Abstract
Background: There is limited literature on risk stratification of patients with acute forearm compartment syndrome. The primary objective of this study was to identify factors associated with poor outcomes in patients with acute forearm compartment syndrome. Methods: We retrospectively identified 130 patients with acute compartment syndrome of 130 forearms treated with fasciotomies from January 2000 to June 2015 at 2 Level 1 trauma centers. Poor outcome was defined as a composite variable, including: (1) death; (2) limb amputation; (3) persistent neurological deficit; and (4) contracture. Patient- and treatment-related variables were collected. Bivariate analyses were used to screen for variables associated with poor outcome, and explanatory variables with a value of P < .05 were included in our multivariable logistic regression analyses. Results: Of the 130 patients, 43 (33%) with acute forearm compartment syndrome had poor outcomes, including 5 deaths, 5 limb amputations, 21 persistent neurological deficits, and 31 contractures. Multivariable logistic regression analyses showed that elevated serum creatine kinase at presentation (P < .05) was associated with poor outcomes in patients with acute forearm compartment syndrome. Receiver operating characteristic curve analysis showed that a serum creatine kinase cutoff of 300 U/L yields 92% sensitivity and a serum creatine kinase cutoff of 10 000 U/L yields 95% specificity for poor outcomes in acute forearm compartment syndrome. Conclusions: Elevated creatine kinase levels above 300 U/L are a useful screening test for the highest risk patients with acute forearm compartment syndrome. Levels above 10 000 U/L may play a role in informed consent and counseling regarding expectations.
Keywords: forearm, anatomy, nerve injury, nerve, diagnosis, trauma, mangled extremity, vascular
Introduction
Acute compartment syndrome is a rare but serious disorder of increased intracompartmental pressure causing decreased tissue perfusion.1 Acute extremity compartment syndrome affects 8 per 100 000 people and is 10 times more common in men than in women.2 The forearm is the most commonly affected location in acute compartment syndrome of the upper extremity.2-4 In general, the treatment for acute compartment syndrome is prompt diagnosis and emergent fasciotomy.5
Prolonged compartment syndrome leads to irreversible tissue ischemia and subsequent necrosis. Muscle ischemia may result in contracture development, whereas nerve ischemia may cause neurological dysfunction, both of which severely affect limb function.6,7 A nonsalvageable limb may prompt the surgeon to perform primary limb amputation. Severe muscle necrosis releases myoglobin, which can lead to kidney failure and ultimately to life-threatening conditions.8 Sequelae of acute compartment syndrome or of the initial injury burden may result in patient death.9,10
In this study, we use “poor outcome” as a composite variable, which we defined as: (1) death; (2) limb amputation; (3) persistent neurological deficit; or (4) contracture. The primary objective of this study was to identify factors associated with poor outcomes in patients with acute forearm compartment syndrome. Our null hypothesis was that poor outcomes are not associated with any identifiable risk factors.
Materials and Methods
Study Design
After institutional review board approval, a retrospective study of all fasciotomies performed for acute forearm compartment syndrome at 2 Level 1 trauma centers over a 15-year period from January 1, 2000 to June 30, 2015 was conducted. To identify patients who underwent forearm fasciotomies for acute compartment syndrome, we queried our institutional patient data repository for International Classification of Disease, Ninth Revision codes 729.71 (nontraumatic compartment syndrome of upper extremity) and 958.91 (traumatic compartment syndrome of upper extremity). The initial query was nonspecific for the forearm, since the diagnosis codes apply to the entire upper extremity. The initial query yielded 438 patients, comprising 260 and 178 patients from the 2 Level 1 trauma centers, respectively.
From the initial cohort of 438 patients, we excluded: (1) 289 miscoded or nonspecifically coded patients with no acute compartment syndrome of the forearm; (2) 15 patients who underwent prophylactic fasciotomies with no clinical signs of acute compartment syndrome; and (3) 4 patients initially treated with fasciotomies at outside hospitals. The final cohort included 130 patients with acute compartment syndrome of 130 forearms treated with fasciotomies. The operative techniques used were chosen at the discretion of the treating surgeon.
Outcome Measures and Explanatory Variables
We defined poor outcome in the treatment of acute forearm compartment syndrome as a composite variable, which included 1 or more of: (1) death; (2) limb amputation; (3) neurological deficit; or (4) contracture. Limb amputation included both below- and above-elbow amputations. Transient neurological deficits that resolved prior to final follow-up were not scored as a poor outcome. Contractures of the digits, wrist, or elbow were included. Neurological deficits and contractures were scored at the time of latest follow-up if they were thought to be sequelae from the acute compartment syndrome.
