Suspected gluteal compartment syndrome: Etiology predicts clinical course, outcomes and resource utilization.

Background: Gluteal Compartment Syndrome (GCS) is a rare subtype of acute compartment syndrome (ACS), complex to diagnose and potentially fatal if left untreated. The incidence of ACS is estimated to be 7.3 per 100,000 in males and 0.7 per 100,000 in females [1-3]. Given its rare occurrence, the incidence of GCS is not well reported. In the case of GCS, the most common etiologies are surgical positioning, prolonged immobilization secondary to substance use or loss of consciousness, and traumatic injury. Clinical findings are pulselessness, pallor, parasthesia, paralysis, and most notably pain out of proportion. Swift diagnosis and treatment are imperative to reduce morbidity and mortality, however the ideal management of GCS is difficult to ascertain given the rare occurrence and variable presentation. Methods: Orthopaedic trauma database at a level 1 trauma center was reviewed to identify patients for whom the orthopaedic service was consulted due to suspicion of gluteal compartment syndrome. This yielded 11 patients between 2011 and 2019. Patients with a measured ΔP greater than 30 upon initial consultation and with a concerning exam requiring monitoring were included. Patient demographics, comorbidities, GCS etiology, laboratory values, physical exam findings, pain scores (0-10) and patient outcomes were collected via chart review. Patient demographic and injury characteristics were summarized using descriptive statistics. Results: Prolonged immobilization patients had worse outcomes including longer hospital stays (40.5 days) compared to trauma patients (4.5 days). All adverse medical outcomes recorded including acute renal failure, prolonged neuropathic pain, cardiopulmonary dysfunction were exclusively experienced by prolonged immobilization patients. Conclusions: Our descriptive study demonstrates the bimodal distribution of GCS patients based on etiology. Prolonged immobilization patients have a longer hospital course and more complications. Our study confirms prior reports and provides information that can be used to counsel patients and families appropriately about treatment and recovery following GCS. Level of evidence: IV. Study type: Epidemiological.

Does Anterior Plating of Pelvic Ring Fractures Increase Infection Risk in Patients With Bladder or Urethral Injuries?

OBJECTIVES: Evaluate the effect of anterior fixation on infection in patients with operative pelvic fractures and bladder or urethral injuries. DESIGN: Retrospective. SETTING: Eight centers. PATIENT SELECTION CRITERIA: Adult patients with closed pelvic fractures with associated bladder or urethral injuries treated with anterior plating (AP), intramedullary screw (IS), or no anterior internal fixation (NAIF, including external fixation or no fixation). OUTCOME MEASURES AND COMPARISONS: Deep infection. RESULTS: There were 81 extraperitoneal injuries and 57 urethral injuries. There was no difference in infection between fixation groups across all urologic injuries (AP: 10.8%, IS: 0%, NAIF: 4.9%, P = 0.41). There was a higher rate of infection in the urethral injury group compared with extraperitoneal injuries (14.0% vs. 2.5%, P = 0.016). Among extraperitoneal injuries, specifically, there was no difference in deep infection related to fixation (AP: 2.6%, IS 0%, NAIF: 2.9%, P = 0.99). Among urethral injuries, there was no statistical difference in deep infection related to fixation (AP: 23.1%, IS: 0%, NAIF: 7.4%, P = 0.21). There was a higher rate of suprapubic catheter (SPC) use in urethral injuries compared with extraperitoneal injuries (57.9% vs. 4.9%, P < 0.0001). In the urethral injury group, SPC use did not have a statistically significant difference in infection rate (SPC: 18.2% vs. No SPC: 8.3%, P = 0.45). Early removal of the SPC before or during the definitive orthopaedic intervention did not significantly affect infection rate (early: 0% vs. delayed: 25.0%, P = 0.16). CONCLUSIONS: Surgeons should approach operative pelvic fractures with associated urologic injuries with caution given the high risk of infection. Further work must be done to elucidate the effect of anterior implants and SPC use and duration. LEVEL OF EVIDENCE: Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.

Bicondylar Tibial Plateau Fractures: What Predicts Infection?

