI as operative time lengthened, with an inflection above 180 minutes[52]. Operative time is a modifiable factor to the extent that surgical volume, implant selection, team familiarity, and case complexity permit.
Other items often cited without shoulder-specific PJI-outcome data
Smoking cessation, preoperative anemia correction, nutritional optimization, OR personnel traffic reduction, intraoperative normothermia, appropriate hair removal, glove changes at key moments, and excellent wound closure are all reasonable, low-harm elements of a perioperative protocol. They are supported to varying degrees by extrapolated evidence from other surgical fields and by surrogate-endpoint orthopaedic data. None has a shoulder-specific randomized controlled trial showing a reduction in PJI. Recommending them is sensible; describing them as 'evidence-based for shoulder PJI reduction' overstates the case.
Preoperative decolonization
Chlorhexidine gluconate (CHG) applied on the skin surface
Home CHG showers are widely used. Their shoulder-specific support is weaker than often assumed. Standard surgical preparation does not eradicate Cutibacterium from the dermis[3], home CHG washes lower skin loads of most bacteria but are specifically less effective against Cutibacterium[4], and the organism can still be isolated from deep cultures at primary shoulder arthroplasty despite prophylaxis[5]. A randomized trial in male shoulder arthroplasty patients comparing home 4% CHG washes to 10% benzoyl peroxide soap found neither agent eliminated Cutibacterium from the skin surface or the incised dermal edge[6]. Cutibacterium repopulates the shoulder skin surface from the sebaceous-gland reservoir within 60 minutes[2].
Benzoyl peroxide (BPO) applied on the skin surface
The BPO shoulder literature now comprises multiple randomized trials. Sabetta and colleagues first reported in 2015 that adding topical 5% BPO cream to standard skin preparation reduced Cutibacterium recovered during shoulder surgery[53]. The 2018 Neer Award trial randomized 80 shoulder-surgery patients to 5% BPO or 4% CHG for three consecutive days; the BPO-treated shoulder had fewer positive cultures than the contralateral untreated control (P = 0.0003), while the CHG-treated shoulder did not differ from its control[7]. A separate small volunteer trial showed a similar BPO surface effect[8]. Scheer and colleagues later reported in a 100-patient randomized trial that BPO reduced Cutibacterium positivity across all phases of open shoulder surgery, from skin incision through wound closure[9].
The picture is not uniformly positive. Heckmann and colleagues showed that topical clindamycin, BPO, and the combination each failed to eliminate Cutibacterium from the dermis in randomized treatment quadrants on the upper back[54]. The Hsu trial on the shoulder was also negative[6]. Taken together, BPO has the most consistent surrogate-endpoint signal of any topical agent in this space, but it reduces rather than eliminates surface colonization and has no shoulder-arthroplasty trial demonstrating reduction in clinical PJI.
Hydrogen peroxide (H2O2)
3% hydrogen peroxide is bactericidal against Cutibacterium at clinically achievable contact times[10]. A nonrandomized controlled trial of 61 primary shoulder arthroplasties reported reduced triple-site (skin + dermis + joint) culture positivity with the addition of an H2O2 wipe to standard preparation[11], and a two-year follow-up of that cohort noted a non-significant trend toward fewer revisions and fewer Cutibacterium infections[12]. Against these: a randomized controlled trial applying H2O2 to the dermis after skin incision showed no difference in culture positivity (20% vs. 16%, p > 0.99)[13], and a 2024 randomized volunteer study found no additional benefit to H2O2-followed-by-CHG over CHG alone, with 78% of shoulders in both arms repopulating from the sebaceous reservoir within 60 minutes[14]. The collective evidence for H2O2 is split, with two studies suggesting a surrogate-endpoint benefit and two showing none; no shoulder-arthroplasty trial has demonstrated a clinical PJI benefit.
Nasal Staphylococcus aureus screening and decolonization
S. aureus is not the dominant shoulder arthroplasty pathogen. Meta-analytic data from hip and knee arthroplasty cohorts suggest screen-and-decolonize protocols lower SSI rates[15]. The largest randomized trial enrolled 613 arthroplasty patients — only 14 (2%) of whom had shoulder arthroplasty — and found zero PJIs in either arm at 2 years, rendering the trial inconclusive[16].
Intraoperative antimicrobial measures
Dilute povidone-iodine joint irrigation
In hip and knee arthroplasty, an early report noted a reduction in acute deep PJI from 0.97% with saline lavage to 0.15% with 0.35% dilute povidone-iodine lavage[23]; a randomized trial in aseptic revision TJA showed a reduction in PJI from 3.4% (saline) to 0.4% (dilute povidone-iodine) (p = 0.038)[24]. Larger cohorts have not replicated this, and a 2025 multicenter randomized trial in high-risk primary THA and TKA found no significant reduction in 3-month PJI or wound-complication rates for dilute povidone-iodine, topical vancomycin powder, or their combination compared with saline[25].
Shoulder-specific data are sparser and focus on microbial surrogates. An observational study of 187 isolates recovered during reverse shoulder arthroplasty reported substantial reduction in recoverable Cutibacterium and coagulase-negative staphylococci after 3 minutes of 0.35% povidone-iodine irrigation[26]. No shoulder-arthroplasty RCT has demonstrated a reduction in clinical PJI attributable to dilute povidone-iodine irrigation. The practice is nonetheless endorsed by WHO, CDC, and ICM guidelines based predominantly on hip, knee, and spine data.
