884662

research-article2019
HANXXX10.1177/1558944719884662HandZhang et al

Surgery Article
HAND

Factors Associated With Poor

1­–7
© The Author(s) 2019
Article reuse guidelines:
Outcomes in Acute Forearm sagepub.com/journals-permissions
DOI: 10.1177/1558944719884662
https://doi.org/10.1177/1558944719884662

Compartment Syndrome hand.sagepub.com

Dafang Zhang1,2 , Stein J. Janssen3, Matthew Tarabochia2,4,

Arvind von Keudell1,2, Brandon E. Earp1,2, Neal Chen2,4 ,
and Philip Blazar1,2

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 life-threatening conditions.8 Sequelae of acute compart-

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 com-
partment syndrome is prompt diagnosis and emergent fasci-
otomy.5
Prolonged compartment syndrome leads to irreversible
tissue ischemia and subsequent necrosis. Muscle isch-
emia may result in contracture development, whereas
nerve ischemia may cause neurological dysfunction, both
of which severely affect limb function.6,7 A nonsalvage-
able limb may prompt the surgeon to perform primary
limb amputation. Severe muscle necrosis releases myo-
globin, which can lead to kidney failure and ultimately to
ment syndrome or of the initial injury burden may result
in patient death.9,10
In this study, we use “poor outcome” as a composite vari-
able, which we defined as: (1) death; (2) limb amputation; (3)
persistent neurological deficit; or (4) contracture. The pri-
mary objective of this study was to identify factors associated
with poor outcomes in patients with acute forearm compart-
ment syndrome. Our null hypothesis was that poor outcomes
are not associated with any identifiable risk factors.
1
Brigham and Women’s Hospital, Boston, MA, USA
2
Harvard Medical School, Boston, MA, USA
3
Amphia Hospital, Breda, The Netherlands
4
Massachusetts General Hospital, Boston, USA
Corresponding Author:
Dafang Zhang, Department of Orthopaedic Surgery, Brigham and
Women’s Hospital, 75 Francis Street, Boston, MA 02115, USA.
Email: dzhang9@partners.org
2 HAND 00(0)
Materials and Methods
Study Design
After institutional review board approval, a retrospective
study of all fasciotomies performed for acute forearm com-
partment 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 fas-
ciotomies for acute compartment syndrome, we queried our
institutional patient data repository for International Classi-
fication of Disease, Ninth Revision codes 729.71 (nontrau-
matic compartment syndrome of upper extremity) and
958.91 (traumatic compartment syndrome of upper extrem-
ity). 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. Tran-
sient neurological deficits that resolved prior to final fol-
low-up were not scored as a poor outcome. Contractures of
the digits, wrist, or elbow were included. Neurological defi-
cits and contractures were scored at the time of latest fol-
low-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 satu-
ration. The following laboratory values were studied: potas-
sium, 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 treat-
ment-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 stan-
dard 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 multi-
variable analyses.
In bivariate analyses, we assessed whether explanatory
variables were associated with our primary outcome mea-
sures 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).
In multivariable logistic regression analyses, we included
all explanatory variables with a value of P < .05 on bivari-
ate analyses to assess which factors were associated with
our primary outcome measure while accounting for poten-
tial 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 perfor-
mance 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 mecha-
nisms of injury were crush injury (24%) and high-energy
blunt trauma (22%). Sixty-seven percent of the acute fore-
arm compartment syndrome resulted from traumatic etiolo-
gies 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
Zhang et al 3