OBJECTIVES: The purpose of this study was to identify the patient, injury, and treatment factors associated with infection of bicondylar plateau fractures and to evaluate whether center variation exists. DESIGN: Retrospective review. SETTING: Eighteen academic trauma centers. PATIENTS/PARTICIPANTS: A total of 1,287 patients with 1,297 OTA type 41-C bicondylar tibia plateau fractures who underwent open reduction and internal fixation were included. Exclusion criteria were follow-up less than 120 days, insufficient documentation, and definitive treatment only with external fixation. INTERVENTION: Open reduction and internal fixation. MAIN OUTCOME MEASUREMENTS: Superficial and deep infection. RESULTS: One hundred one patients (7.8%) developed an infection. In multivariate regression analysis, diabetes (DM) (OR [odds ratio] 3.24; P ≤ 0.001), alcohol abuse (EtOH) (OR 1.8; P = 0.040), dual plating (OR 1.8; P ≤ 0.001), and temporary external fixation (OR 2.07; P = 0.013) were associated with infection. In a risk-adjusted model, we found center variation in infection rates (P = 0.030). DISCUSSION: In a large series of patients undergoing open reduction and internal fixation of bicondylar plateau fractures, the infection rate was 7.8%. Infection was associated with DM, EtOH, combined dual plating, and temporary external fixation. Center expertise may also play a role because one center had a statistically lower rate and two trended toward higher rates after adjusting for confounders. LEVEL OF EVIDENCE: Level IV-Therapeutic retrospective cohort study.

Is the timing of fixation associated with fracture-related infection among tibial plateau fracture patients with compartment syndrome? A multicenter retrospective cohort study of 729 patients.

BACKGROUND: Tibial plateau fractures with an ipsilateral compartment syndrome are a clinical challenge with limited guidance regarding the best time to perform open reduction and internal fixation (ORIF) relative to fasciotomy wound closure. This study aimed to determine if the risk of fracture-related infection (FRI) differs based on the timing of tibial plateau ORIF relative to closure of ipsilateral fasciotomy wounds. METHODS: A retrospective cohort study identified patients with tibial plateau fractures and an ipsilateral compartment syndrome treated with 4-compartment fasciotomy at 22 US trauma centers from 2009 to 2019. The primary outcome measure was FRI requiring operative debridement after ORIF. The ORIF timing relative to fasciotomy closure was categorized as ORIF before, at the same time as, or after fasciotomy closure. Bayesian hierarchical regression models with a neutral prior were used to determine the association between timing of ORIF and infection. The posterior probability of treatment benefit for ORIF was also determined for the three timings of ORIF relative to fasciotomy closure. RESULTS: Of the 729 patients who underwent ORIF of their tibial plateau fracture, 143 (19.6%) subsequently developed a FRI requiring operative treatment. Patients sustaining infections were: 21.0% of those with ORIF before (43 of 205), 15.9% at the same time as (37 of 232), and 21.6% after fasciotomy wound closure (63 of 292). ORIF at the same time as fasciotomy closure demonstrated a 91% probability of being superior to before closure (RR, 0.75; 95% CrI, 0.38 to 1.10). ORIF after fasciotomy closure had a lower likelihood (45%) of a superior outcome than before closure (RR, 1.02; 95% CrI; 0.64 to 1.39). CONCLUSION: Data from this multicenter cohort confirms previous reports of a high FRI risk in patients with a tibial plateau fracture and ipsilateral compartment syndrome. Our results suggest that ORIF at the time of fasciotomy closure has the highest probability of treatment benefit, but that infection was common with all three timings of ORIF in this difficult clinical situation.

Proximal tibia fracture dislocations: Management and outcomes of a severe and under-recognized injury.