The following patient-related factors were studied: age, sex, race, body mass index (BMI), modified Charlson Comorbidity Index, diabetes mellitus, mechanism of injury, and traumatic versus nontraumatic mechanism of injury. The following vital signs on presentation were studied: systolic blood pressure, respiratory rate, and peripheral oxygen saturation. The following laboratory values were studied: potassium, creatinine, blood urea nitrogen (BUN), hemoglobin, hematocrit, platelets, partial thromboplastin time (PTT), prothrombin time (PT), international normalized ratio (INR), total protein, albumin, lactate, base excess, creatine kinase at presentation, and peak creatine kinase. The following treatment-related factors were studied: origin of consult, use of compartment pressure measurement, and time from injury to fasciotomy. Time to fasciotomy was categorized as less than 6 hours, 6 to 24 hours, or more than 24 hours, based on prior literature showing 6 hours7 and 24 hours11 as important benchmarks in acute compartment syndrome.
Statistical Analyses
Categorical variables were presented using frequencies and percentages, and continuous variables using mean and standard deviation as most continuous variables were normally distributed. Due to substantial covariation between BUN and creatinine, hematocrit and hemoglobin, PT/INR and PTT, total protein and albumin, lactate and base excess, and creatine kinase at presentation and at peak, we decided to exclude BUN, hematocrit, PT, PTT, total protein, base excess, and peak creatine kinase from bivariate and multivariable analyses.
In bivariate analyses, we assessed whether explanatory variables were associated with our primary outcome measures using the Fisher exact test for categorical variables and the unpaired t test for continuous variables. Bivariate analyses were complete-case analyses, that is, excluding cases with missing values (missing values are indicated in Tables 1 and 2).
Table 1.
Baseline Characteristics of Patients With Acute Forearm Compartment Syndrome (N = 130).
| Variable | Mean (SD) |
|---|---|
| Age | 45 (16) |
| BMIa | 28 (6.0) |
| Modified Charlson Comorbidity Index | 1.5 (2.4) |
| No. (%) | |
| Male sex | 87 (67) |
| Race | |
| White | 99 (76) |
| Black | 13 (10) |
| Asian | 5 (3.9) |
| Hispanic | 3 (2.3) |
| Unknown/Other | 10 (7.8) |
| Diabetes mellitus | 22 (17) |
| Smoking statusa | |
| Never smoker | 60 (48) |
| Past smoker | 17 (14) |
| Current smoker | 47 (38) |
| Mechanism of injury | |
| Crush injury | 31 (24) |
| High-energy blunt trauma | 28 (22) |
| Penetrating trauma | 15 (12) |
| Intravenous infiltration | 12 (9.2) |
| Vascular injury | 11 (8.5) |
| Otherb | 33 (26) |
| Traumatic mechanism of injury | 87 (67) |
| Time to fasciotomya | |
| <6 hours | 37 (34) |
| 6-24 hours | 31 (29) |
| >24 hours | 41 (38) |
| Compartment pressure measurement | 46 (35) |
| Origin of consult | |
| Emergency department | 92 (71) |
| Otherc | 38 (29) |
Note. BMI = body mass index.
BMI was available for 110 (85%), smoking status for 124 (95%), and time to fasciotomy for 109 (84%) patients.
Other mechanisms of injury include spontaneous bleed (9), low-energy blunt trauma (7), infection (6), burn (3), unclear etiology (3), postoperative bleed (2), electrocution (2), and blast injury (1).
Other origins of consult include: medical floor (8), surgical floor (10), medical intensive care unit (11), surgical intensive care unit (3), operating room (5), and clinic (1).
Table 2.
