Introduction

Femoral periprosthetic fractures above TKA are commonly treated with retrograde intramedullary nailing (IMN). This study determined if TKA design and liner type affect the minimum knee flexion required for retrograde nailing through a TKA.

Periprosthetic femoral shaft fractures are a significant complication of total hip arthroplasty. Plate osteosynthesis with or without onlay strut allograft has been the mainstay of treatment around well-fixed stems. Nonunions are a rare, challenging complication of this fixation method. The number of published treatment strategies for periprosthetic femoral nonunions are limited. In this series, we report the outcomes of a novel orthogonal plating surgical technique for addressing nonunions in the setting of Vancouver B1 and C-type periprosthetic fractures that previously failed open reduction internal fixation (ORIF).

A retrospective chart review of all patients from 2010 to 2014 with Vancouver B1/C total hip arthroplasty periprosthetic femoral nonunions was performed. All patients were treated primarily with ORIF. Nonunion was defined as no radiographic signs of fracture healing nine months post-operatively, with or without hardware failure. Exclusion criteria included open fractures and periprosthetic infections. The technique utilised a mechanobiologic strategy of atraumatic exposure, resection of necrotic tissue, bone grafting with adjuvant recombinant growth factor and revision open reduction internal fixation. Initially, compression was achieved using an articulated tensioning device and application of an anterior plate. This was followed by locked lateral plating. Patients remained non-weight bearing for eight weeks.

Six Vancouver B1/C periprosthetic femoral nonunions were treated. Five patients were female with an average age of 80.3 years (range 72–91). The fractures occurred at a mean of 5.8 years (range 1–10) from their initial arthroplasty procedure. No patients underwent further revision surgery; there were no wound dehiscence, hardware failures, infections, or surgical complications. All patients had a minimum of nine months follow up (mean 16.6, range 9–36). All fractures achieved osseous union, defined as solid bridging callus over at least two cortices and pain free, independent ambulation, at an average of 24.4 weeks (range 6.1–39.7 weeks).

To our knowledge, this is the first case series describing 90–90 locked compression plating using modern implants for periprosthetic femoral nonunions. This is a rare but challenging complication of total hip arthroplasty and we present a novel solution with satisfactory preliminary outcomes. Orthogonal locked compression plating utilising an articulated tensioning device and autograft with adjuvant osteoinductive allograft should be considered in periprosthetic femur fractures around a well-fixed stem. Further biomechanical and clinical research is needed to improve our treatment strategies in this population.

The purpose of this study was to examine the utility of the acetabular component introducer as a tool to intra-operatively predict implant inclination in total hip arthroplasty. This study investigated (1) the correlation between intra-operative photographic assessment of cup inclination using the acetabular introducer and that measured on post-operative radiograph; and (2) the accuracy of intra-operative prediction of abduction angle.

For this study, we prospectively recruited 56 patients scheduled to receive primary hip arthroplasty from one of two senior surgeons. During the procedure, the lead surgeon provided a prediction of the abduction angle based on the alignment of the impactor attached to the cup in its final seated position. A standardized anteroposterior (AP) photograph was then taken of the acetabular impactor in situ. Abduction angles were measured by two observers on the photographs and post-operative AP pelvis radiographs. Linear regression was used to determine the correlation between the angle of the guide measured on the photographs and the actual position of the implant measured on the radiograph. Descriptive statistics were further used to analyze the accuracy of the intra-operative prediction as compared with the abduction angle measured on the photographs.

Measurements of cup position made from post-operative radiographs were significantly correlated with the measurements as assessed by intra-operative photographs (r = 0.34, p = 0.00). Our findings demonstrate that radiological abduction angles tend to be greater than that assessed by intra-operative photographs by a mean of 5.6 degrees (SD = 6.6 degrees; 95% CI = 7.3 to 3.9 degrees). Conversely, surgeon prediction of cup inclination based on the acetabular introducer differed from the radiographic measurements by a mean of 6.8 degrees (SD = 8.7 degrees). There was good agreement between the two observers in both photographic and radiographic measurement (k = 0.95, k = 0.96, respectively).