INTRODUCTION: Proximal tibia fracture dislocations (PTFDs) are a subset of plateau fractures with little in the literature since description by Hohl (1967) and classification by Moore (1981). We sought to evaluate reliability in diagnosis of fracture-dislocations by traumatologists and to compare their outcomes with bicondylar tibial plateau fractures (BTPFs). METHODS: This was a retrospective cohort study at 14 level 1 trauma centers throughout North America. In all, 4771 proximal tibia fractures were reviewed by all sites and 278 possible PTFDs were identified using the Moore classification. These were reviewed by an adjudication board of three traumatologists to obtain consensus. Outcomes included inter-rater reliability of PTFD diagnosis, wound complications, malunion, range of motion (ROM), and knee pain limiting function. These were compared to BTPF data from a previous study. RESULTS: Of 278 submitted cases, 187 were deemed PTFDs representing 4% of all proximal tibia fractures reviewed and 67% of those submitted. Inter-rater agreement by the adjudication board was good (83%). Sixty-one PTFDs (33%) were unicondylar. Eleven (6%) had ligamentous repair and 72 (39%) had meniscal repair. Two required vascular repair. Infection was more common among PTFDs than BTPFs (14% vs 9%, p = 0.038). Malunion occurred in 25% of PTFDs. ROM was worse among PTFDs, although likely not clinically significant. Knee pain limited function at final follow-up in 24% of both cohorts. CONCLUSIONS: PTFDs represent 4% of proximal tibia fractures. They are often unicondylar and may go unrecognized. Malunion is common, and PTFD outcomes may be worse than bicondylar fractures.

Acute Presentation of a Pseudoaneurysm After a Proximal Humerus Shaft Fracture: A Case Report.

CASE: A 69-year-old woman presented with a brachial artery pseudoaneurysm causing median, ulnar, and radial nerve compressive neuropathies 8 weeks after a proximal humerus shaft fracture treated with intramedullary nailing. She underwent a brachial artery bypass with a reverse cephalic vein interposition graft and neurolysis after decompression of a large pseudoaneurysm. Postoperatively, the patient had a normal vascular examination with recovering neurological function. CONCLUSIONS: A high index of suspicion for a brachial artery pseudoaneurysm should be maintained in patients with a displaced proximal humerus shaft fracture, particularly when an abnormal neurovascular examination is present.

Management of the Floating Knee: Ipsilateral Fractures of the Femur and Tibia.

The "floating knee" is defined as fractures of the ipsilateral femur and tibia, which consists of a spectrum of injury, and may be in isolation or part of multiple system trauma for a given patient. A floating knee may compromise limb viability due to severe soft-tissue and vascular injury. Expeditious fracture reduction and patient resuscitation are crucial, while type and timing of provisional and definitive management is guided by the extent of injury to the involved extremity and associated systemic injuries. Numerous surgical techniques are available to treat the floating knee, including external fixation and internal fixation with plates or intramedullary nails. Fracture complexity and severity of soft-tissue injury present challenges, with articular injuries potentially more debilitating in the long term. Complications such as infection, deep vein thrombosis, knee stiffness, nonunion, malunion, and posttraumatic arthrosis after these injuries should be considered.

Wear Particle-induced Priming of the NLRP3 Inflammasome Depends on Adherent Pathogen-associated Molecular Patterns and Their Cognate Toll-like Receptors: An In Vitro Study.

