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The compartment syndrome: Is the intra-compartment pressure a reliable

indicator for early diagnosis?

Article  in  Mathematical Medicine and Biology · October 2016

DOI: 10.1093/imammb/dqw016

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 The compartment syndrome: is the
intra-compartment pressure a reliable indicator for
early diagnosis?
Iftah Nudel
Department of Biomedical Engineering
Ben-Gurion University, Beer-Sheva 8410501, Israel

Luis Dorfmann
Department of Civil and Environmental Engineering
Tufts University, Medford, MA

Gal deBotton∗
Department of Biomedical Engineering
Ben-Gurion University, Beer-Sheva 8410501, Israel
Department of Mechanical Engineering
Ben-Gurion University, Beer-Sheva 8410501, Israel

Abstract

Compartment syndrome occurs when the pressure in an enclosed compartment

increases due to tissue swelling or internal bleeding. As the intra-compartmental
pressure builds up, the blood flow to the tissue or the organ is compromised, re-
sulting in ischemia, necrosis and damage to the nerves and other tissues. At the
present there are no established diagnostic procedures, and clinical observations
such as pain, paralysis and even compartment pressure monitoring are an unreli-
able determinant of the presence of the syndrome. Late diagnosis may result in
fasciotomy, neurological dysfunctions, amputation and even death. Focusing on the
frequently occurring compartment syndrome of the lower leg, this work is aimed to-
ward introducing a coherent, mechanically-motivated analysis of the disease within
∗
corresponding author: debotton@bgu.ac.il, Ben-Gurion Univ., POB 653, Beer-Sheva 8410501, Israel

1
 the framework of poroelasticity. The fascia enclosing the compartment is treated
as an inextensible and impermeable layer, and the tissue inside the compartment is
represented as a fully saturated poroelastic solid. The model quantitatively predicts
the highly nonuniform intra-compartmental pressure buildup as a function of both
time and location. These findings, which are in good agreement with clinical obser-
vations reported in the literature, shed light on the difficulties associated with the
identification of the syndrome and may assist in improved diagnostic procedures.

Keywords Compartment syndrome; Intra-compartmental pressure; Poroelasticity;

Fasciotomy

1 Introduction
Compartment syndrome (CS) is a disease where the intra-compartmental pressure (ICP)
in a confined compartment increases to a level at which the enclosed organs and tissues
dysfunction or fail. The primary pathophysiology for the ICP increase is internal bleeding
or edema that result in swelling of the tissues in the confined compartment. Common
causes for CS are fractures, hemorrhages, constrictive casts and burns. In fact, any
mechanism that causes an increase of the tissue volume in the compartment and hence
an increase of the ICP, may lead to CS (Donaldson et al., 2014; Haller, 2011).
Different treatments for CS have been reported, but there is a broad agreement that
early diagnosis followed by decompression of the compartmental cavity can relieve most
of the symptoms associated with CS. At a later stage a surgical treatment, which is
known as fasciotomy, is required to instantaneously release the ICP. This treatment is
followed by a long rehabilitation period during which patients are partially disabled. A
failure to treat CS on time may result in amputation of limbs or even in death. In essence,
however, the compartment syndrome is a mechanically driven disease.
Two types of limb CS may be distinguished: the chronic exertional (CECS) and the
acute limb CS (ALCS). The first occurs at the lower leg and foot and is usually associated
with physical activity during which an ischemic pain appears. In most cases the pain
ceases when the activity is stopped (Frink et al., 2010; McCallum et al., 2014; Van der
Wal et al., 2014). CECS mostly affects young athletes and soldiers and is probably the
result of a volume increase of the muscle during intensive exercise (Dunn and Waterman,
2014). It is also possible that CECS results from fluid extravasation or a decrease in the
capillary density (Dunn and Waterman, 2014). To the best of our knowledge the etiology
of the CECS are not fully known (Frink et al., 2010; Van der Wal et al., 2014). It is
reported that 14% to 34% of activity related leg pains are associated with CECS (Dunn
and Waterman, 2014). According to a study conducted by Van der Wal et al. (2014)
most patients adapted their life style to the limitations imposed by the disease. The

