Delayed management of high energy femoral shaft fractures is associated with increased complication rates. It has been suggested that there is less urgency to stabilize lower energy femoral shaft fractures. The purpose of this study was to evaluate the effect of surgical delay on 30-day complications following fixation of lower energy femoral shaft fractures.

Patients ≥ 18 years who underwent either plate or nail fixation of low energy (falls from standing or up to three steps' height) femoral shaft fractures from 2005 – 2016 were identified from the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) via procedural codes. Patients with pathologic fractures, fractures of the distal femur or femoral neck were excluded. Patients were categorized into early (< 2 4 hours) or delayed surgery (2–30 days) groups. Bivariate analyses were used to compare demographics and unadjusted rates of complications between groups. A multivariable logistic regression was used to compare the rate of major and minor complications between groups, while adjusting for relevant covariables. Head injury patients and polytrauma patients are not included in the NSQIP database.

Of 2,716 lower energy femoral shaft fracture patients identified, 2,412 (89%) were treated within 1 day of hospital admission, while 304 (11.2%) were treated between 2 and 30 days post hospital admission. Patient age, American Society of Anesthesiologists (ASA) classification score, presence of diabetes, functional status, smoking status, and surgery type (nail vs. plate) were significantly different between groups (p After adjusting for all relevant covariables, delayed surgery significantly increased the odds of 30-day minor complications (p=0.02, OR = 1.48 95%CI 1.01–2.16), and 30-day mortality (p < 0 .001), OR = 1.31 (95%CI 1.03–2.14).

The delay of surgical fixation of femoral shaft fractures appears to significantly increase patients' risk of minor adverse events as well as increase mortality. With only 89% of patients being treated in the 24 hour timeframe that constitutes best practice for treatment of femoral shaft fractures, there remains room for improvement. These results suggest that early treatment of all femoral shaft fractures, even those with a lower energy mechanism of injury, leads to improved outcomes.

Distal radius fractures are the most common adult fractures, yet there remains some uncertainty surrounding optimal treatment modalities. Recently, the rate of operative treatment of these injuries has been increasing, however, predictors of outcomes in patients treated surgically remain poorly understood. The purpose of this study was to evaluate independent predictors of 30-day readmission and complications following internal fixation of distal radius fractures.

Patients ≥18 years who underwent surgical intervention for distal radius fractures between 2005 and 2016 were identified from the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) using procedural codes. Patient demographics, as well as 30-day readmission, complication, and mortality rates were ascertained. Multivariable logistic regression was used to determine independent predictors of 30-day outcomes while adjusting for patient age, sex, American Society of Anaesthesiologists (ASA) class, functional status, smoking status, comorbidities, and Body Mass Index (BMI).

A total of 10,051 patients were identified (average age 58 ±16). All patients received open reduction and internal fixation with no cases of external fixation identified in the data set. Included fractures were 37% extraarticular and 63% intraarticular. Within 30-days of initial fixation 143 (1.42%) patients were readmitted to the hospital, 71 patients experienced a complication, and 18 (0.18%) patients died. After adjusting for relevant covariables, current smoking increased the odds of readmission by 1.73 (95%Confidence interval [95%CI] 1.15 – 2.50), ASA class III/IV vs. I/II increased the odds of readmission by 2.74 (95%CI 1.85 – 4.06), and inpatient surgery vs. outpatient surgery increased the odds of readmission by 2.10 (95%CI 1.46 – 3.03). Current smoking also increased the odds of complications by 2.26 (95%CI 1.32 – 3.87), while ASA class III/IV increased it by 2.78 (95%CI 1.60 – 4.85), inpatient surgery increased it by 2.26 (95%CI 1.37 – 3.74), and dependent functional status increased it by 2.55 (1.16 – 5.64).

In conclusion, patients with severe systemic disease, current smokers and patients undergoing inpatient surgery are at risk for 30-day readmissions and complications following operative treatment of distal radius fractures. In addition, patients with dependent functional statuses are more likely to experience a complication within 30-days.