In conclusion, we found that the intra-operative photographic assessment of acetabular cup inclination by acetabular impactor alignment tends to underestimate the abduction angle by a mean of approximately 5 degrees. In addition, intra-operative surgeon estimation of acetabular inclination did not appear accurate in this study demonstrating that cup position should rely on additional visual cues beyond that captured in the anteroposterior view of the cup introducer.

To investigate differences between the Reamer Irrigator Aspirator and the AO reamer on fat embolism outcome using a porcine model.

All animal procedures were approved and performed in accordance with the Animal Care Committee at St. Michael’s hospital. Following anesthetic administration, the animals were stabilised for thirty minutes. One third of the pig’s blood volume was withdrawn to simulate hemorrhagic shock. Each animal was kept in a state of hypovolemia for an hour before transfusion and resuscitation. Once the animal was stabilised surgical exposure of the distal femur was completed. A 12 mm Reamer Irrigator Aspirator or AO reamer was used depending on which group the animal was assigned to. Blood work was obtained at: baseline, immediately after induction of hypovolemia, one hour post hypovolemia, post stabilization, one minute, five minutes, 1.5 hours and three hours after reaming. The results were analyzed for activation of the coagulation system, platelet and neutrophil activation, and cytokine elevation. ANOVA was the primary tool used to assess statistical significance.

There was no statistical difference between the two reamers with respect to PT, APTT, and fibrinogen. There was a statistical difference in D-dimer at 1.5 and three hours post-reaming, with the RIA showing a lower value. Neither reamer demonstrated any systemic platelet nor neutrophil activation. TNF-alpha spiked immediately post-reaming with the RIA group returning to baseline values and the AO group remaining elevated. There is a spike in IL-1B post reaming in the AO group, however this was not seen in the RIA group. No statistical difference was detected between the two reamers.

All markers for platelet and neutrophil activation and the coagulation cascade were measured at the systemic level. Although there is no statistical difference between the RIA and AO reamer, it is possible that activated cells were removed from the systemic circulation and sequestered as thrombi in the pulmonary microvasculature. This hypothesis may be supported by a drop in platelet count and an increase in D-dimer, with the AO reamer suggesting greater thrombi formation. The trends in IL-1B and TNF-alpha seem to suggest that the RIA abrogates the post-reaming proinflammatory state.

This study was undertaken to assess the contribution of pulmonary fat embolism to systemic platelet activation in a rabbit model of fat embolism. Fifteen NZW rabbits were randomly assigned into one of two groups: fat embolism and control. Fat embolism was induced via intramedullary canal pressurization with a 1–1.5 ml bone cement injection. Only the animals that underwent fat embolism displayed consistent platelet activation, as demonstrated by platelet degranulation and procoagulatory surface expression. These findings suggest that fat embolism plays a role in platelet activation and in the overall activation of hemostasis following trauma.

The objective of this study was to use a recently developed rabbit model of fat embolism to assess the systemic hemostatic response to pulmonary fat embolism.

Our findings demonstrate platelet activation following forced liberation of bone marrow contents into the circulation only in the FE group, as demonstrated by CD62P elevation (a marker of platelet degranulation) and annexin V elevation (a marker of procoagulatory surface expression). Platelet activation also coincided with significantly lower platelet counts in the FE group at two and four hours post embolism, suggesting platelet aggregation.

These findings suggest that fat embolism plays a role in platelet activation and in the overall activation of hemostasis following trauma.

Platelet count decreased significantly at two and four hours post knee manipulation only in the FE group. Annexin V expression increased significantly in the FE group at two and four hours post knee manipulation. Lastly, CD62P expression only increased significantly in the FE group at two hours post knee manipulation

Fifteen New Zealand White male rabbits were randomly assigned into one of two groups: control and fat embolism (FE). In FE group (n=8), the intramedullary cavity was drilled, reamed and pressurized with a 1–1.5 ml bone cement injection. In the control group (n=7), a sham knee incision was made, exposing both femoral condyles, but was immediately closed without further manipulations. All animals were mechanically ventilated for an additional monitoring period of four hours post-surgical closure. For flow cytometric evaluation of platelet activation, blood samples were stained with fluorescence-conjugated antibodies against CD41 (FITC), CD62P (P-selectin) and annexin V (FITC). Platelet events were identified by their characteristic CD41 staining and size and were analyzed using a flow cytometer. All animals were mechanically ventilated for four hours post surgical closure.