Vital Signs and Laboratory Values of Patients With Acute Forearm Compartment Syndrome (N = 130).
| No. (%)a | Mean (SD) | |
|---|---|---|
| Vital signs | ||
| Systolic blood pressure, mm Hg | 106 (82) | 137 (23) |
| Respiratory rate, breaths/min | 98 (75) | 18 (5.0) |
| Peripheral oxygen saturation, % | 63 (48) | 97 (3.7) |
| Laboratory values | ||
| Albumin, g/dL | 104 (80) | 3.7 (0.75) |
| Base excess, mmol/L | 22 (17) | −1.8 (5.8) |
| Blood urea nitrogen, mg/dL | 129 (99) | 18 (11) |
| Creatine kinase at presentation, U/L | 92 (71) | 11 574 (25 829) |
| Creatine kinase at peak, U/L | 92 (71) | 15 370 (30 940) |
| Creatinine, mg/dL | 129 (99) | 1.3 (1.5) |
| Hematocrit, % | 129 (99) | 38 (7.2) |
| Hemoglobin, g/dL | 129 (99) | 13 (2.6) |
| International normalized ratio | 128 (98) | 1.2 (0.33) |
| Lactate, mmol/L | 44 (34) | 2.9 (1.7) |
| Partial thromboplastin time, s | 109 (84) | 38 (29) |
| Platelets, 103/µL | 128 (98) | 218 (88) |
| Potassium, mmol/L | 130 (100) | 4.0 (0.89) |
| Prothrombin time, s | 128 (98) | 15 (3.2) |
| Total protein, g/dL | 103 (79) | 6.4 (1.2) |
Number of nonmissing values per variable including percentage (N = 130) within parentheses.
In multivariable logistic regression analyses, we included all explanatory variables with a value of P < .05 on bivariate analyses to assess which factors were associated with our primary outcome measure while accounting for potential confounding. We used stepwise backward selection of variables in multivariable logistic regression analyses, retaining only those variables with a value of P < .05, as the number of outcomes were relatively low. We used multiple imputation (40 times, chained, predictive mean matching) to account for missing values in multivariable analyses.
We used area under the curve from receiver operating characteristic (ROC) curve analysis to assess the performance of risk factors in predicting a poor outcome and to determine an optimal cutoff value.
A 2-tailed P < .05 was considered significant.
Results
This study included 130 patients who underwent forearm fasciotomies for acute compartment syndrome, of which 87 (67%) were of male sex. Mean age at the time of surgery was 45 years. Mean BMI was 28. Twenty-two patients (17%) had diabetes mellitus. The most common mechanisms of injury were crush injury (24%) and high-energy blunt trauma (22%). Sixty-seven percent of the acute forearm compartment syndrome resulted from traumatic etiologies and the remaining 33% from nontraumatic etiologies. Compartment pressure measurement was used in 46 cases (35%). Thirty-four percent of patients underwent fasciotomies within 6 hours of injury, 29% between 6 and 24 hours of injury, and 38% after 24 hours of injury. The initial evaluation by the treating service was in the emergency department in 71% of cases (Table 1). Patient vital signs and laboratory values on presentation are shown in Table 2.
Poor outcomes occurred in 43 (33%) of 130 patients after fasciotomies for acute forearm compartment syndrome. These included 5 deaths and 5 limb amputations. The remaining 120 patients were followed for a median of 135 days (interquartile range, 58-410 days). At the final follow-up, there were 21 patients with neurological deficits and 31 with contractures. Of the 31 patients with contractures, 23 had contractures of the digits, 20 of the wrist, and 8 of the elbow. Nineteen patients had both neurological deficits and contractures. Bivariate analyses showed that higher BMI (P = .019), mechanism of injury (P = .001), potassium (P < .001), hemoglobin (P = .025), and creatine kinase on presentation (P < .001) were associated with poor outcomes in patients with acute forearm compartment syndrome (Tables 3 and 4). Vital signs on presentation were not found to be associated with poor outcomes.
Table 3.
Bivariate Analyses of Patient, Injury, and Treatment Factors Associated With Poor Outcomes in Patients With Acute Forearm Compartment Syndrome (N = 130).