Closed ankle fractures have been reported to account for 10% off all fractures presenting to the Emergency Department. Many of these injuries require acute surgical management either via direct admission or through defined outpatient surgical pathways. While both methods have been shown to be safe, few studies have examined the cost effectiveness of each clinical scenario. The purpose of this study is to compare cost and resource utilization associated with inpatient and outpatient ankle fracture surgery at a Canadian academic institution.

This is a retrospective chart review of patients who underwent acute ankle fracture surgery at London Health Sciences Centre between 2016 and 2018. Thirty patients who underwent inpatient ankle surgery for closed, isolated ankle fractures at University Hospital were compared to 30 consecutive patients who underwent outpatient ankle surgery for similar fractures at Victoria hospital. Data pertaining to age at time of surgery, sex, BMI, fracture type, operating/recovery room time, and length of hospital stay were collected. All emergency room visits, readmissions and complications within 30 days of surgery were also recorded.

Inpatient and outpatient cohorts were similar with respect to average age (48 vs. 44, P=0.326) and body mass index (29.8 vs. 29.1, P=0.741). There was a greater proportion of patients with an American Society of Anesthesia (ASA) Classification of 3 or greater in the inpatient surgery group (48% vs. 23%). The inpatient group spent an average of 1.2 days in hospital while waiting for surgery and a average of 72 hours in hospital for their entire surgical encounter. The outpatient group spent an average of eight days (at home) waiting for surgery while spending an average of 7.4 hours in hospital during their entire surgical encounter. Outpatient ankle fracture surgery was associated with a cost savings of 35.9% in comparison to inpatient ankle fracture surgery (P < 0 .001). There were no significant differences in the rates of emergency room visits, readmissions, or complications between cohorts.

Preliminary findings suggest that outpatient ankle fracture surgery is appropriate for most patients, requires less hospital resources and is associated with similar rates of readmission and complications as inpatient surgery. An established outpatient surgical pathway may offer significant cost savings in the treatment of the common closed ankle fracture that requires surgical intervention.

This study was designed to compare atypical hip fractures with a matched cohort of standard hip fractures to evaluate the difference in outcomes.

Patients from the American College of Surgeons National Surgical Quality Improvement Program's (NSQIP) targeted hip fracture data file (containing a more comprehensive set of variables collected on 9,390 specially targeted hip fracture patients, including the differentiation of atypical from standard hip fractures) were merged with the standard 2016 NSQIP data file. Atypical hip fracture patients aged 18 years and older in 2016 were identified via the targeted hip fracture data file and matched to two standard hip fracture controls by age, sex, and fracture location. Patient demographics, length of hospital stay, 30-day mortality, major and minor complications, and other hip-specific variables were identified from the database. Binary outcomes were compared using the McNemar's test for paired groups, and continuous outcomes were compared using a paired t-test.

Ninety-five atypical hip fractures were identified, and compared to 190 age, sex, and fracture location matched standard hip fracture controls. There was no statistical difference in body mass index (BMI), race, ASA score, smoking status, timing of fixation, or functional status between the two groups (P>0.05). Thirty-day mortality was significantly higher in the atypical hip fracture group (atypical 7.36%, standard 2.11% p

This is the first study, to our knowledge, that demonstrates an increase in the rate of mortality in atypical hip fractures. Comparing atypical hip fractures with a matched cohort of standard hip fractures revealed a significantly greater 30-day mortality rate with an odds ratio of 3.62 in atypical hip fractures (95% CI 1.03–12.68). Prospective, clinical studies are recommended to further investigate these findings.

The benefit of using a long intramedullary device for the treatment of geriatric intertrochanteric hip fractures is unknown. The InterTAN device (Smith and Nephew, Memphis TN) is offered in either Short (180–200 mm) or Long (260–460 mm) constructs and was designed to provide stable compression across primary intertrochanteric fracture fragments. The objective of our study was to determine whether Short InterTANs are equivalent to Long InterTANs in terms of functional and adverse outcomes for the treatment of geriatric intertrochanteric hip fractures.