The implications of platelet activation following fat embolism are numerous, ranging from adherence and aggregation, to secretion of key components of both the coagulation and inflammatory cascades.

The purpose of this study was to determine the effect of positioning (lateral vs. supine) on pulmonary patho-physiology following pulmonary contusion and fat embolism in a canine model of polytrauma. Platelet and neutrophil activation were assessed using flow-cytometry. There were no significant differences between groups in CD62P and CD11/18 MCF (markers of platelet and neutrophil activation, respectively) following fat embolism. However, only animals in the lateral position displayed significant increases in both measures as compared to baseline values. Lateral positioning may exert an early effect on proinflammatory and coagulation activation, and may play a role in the development of acute lung injury.

It has previously been suggested that acute lung injury can be influenced by patient positioning, be it lateral or supine. The purpose of this study was to determine the effect of positioning on pulmonary pathophysiology associated with concomitant pulmonary contusion and fat embolism in a canine model of polytrauma.

Twelve dogs were randomly assigned to one of two surgical positioning groups, lateral and supine. The dogs were subjected to pulmonary contusion by application of force between 200–250 N/m² for thirty seconds in three areas of one lung. Two hours later, fat embolism was induced via reaming of the ipsilateral femur and tibia and cemented nailing. Two hours later, the dogs were sacrificed. For flow-cytometric evaluation of platelet and neutrophil activation, venous blood samples were stained with fluorescence-conjugated antibodies against CD62P and CD11/18, respectively. There were no significant differences between the groups in CD62P and CD11/18 mean channel fluorescence (MCF) following pulmonary contusion and fat embolism. However, only animals in the lateral positioning group displayed significant increases in CD62P and CD11/18 MCF at two hours following fat embolism as compared to baseline values.

Our findings suggest that lateral positioning, autoregulation and preferential blood flow to the contused non-dependent lung may render lung tissue more susceptible to congestion and lead to activation of both platelets and neutrophils. Lateral positioning may have an early effect on activation of the inflammatory and coagulation cascades and may be significant in the development of posttraumatic acute lung injury.

Purpose: The objective of this study is to investigate the effects of the Reamer-Irrigator-Aspirator (RIA) on fat embolism outcome, as compared to the standard AO reamer, utilizing physiologic parameters as outcome measures.

Methods: All animal procedures were approved by the Animal Care Committee. Fifteen animal experiments were completed. Following anesthesia, each pig was intubated and ventilated. Initial blood samples were analyzed for proper ventilation and acceptable baseline conditions (PaCO2 between 35–40 mm Hg). One third of the pig’s blood volume was withdrawn to simulate hemorrhagic shock. Each animal was kept in a state of hypovolemia for an hour before transfusion and resuscitation. Each pig underwent alternate assignment into either the RIA or AO group. The distal femur was exposed and reamed in a retrograde fashion, followed by cement pressurization with methylmethacrylate. Physiologic measurements included mean arterial pressure (MAP), pulmonary arterial pressure (PAP), partial pressure of arterial oxygen (PaO2), and cardiac output. Upon completion, the animals were euthanized. The data was analyzed using the SPSS statistical program.

Results: One animal in the AO group expired after cement pressurization associated with profound hypotension, pulmonary hypertension and eventual cardiac arrest. There was a statistically significant difference for PaO2 (P = 0.004), cardiac output (P = 0.002), and PAP (P = 0.005) between the AO and RIA groups. That is, by the completion of the experiment the RIA group had higher PaO2, lower PAP, and higher cardiac output measurements as compared to the AO group. There was no statistical significance between the two groups with respect to MAP (P = 0.468).

Conclusions: Using established physiologic parameters, there appears to be a difference between the standard AO reamer and the RIA in terms of fat embolism outcome. The RIA showed a more favorable outcome with respect to PAP, PaO2, and cardiac output. With its simultaneous irrigation and aspiration, the RIA may result in less intramedullary fat displacement into the systemic circulation.