BACKGROUND: Orthopaedic wear particles activate the NLRP3 inflammasome to produce active interleukin 1ß (IL1ß). However, the NLRP3 inflammasome must be primed before it can be activated, and it is unknown whether wear particles induce priming. Toll-like receptors (TLRs) are thought to mediate particle bioactivity. It remains controversial whether pathogen-associated molecular patterns (PAMPs) and/or alarmins are responsible for TLR activation by wear particles. QUESTIONS/PURPOSES: (1) Does priming of the NLRP3 inflammasome by wear particles depend on adherent PAMPs? (2) Does priming of the NLRP3 inflammasome by wear particles depend on TLRs and TIRAP/Mal? (3) Does priming of the NLRP3 inflammasome by wear particles depend on cognate TLRs? (4) Does activation of the NLRP3 inflammasome by wear particles depend on adherent PAMPs? METHODS: Immortalized murine macrophages were stimulated by as-received titanium particles with adherent bacterial debris, endotoxin-free titanium particles, or titanium particles with adherent ultrapure lipopolysaccharide. To study priming, NLRP3 and IL1ß mRNA and IL1ß protein levels were assessed in wild-type, TLR4, TLR2, and TIRAP/Mal macrophages. To study activation, IL1ß protein secretion was assessed in wild-type macrophages preprimed with ultrapure lipopolysaccharide. RESULTS: Compared with titanium particles with adherent bacterial debris, endotoxin-free titanium particles induced 86% less NLRP3 mRNA (0.05 ± 0.03 versus 0.35 ± 0.01 NLRP3/GAPDH, p < 0.001) and 91% less IL1ß mRNA (0.02 ± 0.01 versus 0.22 ± 0.03 IL1ß/GAPDH, p < 0.001). ProIL1ß protein level was robustly increased in wild-type macrophages stimulated by particles with adherent PAMPs but was not detectably produced in macrophages stimulated by endotoxin-free particles. Adherence of ultrapure lipopolysaccharide to endotoxin-free particles reconstituted stimulation of NLRP3 and IL1ß mRNA. Particles with adherent bacterial debris induced 79% less NLRP3 mRNA (0.09 ± 0.004 versus 0.43 ± 0.13 NLRP3/GAPDH, p < 0.001) and 40% less IL1ß mRNA (0.09 ± 0.04 versus 0.15 ± 0.03 IL1ß/GAPDH, p = 0.005) in TLR4 macrophages than in wild-type. Similarly, those particles induced 49% less NLRP3 mRNA (0.22 ± 0.10 versus 0.43 ± 0.13 NLRP3/GAPDH, p = 0.004) and 47% less IL1ß mRNA (0.08 ± 0.02 versus 0.15 ± 0.03 IL1ß/GAPDH, p = 0.012) in TIRAP/Mal macrophages than in wild-type. Particles with adherent ultrapure lipopolysaccharide induced 96% less NLRP3 mRNA (0.012 ± 0.001 versus 0.27 ± 0.05 NLRP3/GAPDH, p = 0.003) and 91% less IL1ß mRNA (0.03 ± 0.01 versus 0.34 ± 0.07 IL1ß/GAPDH, p < 0.001) expression in TLR4 macrophages than in wild-type. In contrast, those particles did not induce less NLRP3 and IL1ß mRNA in TLR2 macrophages. IL1ß protein secretion was equivalently induced by particles with adherent bacterial debris or by endotoxin-free particles in a time-dependent manner in wild-type macrophages. For example, particles with adherent bacterial debris induced 99% ± 2% of maximal IL1ß secretion after 12 hours, whereas endotoxin-free particles induced 92% ± 11% (p > 0.5). CONCLUSIONS: This cell culture study showed that adherent PAMPs are required for priming of the NLRP3 inflammasome by wear particles and this process is dependent on their cognate TLRs and TIRAP/Mal. In contrast, activation of the NLRP3 inflammasome by titanium particles is not dependent on adherent PAMPs. Animal and implant retrieval studies are needed to determine whether wear particles have similar effects on the NLRP3 inflammasome in vivo. CLINICAL RELEVANCE: Our findings, together with recent findings that aseptic loosening associates with polymorphisms in the TIRAP/Mal locus, support that adherent PAMPs may contribute to aseptic loosening in patients undergoing arthroplasty.

Catastrophic Failure of the Acetabular Polyethylene Liner in Ceramic-on-Polyethylene Total Hip Arthroplasty.

INTRODUCTION: Catastrophic polyethylene failure is a rare complication of ceramic-on-polyethylene total hip arthroplasty due to the favorable tribological characteristics of ceramic. Failure of the polyethylene liner can be disastrous, increasing periprosthetic osteolysis, metallosis, and risk of dislocation. Complications associated with ceramic-on-polyethylene articulations have been studied extensively, however, only few reports have described its catastrophic wear. We report such a case of complete wear of the acetabular liner in a ceramic-on-polyethylene prosthesis in a 57-year adult male. CASE REPORT: A 57-year adult male with a history of bilateral total hip arthroplasty presented to our institution with bilateral hip pain worst on the right. Range of motion was limited by pain on the right hip at the extremes of motion. Radiographs revealed severe osteolysis, heterotopic ossification, complete wear of the acetabular liner, bony impingement of the femoral greater trochanter on the acetabular rim and superior migration of the femoral head. All findings were confirmed intraoperatively. Revision of the acetabular components was performed, which successfully alleviated the patient's symptoms. CONCLUSION: Failure of the ceramic-on-polyethylene liner in our patient is due to the use of a non-cross linked polyethylene liner, a highly active lifestyle, and poor follow up. Arthroplasty surgeons should be aware of this complication especially in highly active patients with a conventional polyethylene liner and chronic hip pain.