108 patients with OTA classification 31A–1 and 31A–2 intertrochanteric hip fractures were included in our study and prospectively followed at one of four Canadian Level-1 Trauma Centres. Our primary outcomes included two validated primary outcome measures: the Functional Independence Measure (FIM), to measure function, and the Timed Up and Go (TUG), to measure motor performance. Secondary outcome measures included blood loss, length of procedure, length of stay and adverse events. A pre-injury FIM was measured by retrospective recall and all postoperative outcomes were assessed on postoperative day 3, at discharge, at 6 weeks, 3 months, 6 months and 12 months postoperatively. Unpaired t-tests and Chi-square tests were used for the comparison of continuous and categorical variables respectively between the Short and Long InterTAN groups. A statistically significant difference was defined as p<0.05.

Our study included 71 Short InterTAN and 37 Long InterTAN patients with 31A–1 and 31A–2 intertrochanteric hip fractures. Age, sex, BMI, side, living status and comorbidities were similar between the two groups. The mean operative time was significantly lower in the Short InterTAN group (61 mins) as compared to the Long InterTAN group (71 mins)(p0.05). There were 5 periprosthetic femur fractures in the short InterTAN group versus 1 in the long InterTAN group. Non-mechanical adverse outcomes such as myocardial infarction, pulmonary embolism, urinary tract infections, pneumonia and death all had similar incidence rates between the two InterTAN groups.

Both the Short and Long InterTAN patient cohorts displayed similar improvements in performance and overall function over the course of a year following intertrochanteric hip fracture fixation. The recorded operative times for Short InterTAN fixation were significantly shorter than those recorded for the Long InterTAN patients. Alternatively, a significantly higher proportion of Short InterTAN patients sustained periprosthetic femur fractures within a year of implantation as compared to the Long InterTAN group.

Aims

Compartment syndrome results from increased intra-compartmental pressure (ICP) causing local tissue ischaemia and cell death, but the systemic effects are not well described. We hypothesised that compartment syndrome would have a profound effect not only on the affected limb, but also on remote organs.

Compartment syndrome, a devastating consequence of limb trauma, is characterised by severe tissue injury and microvascular perfusion deficits. We hypothesised that leucopenia might provide significant protection against microvascular dysfunction and preserve tissue viability. Using our clinically relevant rat model of compartment syndrome, microvascular perfusion and tissue injury were directly visualised by intravital video microscopy in leucopenic animals. We found that while the tissue perfusion was similar in both groups (38.8% (standard error of the mean (sem) 7.1), 36.4% (sem 5.7), 32.0% (sem 1.7), and 30.5% (sem 5.35) continuously-perfused capillaries at 45, 90, 120 and 180 minutes compartment syndrome, respectively versus 39.2% (sem 8.6), 43.5% (sem 8.5), 36.6% (sem 1.4) and 50.8% (sem 4.8) at 45, 90, 120 and 180 minutes compartment syndrome, respectively in leucopenia), compartment syndrome-associated muscle injury was significantly decreased in leucopenic animals (7.0% (sem 2.0), 7.0%, (sem 1.0), 9.0% (sem 1.0) and 5.0% (sem 2.0) at 45, 90, 120 and 180 minutes of compartment syndrome, respectively in leucopenia group versus 18.0% (sem 4.0), 23.0% (sem 4.0), 32.0% (sem 7.0), and 20.0% (sem 5.0) at 45, 90, 120 and 180 minutes of compartment syndrome in control, p = 0.0005). This study demonstrates that the inflammatory process should be considered central to the understanding of the pathogenesis of cellular injury in compartment syndrome.

Cite this article: Bone Joint J 2015;97-B:539–43

Purpose: Recent studies have examined the systemic inflammation that occurs following spinal cord injury (SCI) (Gris et al. 2008). It is believed that this systemic inflammation plays a role in the respiratory, renal and hepatic morbidity of SCI patients, ultimately contributing to mortality post-injury. Evidence of this inflammatory response has been shown as early as two hours post SCI (Gris et al. 2008) Intravital microscopy is a powerful tool for assessing inflammation acutely and in ‘real-time’ (Brock et al. 1999). This tool would be useful for demonstrating the acuteness of a systemic inflammatory response post-SCI, and for assessing the degree of inflammation to different severities of SCI. The liver has been shown to play a particularly important role in the initiation and progression of the early systemic inflammatory response to spinal cord injury (SCI), therefore the purpose was to evaluate hepatic inflammation immediately after SCI. We hypothesized that SCI would cause immediate leukocyte recruitment and that the magnitude of inflammation would increase with increasing severity of cord injury.