This study was undertaken to assess the contribution of fat embolism (FE) to the development of acute lung injury in the presence of resuscitated hemorrhagic shock. Twenty-seven NZW rabbits were randomly assigned into four groups: resuscitated hemorrhagic shock and FE (HR/FE), resuscitated hemorrhagic shock, FE, and control. FE was induced via intramedullary femoral canal pressurization using a 1–1.5 ml bone cement injection. Only HR/FE animals displayed significant proinflammatory cytokine release as compared to controls. These findings suggest that the combination of resuscitated shock with FE initiates an inflammatory response, which may lead to the development of fat embolism syndrome.

The objective of this study was to assess the contribution of fat embolism caused by intramedullary femoral canal pressurization to the development of acute lung injury in the presence of resuscitated hemorrhagic shock.

Only the animals that underwent resuscitated shock and fat embolism displayed amplified BALF proinflammatory cytokine expression.

These findings suggest that the combination of resuscitated shock with fat embolism initiates an inflammatory response, which may play a role in the development of fat embolism syndrome.

Only HR/FE BALF IL-8 and MCP-1 levels were significantly higher than controls (0.72 ng/ml vs. 0.26ng/ ml, p=0.03; 18.3 ng/ml vs. 2.0 ng/ml, p=0.01, respectively).

Twenty-seven NZW rabbits were randomly assigned into four groups: resuscitated hemorrhagic shock + fat embolism (HR/FE), resuscitated hemorrhagic shock (HR), fat embolism (FE), and control. Shock was induced via carotid bleeding for one-hour prior to resuscitation. For FE induction, the intramedullary cavity was drilled, reamed and pressurized with a 1–1.5 ml bone cement injection. Four hours later, postmortem bronchoalveolar lavage was performed through the right mainstem bronchus. Analyses of bronchoalveolar lavage fluid (BALF) of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) were carried out in triplicate and blinded fashion using the ELISA technique.

Our findings suggest that FE by itself does not initiate inflammatory lung injury, as there were no apparent differences between the control and FE cytokine levels. Only the HR/FE animals revealed elevated levels of pro-inflammatory cytokines in BALF. These findings are in agreement with our previous results, which displayed neutrophil activation only in the HR/FE group.

The purpose of this study was to determine the effect of positioning (lateral vs. supine) on pulmonary pathophysiology following pulmonary contusion and fat embolism in a canine model of polytrauma. Platelet and neutrophil activation were assessed using flow-cytometry. There were no significant differences between groups in CD62P and CD11/18 MCF (markers of platelet and neutrophil activation, respectively) following fat embolism. However, only animals in the lateral position displayed significant increases in both measures as compared to baseline values. Lateral positioning may exert an early effect on proinflammatory and coagulation activation, and may play a role in the development of acute lung injury.

It has previously been suggested that acute lung injury can be influenced by patient positioning, be it lateral or supine. The purpose of this study was to determine the effect of positioning on pulmonary pathophysiology associated with concomitant pulmonary contusion and fat embolism in a canine model of polytrauma.

Twelve dogs were randomly assigned to one of two surgical positioning groups, lateral and supine. The dogs were subjected to pulmonary contusion by application of force between 200–250 N/m² for thirty seconds in three areas of one lung. Two hours later, fat embolism was induced via reaming of the ipsilateral femur and tibia and cemented nailing. Two hours later, the dogs were sacrificed. For flow-cytometric evaluation of platelet and neutrophil activation, venous blood samples were stained with fluorescence-conjugated antibodies against CD62P and CD11/18, respectively.

There were no significant differences between the groups in CD62P and CD11/18 mean channel fluorescence (MCF) following pulmonary contusion and fat embolism. However, only animals in the lateral positioning group displayed significant increases in CD62P and CD11/18 MCF at two hours following fat embolism as compared to baseline values.

Our findings suggest that lateral positioning, autoregulation and preferential blood flow to the contused non-dependent lung may render lung tissue more susceptible to congestion and lead to activation of both platelets and neutrophils. Lateral positioning may have an early effect on activation of the inflammatory and coagulation cascades and may be significant in the development of posttraumatic acute lung injury.