2
process of recovery following a surgical treatment is relatively long and in the military,
for example, at least 25% of the soldiers are unable to return to full duty at the end of
the medical treatment (Dunn and Waterman, 2014; McCallum et al., 2014; Waterman et
al., 2013).
ALCS, usually following physical trauma, is caused by diffuse bleeding or edema in a
confined muscle compartment which is surrounded by an impermeable fascia and located
adjacent to a bone (Frink et al., 2010; Kalns et al., 2011). The fascia is inextensible and
limits the volume expansion of the swelling muscle tissue, thus resulting in an increase
of the ICP. This leads to a reduced transmural pressure gradient between microcircula-
tion and interstitium and ischemia follows (Frink et al., 2010). In patients with ALCS
irreversible damage to the nerves and muscles may occur within 5 to 6 hours of ischemia
(Frink et al., 2010). However, muscles necrosis was also reported for as little as 3 hours
from the onset of the injury (Frink et al., 2010; Vaillancourt et al., 2004). Current under-
standing suggests that the rapid progress of ALCS results from positive feedback within
the compartment involving increasing vascular permeability (Kalns et al., 2011). Late
diagnosis might lead to significant neurological dysfunction, amputation or even death
(Donaldson et al., 2014).
Early identification of compartment syndrome is considered of critical importance and
can significantly reduce the physical, financial and vocational disabilities experienced by
the patient (Ali et al., 2014; Köstler et al., 2004). The clinical observations of pain, pallor,
parasthesia, paresis or paralysis are an unreliable determinant of the presence of CS (Ali
et al., 2014; Dunn and Waterman, 2014; Goaley et al., 2007). Nonetheless, at the present
these observations, together with compartment pressure monitoring, are identified as the
most useful methods in the diagnosis of the CS (Ali et al., 2014; Giannoudis et al., 2009).
Moreover, patients at risk for CS require repeated examinations (Frink et al., 2010). The
ICP provides an indirect measure of tissue damage and perfusion (Köstler et al., 2004).
Variations in both time of ischemia and pressure magnitude during ischemia need to be
more closely defined to ensure accurate diagnoses of the CS (Frink et al., 2010; Kalns et
al., 2011; Köstler et al., 2004).
Currently, there is no consensus regarding the threshold pressure level for the CS
of the limb (Ali et al., 2014). A compartment pressure between 30 and 50 mmHg is
considered critical and fasciotomy is recommended (Goaley et al., 2007; Köstler et al.,
2004). However, different suggestions exist of which differential pressure should be used
as an indicator (Frink et al., 2010). The perfusion pressure is considered reliable in
patients with high absolute blood pressure and may avoid unnecessary fasciotomies (Ali
et al., 2014; Köstler et al., 2004). Whitesides Jr et al. (1975) proposed to monitor the
difference between the diastolic blood pressure and the ICP in order to detect ALCS.
This measure takes into account the ability of the blood pressure to supply an adequate

3
tissue perfusion (Donaldson et al., 2014). A pressure difference less than 30 mmHg is
suggested as a critical value for fasciotomy (Donaldson et al., 2014; McQueen and Court-
Brown, 1996; White et al., 2003; Whitesides Jr et al., 1975). Since the differential pressure
method accounts for physiological variabilities, it is considered superior and more reliable
than methods based on absolute ICP measurements.
Although the pathophysiolgy of CECS is not fully understood, near infrared spec-
troscopy has shown that an increase of compartment pressure results in decreased muscle
oxygenation (Roberts and Franklyn-Miller, 2012; Van Den Brand et al., 2005). Further
research is needed to determine an appropriate diagnostic protocol for this condition
(Roberts and Franklyn-Miller, 2012). Thus, there is a clear need to raise the clinician’s
awareness and to improve guidelines to interpret results and their clinical relevance.
The lack of a firm diagnostic procedure results in diagnosis by method of elimination, a
long process that is accompanied by suffering of the patients (Engelbert and Turnipseed,
2014). In the course of the present work it will be demonstrated that the increase of
the ICP is not spatially uniform. This may explain why the common methods of ICP
measurements do not provide a firm indication of the presence of CS.

1.1 The muscle as poroelastic material

We introduce a quantitative analysis of the CS capable of predicting the development
of muscle edema and the increase of ICP following the absorption of blood. To this
end we employ the widely-used theory of poroelasticity and treat the muscle tissue as
a poroelastic solid. The theory of poroelasticity has been used in the past to describe
the mechanical behavior of biological tissues such as brain, cartilage and edematous soft
tissues (Grillo et al., 2015; Li et al., 2013).
To the best of the authors’ knowledge no mechanically-motivated analysis of the CS
is reported in the literature. Nonetheless, various treatments of muscle tissue as a porous
material have been reported (Abraham et al., 2012; Morrow et al., 2013; Vankan et al.,
1996; Yang and Taber, 1991). In a manner resembling the confinement of the brain in
the skull, the muscle is confined in a limited space by the stiff fascia that restricts its
deformation. Accordingly, following recent works in which the brain tissue was analyzed
within the framework of linear poroelasticity (Li et al., 2013; Smillie et al., 2005; Tully
and Ventikos, 2011; Wirth and Sobey, 2009), in this work we too consider the muscle as
a linear poroelastic material. This approach also agrees with the findings of Franceschini
et al. (2006), who concluded that a general constitutive model for the brain tissue should
reduce to the linear theory of poroelasticity under the small deformations induced by
consolidation.