Method: Male Wistar rats (200–225g) were randomly assigned to one of the following groups: uninjured, trauma-injured (laminectomy and no cord injury), cord compressed or cord transected. Spinal cord-injured rats were anesthetized by isoflurane, a dorsal laminectomy was performed, and the 4th thoracic spinal segment was injured by a moderately severe clip-compression injury or by a severe complete cord transection injury. Uninjured rats and trauma-injured rats served as controls. At 0.5 and 1.5 h after SCI rats had the left lobe of their livers externalized and visualized using intravital video microscopy.

Results: At 0.5 hours the total number of leukocytes per post-sinusoidal venule was significantly increased after cord compression and cord transection compared to that in uninjured and trauma-injured rats (P< 0.05). Of these leukocytes significantly more were either adherent or rolling along venule walls compared to uninjured and trauma-injured rats (P< 0.05). Of the rolling leukocytes 2–fold more were observed after cord transection compared to cord compression. At 1.5 h the total number of leukocytes per post-sinusoidal venule and the number of adherent leukocytes was significantly increased only after cord transection.

Conclusion: Injury to the spinal cord but not trauma alone causes immediate leukocyte recruitment to the liver within 0.5 h after injury. Also, leukocyte recruitment increases with increasing severity of injury. This is the first study to use intravital microscopy to visualize systemic inflammation in the liver following SCI.

Purpose: Severe compartment syndrome is associated with renal failure, end organ damage, and systemic inflammatory response syndrome (SIRS). Intravital videomicroscopy (IVVM) is a useful tool to study capillary perfusion and inflammation in end organs such as the liver and lungs. In this study, the systemic effect of hindlimb compartment syndrome was studied using hepatic IVVM. The purpose was to measure the effect of increased hindlimb intracompartmental pressure on hepatocyte viability, inflammation, and blood flow in a rodent model.

Method: Ten Wistar rats were randomised into control (C) and Compartment Syndrome (CS) groups. Animals were anaesthetized with 5 % isoflurane. Mean arterial pressure was monitored using a carotid artery catheter. Elevated intracompartmental pressure (EICP) was induced by saline infusion into the anterior compartment of the hind limb and maintained for 2 hours between 30–40mmHg in the CS group. Two hours following fasciotomy, the liver was analyzed using IVVM to quantify capillary perfusion as a measure of microvascular dysfunction. The numbers of adherent and rolling leukocytes in venules and sinusoids were quantified to measure the inflammatory response. Irreversible hepatocyte injury was measured using a fluorescent vital dye which labels the nuclei of severely injured cells.

Results: Hepatocellular injury was significantly higher in the CS group (325±103 PI labeled cells/10-1 mm2) compared to controls (30±12 PI labeled cells/10-1 mm2)(p=0.0087). The number of adherent venular white blood cells (WBC) was significantly higher for the CS group (5±2/hpf) than controls (0.2±0.2)(p=0.0099). Volumetric blood flow was not significantly different between CS and controls.

Conclusion: After only 2 hours of compartment syndrome in this animal model, the number of activated white blood cells increased 25-fold and liver cellular injury increased 10-fold compared to controls. Marked systemic inflammation and hepatocellular damage was detected in response to isolated limb compartment syndrome. Compartment syndrome is a low-flow ischemia/reperfusion injury with a profound inflammatory response. Further research into the severe end-organ damage associated with compartment syndrome is required.

Purpose: Compartment syndrome is a limb-threatening complication of skeletal trauma. Both ischemia and inflammation may be responsible for tissue necrosis in compartment syndrome (CS). In this study, normal rodents were compared with neutropenic animals to determine the importance of inflammation as a mechanism of cellular damage using techniques of intravital videomicroscopy (IVVM) and histochemical staining.