This study was undertaken to assess the contribution of pulmonary fat embolism caused by intramedullary femoral canal pressurization to the development of acute lung injury in the presence of resuscitated hemorrhagic shock. Twenty-seven NZW rabbits were randomly assigned into one of four groups: resuscitated hemorrhagic shock and fat embolism, resuscitated hemorrhagic shock, fat embolism, and control. Fat embolism was induced via intramedullary cavity with a 1–1.5 ml bone cement injection. Only the animals that underwent resuscitated shock and fat embolism displayed amplified neutrophil activation and alveolar infiltration. These findings suggest that the combination of resuscitated shock with fat embolism initiates an inflammatory response, which may play a role in the development of fat embolism syndrome.

The objective of this study was to assess the contribution of pulmonary fat embolism caused by intramedullary femoral canal pressurization to the development of acute lung injury in the presence of resuscitated hemorrhagic shock.

Only the animals that underwent resuscitated shock and fat embolism displayed amplified neutrophil activation and alveolar infiltration.

These findings suggest that the combination of resuscitated shock with fat embolism initiates an inflammatory response, which may play a role in the development of fat embolism syndrome.

CD11b mean channel florescence was only significantly elevated in the HR/FE group at two and four hours post knee manipulation. Moreover, greater infiltration of alveoli by leukocytes was only significantly higher in the HR/FE group as compared to controls.

Twenty-seven NZW rabbits were randomly assigned into one of four groups: resuscitated hemorrhagic shock + fat embolism (HR/FE), resuscitated hemorrhagic shock (HR), fat embolism (FE), and control. Hypovolemic shock was induced via carotid bleeding for one-hour prior to resuscitation. For fat embolism induction, the intramedullary cavity was drilled, reamed and pressurized with a 1–1.5 ml bone cement injection. For evaluation of neutrophil activation, blood was stained with antibodies against CD45 and CD11b and analyzed with a flow cytometer. Animals were mechanically ventilated for four hours post surgical closure. Postmortem thoracotomy was performed, and three stratified random blocks of each lung were processed for histological examination.

Our findings suggest that FE by itself does not cause lung injury, as there were no apparent differences between the control and FE animals. Only the HR/FE animals revealed a higher number of infiltrating neutrophils into alveolar spaces and greater neutrophil activation.

The purpose of this study was to determine the effect of positioning (lateral vs. supine) on pulmonary pathophysiology following pulmonary contusion and fat embolism in a canine model of polytrauma. Platelet and neutrophil activation were assessed using flow-cytometry. There were no significant differences between groups in CD62P and CD11/18 MCF (markers of platelet and neutrophil activation, respectively) following fat embolism. However, only animals in the lateral position displayed significant increases in both measures as compared to baseline values. Lateral positioning may exert an early effect on proinflammatory and coagulation activation, and may play a role in the development of acute lung injury.

It has previously been suggested that acute lung injury can be influenced by patient positioning, be it lateral or supine. The purpose of this study was to determine the effect of positioning on pulmonary pathophysiology associated with concomitant pulmonary contusion and fat embolism in a canine model of polytrauma.

Twelve dogs were randomly assigned to one of two surgical positioning groups, lateral and supine. The dogs were subjected to pulmonary contusion by application of force between 200–250 N/m² for thirty seconds in three areas of one lung. Two hours later, fat embolism was induced via reaming of the ipsilateral femur and tibia and cemented nailing. Two hours later, the dogs were sacrificed. For flow-cytometric evaluation of platelet and neutrophil activation, venous blood samples were stained with fluorescence-conjugated antibodies against CD62P and CD11/18, respectively.

There were no significant differences between the groups in CD62P and CD11/18 mean channel fluorescence (MCF) following pulmonary contusion and fat embolism. However, only animals in the lateral positioning group displayed significant increases in CD62P and CD11/18 MCF at two hours following fat embolism as compared to baseline values.

Our findings suggest that lateral positioning, autoregulation and preferential blood flow to the contused non-dependent lung may render lung tissue more susceptible to congestion and lead to activation of both platelets and neutrophils. Lateral positioning may have an early effect on activation of the inflammatory and coagulation cascades and may be significant in the development of posttraumatic acute lung injury.