Posterior dislocation of the hinge-post extension in a rotating hinge total knee prosthesis.

The rotating hinge knee prosthesis is a popular intervention in patients lacking stability with highly constrained total knee arthroplasty. Despite improvements in design, nonmechanical and mechanical complications continue to be a problem. Dislocation of the hinge has been widely described, mainly due to the component fracture. Few reports describe isolated dislocation of the rotating stem. We report a case of isolated disengagement of the rotating hinge mechanism, due to severe flexion gap imbalance, leading to subsequent posterior dislocation of the hinge and anterior knee dislocation, in a patient with a history of multiple total knee arthroplasty revisions. This case suggests the importance of the soft tissue balancing, the adequate patellar tracking, and use of a long cylindrical, minimally tapered rotating stem in hinge arthroplasty to minimize hinge dislocation.

Nerve allografts and conduits in peripheral nerve repair.

Since the last update on nerve conduits and allograft in 2000, investigations have established the efficacy of these alternatives to autograft in the repair of small sensory neural gaps. However, limited insights into the biology of the regenerating nerve continue to preclude intelligent conduit design. Ongoing discoveries in neuroscience and biomaterial engineering hold promise for the eventual development of allograft and conduits with potential of surpassing nerve autografts in clinical efficacy. In this review, we summarize the history, recent advances, and emerging developments in nerve conduits and allograft.

Original article Muscle extracellular matrix degradation and contractibility following tendon rupture and disuse.

Muscle extracellular matrix (ECM) plays an important role in maintaining muscular integrity and force transduction. However, the role of ECM in skeletal muscle atrophy remains unknown. In this study, we employed two clinically relevant mouse models of Achillotenotomy and hindlimb suspension to simulate Achilles tendon rupture and hindlimb disuse. The gastrocnemius was harvested following two weeks of treatment. We hypothesized that degradation of muscle ECM basement membrane lead to dysfunction of muscle contractility. Our results demonstrated a significant reduction of gastrocnemius single twitch force, isometric tetanic force, and contraction velocity following tendon rupture (p<0.001), but not disuse. Additionally, up-regulation of matrix metalloproteinase-2 (MMP-2) was observed only after tendon rupture (p=0.00234). These findings suggest that ECM remodeling and basement membrane degradation due to MMP-2 may be responsible for declined muscle contractibility. Inhibiting ECM degradation enzymes may be a potential treatment strategy for skeletal muscle atrophy after tendon rupture.

Comparison of tissue oxygenation and compartment pressure following tibia fracture.

OBJECTIVE: We investigated the ability of direct continuous measurement of intramuscular tissue oxygenation (PmO(2)) to detect acute ischaemia in the leg in patients at risk for acute extremity compartment syndrome. Following tibia fracture treated by intramedullary nailing, we compared the proportions of PmO(2) and compartment pressure (CP) measurements that met the warning criteria for compartment syndrome. METHODS: Participants included 10 patients sustaining acute isolated closed tibia shaft fractures treated by intramedullary nailing. A tissue oxygenation probe and a CP probe were percutaneously placed into the anterior compartment of the leg. PmO(2) and CP in the anterior compartment were measured in the injured leg for 48 h postoperatively. Measurements meeting the warning criteria were defined as PmO(2) < 10 mmHg, CP > 30 mmHg and perfusion pressure ΔP < 30 mmHg. RESULTS: None of the patients developed compartment syndrome. Comparison of CP and PmO(2) showed a CP > 30 mmHg in 50.39% of CP measurements in all patients and a PmO(2) < 10 mmHg in 0.75% of PmO(2) measurements in two patients (P = 0.005). Comparison of ΔP and PmO(2) showed a ΔP < 30 mmHg in 31.01% of ΔP measurements in nine patients and a PmO(2) < 10 mmHg in 0.76% of PmO(2) measurements in one patient (P = 0.01). CONCLUSION: In the absence of compartment syndrome, pressure measurements following tibia fracture treated with intramedullary nailing often met the warning criteria, whereas PmO(2) did not, suggesting that measurement of intramuscular tissue oxygenation may represent a potential method for the identification of acute compartment syndrome that deserves continued investigation.