| Comparison group (n = 87) |
Poor outcome group (n = 43) |
P value | |
|---|---|---|---|
| Mean (SD) | Mean (SD) | ||
| Age | 45 (16) | 45 (16) | .875 |
| BMIa | 27 (5.5) | 30 (6.6) | .019 |
| Modified Charlson Comorbidity Index | 1.6 (2.3) | 1.3 (2.6) | .574 |
| No. (%) | No. (%) | P value | |
| Male sex | 60 (69) | 27 (63) | .555 |
| Race | |||
| White | 64 (74) | 35 (81) | .908 |
| Black | 10 (12) | 3 (6.8) | |
| Asian | 4 (4.7) | 1 (2.3) | |
| Hispanic | 2 (2.3) | 1 (2.3) | |
| Unknown/Other | 7 (8.1) | 3 (6.8) | |
| Diabetes mellitus | 16 (18) | 6 (14) | .623 |
| Smoking statusa | |||
| Never smoker | 42 (49) | 18 (46) | .964 |
| Past smoker | 11 (13) | 6 (15) | |
| Current smoker | 32 (38) | 15 (38) | |
| Mechanism of injury | |||
| Crush injury | 14 (16) | 17 (40) | .001 |
| High-energy blunt trauma | 18 (21) | 10 (23) | |
| Penetrating trauma | 15 (17) | 0 (0) | |
| Intravenous infiltration | 11 (13) | 1 (2.3) | |
| Vascular injury | 7 (8.0) | 4 (9.3) | |
| Otherb | 22 (25) | 11 (26) | |
| Traumatic mechanism of injury | 56 (64) | 31 (72) | .430 |
| Time to fasciotomya | |||
| <6 hours | 26 (34) | 11 (33) | .148 |
| 6-24 hours | 18 (24) | 13 (39) | |
| >24 hours | 32 (42) | 9 (27) | |
| Compartment pressure measurement | 28 (33) | 17 (41) | .441 |
| Origin of consult | |||
| Emergency department | 60 (69) | 32 (74) | .533 |
| Otherc | 27 (31) | 11 (26) | |
Note. Bold indicates statistical significance. BMI = body mass index.
BMI was available for 110 (85%), smoking status for 124 (95%), and time to fasciotomy for 109 (84%) patients.
Other mechanisms of injury include spontaneous bleed (9), low-energy blunt trauma (7), infection (6), burn (3), unclear etiology (3), postoperative bleed (2), electrocution (2), and blast injury (1).
Other origins of consult include: medical floor (8), surgical floor (10), medical intensive care unit (11), surgical intensive care unit (3), operating room (5), and clinic (1).
Table 4.
Bivariate Analyses of Vital Signs and Laboratory Values Associated With Poor Outcomes in Patients With Acute Forearm Compartment Syndrome (N = 130).
| Comparison group (n = 87) |
Poor outcome (n = 43) |
P value | |
|---|---|---|---|
| Mean (SD) | Mean (SD) | ||
| Vital signs | |||
| Systolic blood pressure, mm Hg | 138 (22) | 134 (25) | .410 |
| Respiratory rate, breaths/min | 18 (2.8) | 19 (7.4) | .216 |
| Peripheral oxygen saturation, % | 97 (2.7) | 96 (5.8) | .168 |
| Laboratory values | |||
| Albumin, g/dL | 3.7 (0.75) | 3.6 (0.74) | .223 |
| Creatine kinase at presentation, U/L | 2619 (6266) | 25 269 (36 547) | <.001 |
| Creatinine, mg/dL | 1.3 (1.8) | 1.3 (0.84) | .974 |
| Hemoglobin, g/dL | 13 (2.6) | 14 (2.5) | .025 |
| International normalized ratio | 1.2 (0.33) | 1.3 (0.32) | .442 |
| Lactate, mmol/L | 2.6 (1.5) | 3.3 (1.9) | .186 |
| Partial thromboplastin time, s | 35 (23) | 42 (37) | .255 |
| Platelets, 103/µL | 213 (85) | 226 (94) | .387 |
| Potassium, mmol/L | 3.9 (0.55) | 4.4 (1.3) | <.001 |
Note. Number of nonmissing values per variable indicated in Table 2. Bold indicates statistical significance.
Multivariable logistic regression analyses showed that serum creatine kinase (P = .003) was the only factor independently associated with poor outcomes in patients with acute forearm compartment syndrome (Table 5). Higher creatine kinase levels are correlated with higher percentage of patients with poor outcomes (Table 6).
Table 5.
Multiple Imputeda Stepwise Backward Multivariable Logistic Regression Analyses of Risk Factors Associated With Poor Outcomes in Patients With Acute Forearm Compartment Syndrome (N = 130).
| Odds ratio (95% confidence interval) | P value | |
|---|---|---|
| Creatine kinase at presentation, U/L | 1.00006 (1.00002-1.00010) | .003 |
Table 6.