Table 1.  Baseline Characteristics of Patients With Acute and 31 with contractures. Of the 31 patients with contrac-
Forearm Compartment Syndrome (N = 130). tures, 23 had contractures of the digits, 20 of the wrist, and
Variable Mean (SD) 8 of the elbow. Nineteen patients had both neurological
deficits and contractures. Bivariate analyses showed that
Age 45 (16) higher BMI (P = .019), mechanism of injury (P = .001),
BMIa 28 (6.0) potassium (P < .001), hemoglobin (P = .025), and creatine
Modified Charlson Comorbidity Index 1.5 (2.4) kinase on presentation (P < .001) were associated with
  No. (%) poor outcomes in patients with acute forearm compartment
syndrome (Tables 3 and 4). Vital signs on presentation were
Male sex 87 (67) not found to be associated with poor outcomes.
Race
Multivariable logistic regression analyses showed that
 White 99 (76)
serum creatine kinase (P = .003) was the only factor inde-
 Black 13 (10)
pendently associated with poor outcomes in patients with
 Asian 5 (3.9)
acute forearm compartment syndrome (Table 5). Higher
 Hispanic 3 (2.3)
 Unknown/Other 10 (7.8)
creatine kinase levels are correlated with higher percentage
Diabetes mellitus 22 (17) of patients with poor outcomes (Table 6).
Smoking statusa The ROC analysis showed that serum creatine kinase on
  Never smoker 60 (48) presentation has potential use as a predictor of poor out-
  Past smoker 17 (14) comes in acute forearm compartment syndrome (Table 7).
  Current smoker 47 (38) Lower creatine kinase cutoff levels are more sensitive to
Mechanism of injury poor outcomes, whereas higher creatine kinase cutoff levels
  Crush injury 31 (24) are more specific. A serum creatine kinase cutoff of 300 U/L
  High-energy blunt trauma 28 (22) exhibits greater than 90% sensitivity for poor outcomes, but
  Penetrating trauma 15 (12) with only 35% specificity. By contrast, a serum creatine
  Intravenous infiltration 12 (9.2) kinase cutoff of 10 000 U/L exhibits 95% specificity for
  Vascular injury 11 (8.5) poor outcomes, but with only 43% sensitivity.
 Otherb 33 (26) We did not find independent association of mechanism
Traumatic mechanism of injury 87 (67) of injury or time to fasciotomy in the multivariable logistic
Time to fasciotomya regression analysis.
  <6 hours 37 (34)
  6-24 hours 31 (29)
  >24 hours 41 (38) Discussion
Compartment pressure measurement 46 (35) Acute compartment syndrome of the upper extremity is a
Origin of consult limb- and life-threatening disorder. Early diagnosis and
  Emergency department 92 (71) emergent surgical fasciotomy are paramount to avoid irre-
 Otherc 38 (29) versible tissue ischemia, neurological deficits, and contrac-
Note. BMI = body mass index. tures.6,7 There has been limited literature that risk-stratifies
a
BMI was available for 110 (85%), smoking status for 124 (95%), and time patients with acute forearm compartment syndrome. The
to fasciotomy for 109 (84%) patients. emergent nature of compartment syndrome pathophysiol-
b
Other mechanisms of injury include spontaneous bleed (9), low-
ogy makes prospective studies difficult. We have shown in
energy blunt trauma (7), infection (6), burn (3), unclear etiology (3),
postoperative bleed (2), electrocution (2), and blast injury (1). this retrospective cohort study that serum creatine kinase
c
Other origins of consult include: medical floor (8), surgical floor (10), levels on presentation are associated with poor outcomes in
medical intensive care unit (11), surgical intensive care unit (3), operating patients with acute forearm compartment syndrome.
room (5), and clinic (1).
The major strength of our study is our large sample size
of heterogeneous patients with acute forearm compartment
by the treating service was in the emergency department in syndrome over a 15-year period. Our results support prior
71% of cases (Table 1). Patient vital signs and laboratory findings by Duckworth et al7 that this is primarily a disease
values on presentation are shown in Table 2. of young men. Compartment pressure measurements are
Poor outcomes occurred in 43 (33%) of 130 patients used as an adjunct to diagnosis in approximately one-third
after fasciotomies for acute forearm compartment syn- of cases both in our study and in prior literature.7 Kalyani
drome. These included 5 deaths and 5 limb amputations. et al,6 in a systematic review of the literature, reported a
The remaining 120 patients were followed for a median of 42% complication rate in acute forearm compartment syn-
135 days (interquartile range, 58-410 days). At the final drome, the most common complication being neurological
follow-up, there were 21 patients with neurological deficits deficit at 21%. The rates of neurological deficit (17%) and
4 HAND 00(0)

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)
a
Number of nonmissing values per variable including percentage (N = 130) within parentheses.

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 cre-
atine 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. Cre-
atine 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 syn-
drome is so great that surgeons may value a sensitive
screening test for the highest risk patients with acute fore-
arm 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 fasciot-
omy to be important to normal function without neuro-
logical deficits and the need for reconstructive
procedures.2,7,11 It is difficult retrospectively to determine
the exact time of onset of compartment syndrome physi-
ology after an injury or insult. We attempted to mitigate
inaccuracies by evaluating time from injury to fasciot-
omy, which can be more objectively defined than time
from onset of symptoms or signs to fasciotomy. More-
over, we separated time to fasciotomy into 3 broad cate-
gories: 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 selec-
tion 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 out-
comes. Moreover, a large proportion of our study cohort
Zhang et al 5

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)

  Mean (SD) Mean (SD) P value
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.

a
BMI was available for 110 (85%), smoking status for 124 (95%), and time to fasciotomy for 109 (84%) patients.
b
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).
c
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).