A mouse model of massive rotator cuff tears.

BACKGROUND: Rotator cuff tears are the most common tendon injury seen in orthopaedic patients. Muscle atrophy and fatty infiltration in rotator cuff muscles are considered among the key factors responsible for the failure of attempted repair of a massive rotator cuff tear. However, the pathophysiology of rotator cuff muscle atrophy and fatty infiltration remains largely unknown, partly because of the lack of appropriate small animal models. The goal of this study was to develop a mouse model of muscle atrophy and fatty infiltration after a rotator cuff tear. We also sought to study the role of denervation on muscle atrophy and fatty infiltration after a rotator cuff tear. METHODS: Adult wild-type FVB/N mice were randomly divided into three groups. Mice in different groups received unilateral complete supraspinatus and infraspinatus tendon transection, suprascapular nerve transection, or both procedures. Sham surgery was performed on the contralateral shoulder to serve as a control. Mice were killed twelve weeks after surgery. Histological analysis and high-resolution magnetic resonance imaging were used to evaluate muscle atrophy and fat infiltration after a rotator cuff tear. RESULTS: Significant and consistent muscle atrophy and fatty infiltration were observed in the rotator cuff muscles after rotator cuff tendon transection. We further found that denervation significantly increases the amount of muscle atrophy and fatty infiltration after a rotator cuff tear. CONCLUSIONS: We successfully developed a novel mouse model of a massive rotator cuff tear, which simulates major pathological changes, including muscle atrophy and fatty infiltration after massive rotator cuff tears seen in patients.

A rat model of massive rotator cuff tears.

Rotator cuff tears (RCTs) are the most common tendon injury seen in orthopedic patients. Massive RCT does not heal spontaneously and results in poor clinical outcomes. Muscle atrophy and fatty infiltration in rotator cuff muscles are major complications of chronic massive RCT and are thought to be the key factors responsible for the failure of attempted massive RCT repair. However, the pathophysiology of rotator cuff muscle atrophy and fat infiltration remains largely unknown, and no small animal model has been shown to reproduce the histologic and molecular changes seen in massive RCT. In this article, we report a novel rat massive RCT model, in which significant and consistent muscle atrophy and fat infiltration were observed in the rotator cuff muscles after rotator cuff tendon transection and denervation. The supraspinatus and infraspinatus muscle lost 25.4% and 28.9% of their wet weight 2 weeks after complete tendon transection, respectively. Six weeks after surgery, the average wet weight of supraspinatus and infraspinatus muscles decreased 13.2% and 28.3%, respectively. Significant fat infiltration was only observed in infraspinatus 6 weeks after tendon transection.

Role of AP-1 and RE-1 binding sites in matrix metalloproteinase-2 transcriptional regulation in skeletal muscle atrophy.

Previous work has suggested that an extracellular matrix degrading enzyme-matrix metalloproteinase-2 (MMP-2) plays an important role in the development of muscle atrophy. However, the transcriptional regulation mechanism of MMP-2 in skeletal muscle atrophy remains largely unknown. Using transgenic MMP-2 promoter reporter mice, we have demonstrated that AP-1 and RE-1 binding sites in the MMP-2 promoter region, coupled with increased binding of Fra-1, Fra-2 and AP-2, play a critical role in MMP-2 transcriptional regulation in muscle atrophy. Novel information gained from this study has improved our understanding of in vivo transcriptional regulation of MMP-2 in skeletal muscle atrophy.