Relationship Between Serum Creatine Kinase on Presentation on a Logarithmic Scale and Percentage of Patients With Poor Outcomes After Acute Forearm Compartment Syndrome.
| Serum creatine kinase level, U/L | Patients with poor outcomes (n) | Total patients (n) | Percent with poor outcomes |
|---|---|---|---|
| 0-250 | 1 | 18 | 6 |
| 251-1250 | 14 | 41 | 34 |
| 1251-6250 | 2 | 7 | 29 |
| 6251-31 250 | 8 | 14 | 57 |
| 31 251-156 250 | 11 | 12 | 92 |
The ROC analysis showed that serum creatine kinase on presentation has potential use as a predictor of poor outcomes in acute forearm compartment syndrome (Table 7). Lower creatine kinase cutoff levels are more sensitive to poor outcomes, whereas higher creatine kinase cutoff levels are more specific. A serum creatine kinase cutoff of 300 U/L exhibits greater than 90% sensitivity for poor outcomes, but with only 35% specificity. By contrast, a serum creatine kinase cutoff of 10 000 U/L exhibits 95% specificity for poor outcomes, but with only 43% sensitivity.
Table 7.
Sensitivity, Specificity, and Area Under the Curve of Serum Creatine Kinase on Presentation as a Predictor of Poor Outcome in Acute Forearm Compartment Syndrome.
| Serum creatine kinase level cutoff, U/L | Sensitivity, % | Specificity, % | AUC, % |
|---|---|---|---|
| 100 | 97 | 4 | 41 |
| 300 | 92 | 35 | 58 |
| 1000 | 65 | 73 | 70 |
| 3000 | 54 | 82 | 71 |
| 10 000 | 43 | 95 | 74 |
| 30 000 | 30 | 98 | 70 |
| 100 000 | 5 | 100 | 61 |
Note. AUC = Area Under the Curve.
We did not find independent association of mechanism of injury or time to fasciotomy in the multivariable logistic regression analysis.
Discussion
Acute compartment syndrome of the upper extremity is a limb- and life-threatening disorder. Early diagnosis and emergent surgical fasciotomy are paramount to avoid irreversible tissue ischemia, neurological deficits, and contractures.6,7 There has been limited literature that risk-stratifies patients with acute forearm compartment syndrome. The emergent nature of compartment syndrome pathophysiology makes prospective studies difficult. We have shown in this retrospective cohort study that serum creatine kinase levels on presentation are associated with poor outcomes in patients with acute forearm compartment syndrome.
The major strength of our study is our large sample size of heterogeneous patients with acute forearm compartment syndrome over a 15-year period. Our results support prior findings by Duckworth et al7 that this is primarily a disease of young men. Compartment pressure measurements are used as an adjunct to diagnosis in approximately one-third of cases both in our study and in prior literature.7 Kalyani et al,6 in a systematic review of the literature, reported a 42% complication rate in acute forearm compartment syndrome, the most common complication being neurological deficit at 21%. The rates of neurological deficit (17%) and overall poor outcome (33%) in our study support these prior findings.
Creatine kinase is an enzyme expressed in various cell types, and serum creatine kinase is commonly used as a measure of muscle ischemia. Elevated serum creatine kinase level in acute extremity compartment syndrome is most likely a measure of the extent of intracompartmental myonecrosis. The relationship between higher creatine kinase and greater local tissue damage accounts for its association with poor outcomes such as limb amputation, contracture, and neurological deficits. Elevated creatine kinase in the setting of muscle necrosis is associated with acute renal failure, the risk of which is compounded by hypovolemia and sepsis.12 The association between creatine kinase and mortality may be also related to total bodily injury.
Evidence to guide interpretation of serum biomarkers in the setting of acute compartment syndrome is limited. Creatine kinase has previously been proposed as an adjunct serum test for the diagnosis of acute extremity compartment syndrome13,14; however, its role in prognostication has not been investigated. Although a creatine kinase level of 10 000 U/L was found to be the optimal cutoff by ROC analysis, the morbidity of missed acute compartment syndrome is so great that surgeons may value a sensitive screening test for the highest risk patients with acute forearm compartment syndrome, at the cost of specificity. We propose a creatine kinase level of 300 U/L as a sensitive cutoff and a level of 10 000 U/L as a specific cutoff for poor outcomes in acute forearm compartment syndrome. When creatine kinase reaches 300 U/L, the surgeon may more aggressively consider fasciotomy in the correct clinical context, at a time when extensive myonecrosis has not yet occurred. A creatine kinase level of 10 000 U/L or above is useful for patient counseling because it more accurately predicts a poor final outcome.