(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 devel-
opment of acute compartment syndrome, and clinical
vigilance is required for suspected cases. Other reasons
for the large percentage of late fasciotomies include grad-
ually evolving nontraumatic processes, such as a pro-
longed 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, ampu-
tation, 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 mea-
sure. 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
6 HAND 00(0)

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)

  Mean (SD) Mean (SD) P value

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.

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

Note. Bold indicates statistical significance.

a
Missing values were imputed using multiple chained imputation (40×); see Tables 1 and 2 for missing values.

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

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.

Zhang et al 7
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 sus-
ceptible to the weaknesses of retrospective studies. Labora-
tory studies were collected at the discretion of the treating
team at the time of injury. Serum biomarkers, such as cre-
atine 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 fol-
low-up may have negatively affected our ability to detect
risk factors associated with poor outcomes. Underdocu-
mentation 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 compart-
ment 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 con-
tractures may have resulted from inadequate therapy.
Finally, our study was performed at 2 Level 1 trauma cen-
ters in a major metropolitan area, which may limit the gen-
eralizability 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 associ-
ated 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 out-
comes in these patients. Patients with elevated creatine
kinase levels should not be undertriaged. The most impor-
tant aspect of management of acute compartment syndrome
is prompt diagnosis and emergent fasciotomy. After com-
partment 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 pri-
mary limb amputation or nonoperative medical manage-
ment may be advantageous in select cases.
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 stan-
dards 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
References
1. Prasarn ML, Ouellette EA. Acute compartment syn-
drome of the upper extremity. J Am Acad Orthop Surg.
2011;19(1):49-58.
2. McQueen MM, Gaston P, Court-Brown CM. Acute com-
partment syndrome. Who is at risk? J Bone Joint Surg Br.
2000;82:200-203.
3. Bodansky D, Doorgakant A, Alsousou J, et al. Acute com-
partment syndrome: do guidelines for diagnosis and manage-
ment make a difference? Injury. 2018;49(9):1699-1702.
4. Elliott KG, Johnstone AJ. Diagnosing acute compartment
syndrome. J Bone Joint Surg Br. 2003;85(5):625-632.
5. von Keudell AG, Weaver MJ, Appleton PT, et al. Diagnosis
and treatment of acute extremity compartment syndrome.
Lancet. 2015;386(10000):1299-1310.
6. Kalyani BS, Fisher BE, Roberts CS, et al. Compartment syn-
drome of the forearm: a systematic review. J Hand Surg Am.
2011;36(3):535-543.
7. Duckworth AD, Mitchell SE, Molyneux SG, et al. Acute
compartment syndrome of the forearm. J Bone Joint Surg Am.
2012;94: e63.
8. Mitas P, Vejrazka M, Hruby J, et al. Prediction of compart-
ment syndrome based on analysis of biochemical parameters.
Ann Vasc Surg. 2014;28(1):170-177.
9. Jensen SL, Sandermann J. Compartment syndrome and fasci-
otomy in vascular surgery. A review of 57 cases. Eur J Vasc
Endovasc Surg. 1997;13(1):48-53.
10. Rush DS, Frame SB, Bell RM, et al. Does open fasciotomy
contribute to morbidity and mortality after acute lower
extremity ischemia and revascularization. J Vasc Surg.
1989;10(3):343-350.
11. Rorabeck CH. The treatment of compartment syndromes of
the leg. J Bone Joint Surg Br. 1984;66(1):93-97.
12. Ward MM. Factors predictive of acute renal failure in rhabdo-
myolysis. Arch Intern Med. 1988;148(7):1553-1557.
13. Orrapin S, Orrapin S, Arwon S, et al. Predictive factors for
post-ischemic compartment syndrome in non-traumatic
acute limb ischemia in a lower extremity. Ann Vasc Dis.
2017;10(4):378-385.
14. Valdez C, Schroeder E, Amdur R, et al. Serum creatine kinase
levels are associated with extremity compartment syndrome.
J Trauma Acute Care Surg. 2013;74(2):441-447.