Method: Forty Wistar rats were randomised. Twenty animals served as a control (group C). Twenty rats were rendered neutropenic using cyclophosphamide (250mg/kg) (group N). Animals were anaesthetised with 5 % isoflurane. Elevated intracompartmental pressure was induced by saline infusion into the anterior hindlimb compartment and maintained at 30–40 mmHg for 0, 15, 45 or 90 minute time intervals. Following fasciotomy, the EDL muscle was analyzed using IVVM to quantify tissue injury, capillary perfusion, and inflammatory response.

Results: The proportion of injured cells decreased in group N compared to group C at all time intervals of EICP (p< 0.05). The proportion of injured cells in group N was 8 % after 0 minutes EICP, and 12, 15, and 10 % at 15, 45, and 90 min of EICP. In group C injured cells increased from 8 % to 20, 22, and 21 % at 15, 45, and 90 minutes EICP respectively. Groups N and C both demonstrated a time-dependent reduction in capillary perfusion. In group N continuously-perfused capillaries decreased from 79±4/mm with 0 min of EICP, to 48±11/mm (15min), 36±7/mm (45min), and 24±10/mm (90min) (p < 0.05). Overall, There was no difference between groups N and C with regards to perfusion (p> 0.05).

Conclusion: This study demonstrates the importance of inflammation as a cause of injury in compartment syndrome. There was a 50% decrease in injury in neutropenic animals compared to controls after 90 minutes of elevated intracompartmental pressure. Microvascular perfusion analysis demonstrated a time-dependent decrease in capillary perfusion in both neutropenic and control animals. Blocking of the inflammatory response via neutropenia was protective against tissue injury. These results provide evidence toward a potential therapeutic benefit for anti-inflammatory treatment of elevated intra-compartmental pressure.

Purpose: Indomethacin may preserve tissue viability in compartment syndrome. The mechanism of improved tissue viability is unclear, but the anti-inflammatory effects may alter the relative contribution of tissue necrosis versus apoptosis to cellular injury. Existing studies have only considered indomethacin administration prior to induction of compartment syndrome. The purpose of this study was to determine the effect of timing of indomethacin administration on muscle damage in compartment syndrome, and to assess apoptosis as a cause of tissue demise.

Method: Twenty-four Wistar rats were randomized to elevated intracompartmental pressure (EICP) for either 45 or 90 minutes (30mm Hg). In the 45 min group, indomethacin was withheld (group 1), given prior to induction of EICP (group 2) or given 15 min prior to fasciotomy (group 3). In the 90 min group, indomethacin was withheld (group 4) or provided 30 or 60 minutes prior to fasciotomy (groups 5 and 6). Intravital microscopy and histochemical staining assessed capillary perfusion, cell damage and inflammatory activation within EDL muscle. Apoptosis was assessed using ELISA staining for caspase-3. Groups were compared with one-way ANOVA (p< 0.05).

Results: Perfusion improved in indomethacin-treated groups. Nonperfused capillaries decreased from group 1 (50.1±2.5), to groups 2 (38.4±1.8) and 3 (14.13±1.73)(p< 0.0001). Similarly, groups 5 and 6 had 25% fewer non-perfused capillaries compared to group 4 (p< 0.0001). Tissue viability improved in indo-methacin-treated groups. Groups 2 and 3 showed fewer damaged cells (1±0.5% and 8.7±2%) compared to group 1 (20±14%)(p< 0.0001). Groups 5 and 6 showed decreased cell damage (13±1% and 11±1%) compared to group 4 (18±1%) (p< 0.01). Apoptotic activity was present in compartment syndrome. At 30 minutes there were elevated caspase levels in EICP groups (0.47±0.08) compared to controls (0.19±0.02). However, indomethacin treated groups did not differ from controls with regards to caspase levels (p> 0.05).

Conclusion: Indomethacin decreased cell damage and improved perfusion in compartment syndrome. The benefits of indomethacin were partially time dependent; some improvement in tissue viability occurred regardless of timing of administration. Although apoptosis was common in compartment syndrome, the protective effect of indomethacin does not appear to be related to apoptosis.