It was surprising that time to fasciotomy was not found to be significantly associated with poor outcomes in our study. Multiple prior studies have shown prompt fasciotomy to be important to normal function without neurological deficits and the need for reconstructive procedures.2,7,11 It is difficult retrospectively to determine the exact time of onset of compartment syndrome physiology after an injury or insult. We attempted to mitigate inaccuracies by evaluating time from injury to fasciotomy, which can be more objectively defined than time from onset of symptoms or signs to fasciotomy. Moreover, we separated time to fasciotomy into 3 broad categories: less than 6 hours, 6 to 24 hours, and more than 24 hours from injury. Despite these broad categories, time from injury to fasciotomy could not be ascertained for 16% of our cohort, which is a potential source of selection bias. The substantial noise in our time to fasciotomy data may have contributed to the nonsignificance of the effect. It is possible that with an increased sample size or with better signal-to-noise ratio, we could have found an association between time to fasciotomy and poor outcomes. Moreover, a large proportion of our study cohort (38%) underwent fasciotomy more than 24 hours after injury. This finding supports conventional wisdom that a proportion of injured patients are at risk of the late development of acute compartment syndrome, and clinical vigilance is required for suspected cases. Other reasons for the large percentage of late fasciotomies include gradually evolving nontraumatic processes, such as a prolonged decubitus injury, failure to recognize compartment syndrome in polytraumatized patients, and late transfers to our tertiary referral centers.
There are other limitations to our study. First, we used a composite primary outcome measure, and therefore, we are unable to comment on separate risk factors for death, amputation, neurological deficit, or contracture. While not ideal, the use of a composite variable allowed us to study this rare phenomenon. Moreover, deaths from all causes, not only renal failure, were included in our composite outcome measure. We felt that mortality from any cause was a negative end point warranting inclusion in our analysis; however, we cannot rule out that had these patients survived their initial injuries, they would have exhibited good function at follow-up. Post hoc analysis with the 5 deceased patients in the control group showed no statistically significant difference in any associations that we found. Second, this study is susceptible to the weaknesses of retrospective studies. Laboratory studies were collected at the discretion of the treating team at the time of injury. Serum biomarkers, such as creatine kinase, may have been collected preferentially or more frequently in more critically ill patients or in patients with concern for renal injury. This could have resulted in selection bias, making creatine kinase less predictive of poor outcomes than our results would suggest. Loss to follow-up may have negatively affected our ability to detect risk factors associated with poor outcomes. Underdocumentation of a neurological deficit or contracture at final follow-up may have resulted in reporting bias. Therefore, the actual rate of poor outcomes in acute forearm compartment syndrome may be higher than reported. Conversely, it is impossible to fully know whether neurological deficits and contractures were the result of compartment syndrome or a separate, distinct injury. We cannot rule out that contractures may have resulted from inadequate therapy. Finally, our study was performed at 2 Level 1 trauma centers in a major metropolitan area, which may limit the generalizability of our results to other settings.
To our knowledge, we have reported on the largest cohort of acute forearm compartment syndrome treated with surgical fasciotomy. Serum creatine kinase is associated with poor outcomes in patients with acute forearm compartment syndrome. Serum creatine kinase level above 300 U/L is a sensitive predictor, and serum creatine kinase level above 10 000 U/L is a specific predictor of poor outcomes in these patients. Patients with elevated creatine kinase levels should not be undertriaged. The most important aspect of management of acute compartment syndrome is prompt diagnosis and emergent fasciotomy. After compartment release, appropriate multiorgan supportive care may play a role in the metabolic derangement often seen in compartment syndrome. A serum creatine kinase level above 300 U/L may portend a poor outcome and may prompt surgeons to perform compartment releases. A serum creatine kinase level above 10 000 U/L is predictive of a poor outcome and can be used in patient counseling and setting expectations. It remains unclear whether primary limb amputation or nonoperative medical management may be advantageous in select cases.
Footnotes
Ethical Approval: The study was performed with institutional review board approval.
Statement of Human and Animal Rights: All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2008.
Statement of Informed Consent: Informed consent was waived in this retrospective study.
Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.
ORCID iDs: Dafang Zhang 
https://orcid.org/0000-0003-0155-8244
Neal Chen
https://orcid.org/0000-0001-7527-1110
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