Subcutaneous povidone-iodine lavage
A distinct approach — povidone-iodine applied to the subcutaneous layer after skin incision, rather than joint-space lavage before closure — was tested in a 120-patient randomized, single-blinded trial. Subcutaneous povidone-iodine applied after deltoid fascia exposure significantly reduced Cutibacterium surgical-field culture positivity compared with no-additional-preparation control[35].
Subcutaneous chlorhexidine gluconate lavage
Two randomized trials published in 2025 tested 0.05% chlorhexidine gluconate as an intraoperative adjunct to reduce Cutibacterium contamination in primary shoulder arthroplasty. The results were mixed. One reported a pooled deep-culture odds ratio of 2.21 favoring CHG over saline (n = 126, single surgeon)[31]. The other reported no difference (n = 56, single surgeon); the CHG arm was numerically (but not statistically significantly) worse (10.08% vs. 5.77%)[32]. In a dermal biopsy subgroup, the CHG arm was 13% positive and the control arm was 0% (p = 0.115)[32].
It would be of interest to know how subcutaneous CHG compares head-to-head with subcutaneous povidone-iodine.
Topical (intrawound) vancomycin powder
Meta-analyses of predominantly retrospective hip and knee arthroplasty studies have reported reductions in PJI with intrawound vancomycin powder[27][28]. In a prospective multicenter RCT in high-risk primary THA and TKA, topical vancomycin powder (alone or with dilute povidone-iodine) produced no statistically significant reduction in 3-month PJI compared with saline[25]. Shoulder-specific data consist of a single retrospective cohort: 422 shoulder arthroplasties that received intrawound vancomycin powder embedded in a collagen sponge compared with 405 historical controls. The study reported a reduction in PJI without an increase in aseptic wound complications[29]. The comparison is to historical rather than concurrent controls. No prospective, randomized trial in shoulder arthroplasty has tested intrawound vancomycin powder for the outcome of PJI.
Operating room environment
No widely used OR environment measure for shoulder PJI prevention has high-quality, shoulder-specific outcome evidence demonstrating a reduction in clinical PJI. Most data extrapolate from hip and knee arthroplasty or rely on surrogate endpoints.
Surgical drapes
Adhesive drapes — iodine-impregnated or not — reduce wound contamination in a meta-analysis (OR 0.49; 95% CI 0.34–0.72), but the two studies reporting SSI found zero infections in both arms, leaving the clinical infection benefit indeterminate[36]. WHO conditionally recommends against plastic adhesive incise drapes — with or without antimicrobial properties — for SSI prevention[37]. No shoulder-specific draping study has demonstrated PJI reduction.
Surgical hoods and helmet systems
The distinction between older Charnley-type body exhaust suits and modern positive-pressure surgical helmet systems matters. Older systems showed reduced air and wound contamination in most studies; modern helmet systems have not[38]. A 2025 systematic review found that helmet systems frequently harbor microbes and that their exhaust fans can contaminate the sterile field — some systems exhaust air laterally at the level of the surgical wound[39][40]. Simulated studies have shown surgical helmets can actually increase particle and microbial emission rates compared with standard surgical clothing[41]. The CDC 2017 guidelines classified space suits as an 'unresolved issue'[42]. The most directly relevant shoulder-specific evidence is a 2024 New Zealand Joint Registry analysis of 16,000 primary shoulder arthroplasties, which found no difference in all-cause revision or revision for deep infection between surgical helmet systems and conventional gowns[43].
Laminar airflow and closed-incision NPWT
Major guidelines recommend against laminar airflow for arthroplasty SSI prevention[37][44]. A single shoulder-arthroplasty RCT of a localized laminar flow device (n = 43) demonstrated reduced airborne CFUs near the wound but no infections occurred in either group[45]. Closed-incision negative pressure wound therapy has broad SSI-reduction evidence across surgical specialties[46][47][48], but no trial has specifically evaluated it for shoulder arthroplasty PJI.
Putting all this together
Weight-based IV cefazolin, administered within the guideline window, is the one intervention with robust shoulder-specific outcome data for PJI reduction[17,18]. When vancomycin is required, complete infusion before incision matters[19]. Beyond that, the evidence base consists almost entirely of either extrapolation from hip and knee arthroplasty or surrogate endpoints that have a known and unresolved dissociation from clinical PJI[1][32][34].
Several patient-side measures are supported by shoulder-specific data on associated infection risk: perioperative HbA1c screening and optimization in patients with diabetes[49], deferring elective arthroplasty ≥4 weeks (ideally ≥3 months) after any ipsilateral corticosteroid injection[50,51], and minimizing operative time[52]. Smoking cessation, nutritional optimization, anemia correction, normothermia, traffic reduction, and careful wound closure are reasonable — but are not 'evidence-based for shoulder PJI reduction' in the strong sense of that phrase.
Multiple inexpensive, low-harm adjuncts — BPO, H2O2, subcutaneous povidone-iodine, dilute povidone-iodine joint lavage, intrawound vancomycin, subcutaneous CHG — reduce surrogate endpoints with varying consistency.
Nevertheless, because shoulder PJI is serious and difficult to treat, prevention is the preferred strategy. Surgeons should consider adding such low-harm, low cost adjuncts on biological-plausibility grounds, even though robust evidence supporting their efficacy in reducing PJI is lacking.
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Lots to consider!
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