Purpose: This study determined the relative role of inflammation and ischemia in cell damage using an animal model of compartment syndrome.

Method: Forty adult Wistar rats were studied according to a protocol approved by the animal care committee at our institution. Twenty rats were used as control animals, while an additional 20 rats were pretreated with cyclophosphamide to create a leucocyte-deplete state. Animals were anesthetized using 5% isoflurane. Mean arterial pressure was maintained at 80 mm Hg and core temperature was maintained at 36 degrees. Animals were then randomly assigned to one of 4 groups, in which hindlimb compartment pressure was maintained at 30 mm Hg for 0, 15, 45, or 90 minutes. Intravital microscopy was then utilized to study capillary perfusion, white blood cell activation, and cellular damage in the hindlimb EDL muscle.

Results: Inflammation: White blood cell activation was dampened in the neutropenic animals by approximately 85 % at all time periods. Capillary Perfusion: Perfusion was similar between the neutropenic and control animals. Both groups demonstrated a gradual decrease in the number of continuously perfused capillaries, from 80 % at 0 min of elevated intracompartmental pressure (EICP) to 30 % after 90 minutes of EICP. Cellular damage: Cellular damage, measured using a differential staining technique, decreased by 55 % in the neutropenic group after 90 minutes of EICP (p< 0.005).

Conclusion: Compartment syndrome is an important clinical problem resulting in severe muscle damage. In this study, inflammation was confirmed as an important causative element of cell damage. Based upon the results of this study, adjuvant treatment to fasciotomy designed to reduce inflammation and cellular damage may have important clinical benefit.

Purpose: This study was designed to determine whether indomethacin, a potent anti-inflammatory agent, reduces muscle damage secondary to elevated ICP.

Method: 16 adult Wistar rats were randomized to 4 groups. In group 1 (control), no intervention occurred. Group 2 (indo) rats were administered indomethacin (12mg/kg) with no elevation of ICP. Group 3 (CS) rats had elevated ICP (30–40mmHg × 45 minutes) using saline injection. Group 4 rats (CS/indo) had elevated ICP and indomethacin administration. After 45 minutes, hindlimb fasciotomy was performed. The extensor digitorum longus muscle was reflected onto an intravital microscope. Capillary perfusion was measured by comparing the number of continuously perfused capillaries to intermittent and non perfused capillaries. Inflammation was determined using the number of activated (rolling and adherent) white blood cells. Muscle cell damage was measured using differential fluorescent staining. Perfusion, inflammation, and muscle damage were compared in all 4 groups using a one-way ANOVA (p< 0.05).

Results: Perfusion: Indomethacin treatment (CS/indo) increased the proportion of intermittently perfused capillaries (39.1 ± 2.2 vs 30.3 ± 2.7) and decreased nonperfused capillaries (38.4 ± 1.8 vs 50.1 ±2.5) compared to CS (p=0.0002). Control and indo groups demonstrated more continuously perfused capillaries compared to CS or CS/indo groups (p0.05).

Conclusion: Treatment of elevated ICP with indomethacin improved microvascular perfusion and reduced cell damage. The protective mechanism of indomethacin is unknown, but may be related to an anti-oxidative and vasodilatory effect. Treatment of elevated intracompartmental pressure with indomethacin dramatically reduces muscle damage and may have important future clinical benefit. Further research is required to determine the mechanism of action.

Elevated intracompartmental pressure (ICP) results in tissue damage due to impaired microcirculatory function. The nature of microcirculatory impairment in elevated ICP is not well understood. This study was designed to measure the effects of increased ICP on skeletal muscle microcirculation, inflammation and cell viability using intravital videomicroscopy.

Twenty adult male Wistar rats were randomised to four groups: the control group (control) had no intervention; while three experimental groups had elevated ICP maintained for fifteen (15m), 45 (45m), or ninety (90m) minutes. Compartment pressure was continuously monitored and controlled between 30¡V40mmHg in the posterior hindlimb using saline infusion into the anterior hindlimb. Mean arterial pressure was maintained between 80 and 120mmHg. Fasciotomy was then performed and the Extensor Digitorum Longus muscle studied using intravital videomicroscopy. Perfusion was measured by comparing the numbers of continuous, intermittent, and nonperfused capillaries. Inflammation was measured by counting the number of activated (rolling and adherent) leukocytes in post-capillary venules. Muscle cellular Injury was measured using fluorescent vital staining of injured cell nuclei.

Perfusion: The number of continuously perfused capillaries decreased from 77 ± 3/mm (control) to 46 ± 10/mm (15m),40±10/mm(45m)and27±8/mm(90m)(p< 0.05). Non-perfused capillaries increased from 13 ± 1 (control) to 16 ± 4 (15m), 30 ± 7 (45m), and 39 ± 5 (90m) (p< 0.05). Inflammation: Activated leukocytes increased from 3.6 ± 0.7/(100ƒÝ)2 (control) to 5.9 ± 1.3 (15m), 8.6 ± 1.8 (45m), and 10.9 ± 3.0/(100ƒÝ)2 (90m) (p< 0.01). Injury: The proportion of injured cells increased from 5 ± 2 % in the control group to 12 ± 3 (15m), 16 ± 7 (45m) and 20 ± 3 % (90m) (p< 0.05).

As little as fifteen minutes of 30mmHg ICP caused irreversible muscle damage and microvascular dysfunction. With increased duration, further decreases in capillary perfusion and increases in injury are noted. A severe inflammatory response accompanies elevated ICP. The role of inflammation in compartment syndrome is unknown, but may contribute to cell injury and reduced capillary perfusion.

A predictive model for final kyphosis was tested by evaluating the radiographs of forty-three patients with traumatic burst fractures. Since clinical outcomes are related to final kyphosis in the ambulatory patient rather than on the initial supine injury radiograph, the ability to predict final kyphosis is beneficial in determining treatment. This study demonstrated that in the appropriately selected patient for conservative care, the limit of final-kyphosis(Kf) can be predicted from the intial-kyphosis(KI) , such that Kf= < KI+.5KI . Outliers from this equation were patients who had unrecognized posterior column fractures, superior and inferior end-plate fractures, and/or multiple level of injury.

The purpose of this study was to define a prediction model that afforded clinicians the ability to define final kyphosis from initial supine films in order to guide the management of stable burst fractures.

This study has demonstrated that as a rule of thumb, the final absolute kyphosis for stable burst fractures can be expected to be up to Ki (initial absolute kyphosis) + 1.5Ki. Outliers were found to be fractures with unrecognized posterior element injury, both superior and inferior endplate fractures and multiple level injuries.

The final kyphosis is clinically more relevant than the initial kyphosis in terms of functional outcome after conservative management. A prediction model for final kyphosis based on initial injury films can help guide the clinician for optimal management.

Retrospective radiographic analysis was performed on forty-three patients with a minimum follow up six months. All patients suffered traumatic burst fractures, which were deemed stable as to be satisfactorily managed in a brace. Serial radiographs were used to determine initial (Ki) and final (Kf), Kyphosis angles. Predicted Kf was determined using the equation Kf =Ki + 1.5 Ki. The initial absolute kyphosis was the measured kyphosis using the Cobb technique and including the loss of the expected normal lordosis of that spinal segment. Inclusion criteria included burst fractures at between levels T10 – L3 in the neurologically intact patient.

The equation accurately predicted the final outcome , Kf, in 70 % of the cases. In 20% of the cases, the Kf was less than expected. (Acceptable clinical result). In 10% of the cases, Kf was greater than predicted or achieved a clinically unacceptable kyphotic angulation requiring secondary surgery. In this group of outliers, post-hoc analysis identified unrecognized posterior element injury, both superior and inferior endplate fractures and multiple level injuries.

In traumatic burst fractures, the goal of management is to protect the spine during healing while maintaining an acceptable alignment, which will not lead to late pain and deformity. A final absolute kyphosis angle, Kf, from twenty to thirty degrees has been variably regarded as a threshold to obtain a good clinical outcome. Criteria for stability have been previously documented, however variables are based on initial presentation. Aside from careful classification of the fracture type, the current “rule of thumb” prediction model for Kf may further help the clinician with management decisions.