4
 Anterior
tibial artery

Anterior Deep posterior

compartment compartment

Tibia

Gal deBotton

Lateral Fibula
compartment

Superficial posterior compartment

Figure 1: Schematic representation of the cross section of the lower leg with the four
muscle compartments.

2 Analytical model of the compartment syndrome

We begin our analysis with a brief summary of the poroelsticity theory that was developed
by Biot (1941) to describe the flow of water through a porous skeleton. In terms of the
strain tensor ε and the pressure of the interpenetrating fluid P , the stress in the mixture
is
P
σ = 2µε + λ(trε)I − κ I, (1)
H
where µ and λ are the two Lamè coefficients and the coefficient 1/H quantifies the
compressibility of the material for a change in the fluid pressure. Here κ = λ + 23 µ is the
modulus of compression of the fully drained porous muscle tissue or, equivalently, of the
muscle tissue in case the fluid is free to flow out of the pores (i.e., P = 0). The stress is
required to satisfy the equilibrium equation divσ = 0.
The variation of fluid content in a unit volume of the solid is

1 P
θ= trσ + , (2)
3H R

where the ratio 1/R measures the change in the fluid content for a given change in the
liquid pressure. By taking the trace of Eq. (1) together with Eq (2), we note that if the
fluid is free to flow out of the tissue then the ratio between the amount of liquid squeezed
out to the tissue volume change is given by the ratio κ/H. The continuity equation,
assuming incompressibility of the fluid phase, requires that the change of fluid content is
equal to the amount of fluid crossing the surrounding surface. It has the form

∂θ
+ divq = 0, (3)
∂t

5
 Gal deBotton

Lateral Fibula
compartment

Superficial posterior compartment

Fascia

b
a

Artery

Muscle tissue

Figure 2: Axisymmetric model of the anterior compartment with the anterior tibial artery
at the center.

where t is the time and q is the liquid flow. The remaining equation is Darcy’s law that
describes the fluid flow in terms of the pressure gradient

q = −k gradP, (4)

where k is the coefficient of permeability under the assumption that the medium is
isotropic with respect to the permeability.
By making use of (1) in (2) and substituting the resulting expression for θ together
with the expression for q from Darcy’s law in the continuity equation (3), we end with
the relation  
κ ∂(trε) 1 κ ∂P
k div(gradP ) = + − 2 . (5)
H ∂t R H ∂t
We now focus our attention on the anterior compartment of the lower leg shown
schematically in Fig. 1. Herein we approximate the geometry of the compartment as
a long cylindrical shaped region with a circular cross-sectional area. In the analytical
model we assume that the muscle tissue envelops the anterior tibial artery and is enclosed
by an inextensible and impermeable fascia, see Fig. 2. The compartment is represented
as a fully saturated, isotropic and poroelastic mixture of muscle tissue and a distribution
of capillary size blood vessels that deliver oxygen to the muscle fibers.
The region occupied by the compartment is defined as a thick-walled tube whose
geometry is specified by

a 6 r 6 b, 0 6 φ 6 2π, 06z6l with l > b, (6)

where a is the radius of the anterior tibial artery, b is the outer radius of the compartment
and l is the length of the compartment, all of which are constants. The cylindrical polar
coordinates (r, φ, z) are associated with the unit vectors er , eφ , ez , respectively. Consider
an axisymmetric deformation defined by the displacement vector u = ur (r, t)er such that

6
the circular cylindrical shape is maintained. The non-zero components of the infinitesimal
strain tensor ε are
∂ur ur
εr = , εφ = , (7)
∂r r
and we note that trε = εr + εφ .
The sole nontrivial equilibrium equation for the conditions specified above is

∂σr 1
+ (σr − σφ ) = 0. (8)
∂r r

With the aid of (1) we rewrite this equation in the form

∂  κ 
(2µ + λ)(εr + εφ ) − P = 0, (9)
∂r H
∂εφ 1
where we have made use of the relation ∂r
= (ε
r r
− εφ ) that follows from (7), and
assumed that P = P (r, t).
For the problem at hand the general relation (5) reduces to

∂ 2P
   
1 ∂P κ ∂(εr + εφ ) 1 κ ∂P
k 2
+ = + − 2 . (10)
∂r r ∂r H ∂t R H ∂t

Integrating Eq. (9) with respect to r and substituting the resulting expression for the
sum εr + εφ in (10) leads to

∂ 2P 1 ∂P N ∂P
+ = + f (t), (11)
∂r2 r ∂r k ∂t

where f (t) is an unknown function of time only and

κ2 1 κ
N= 2
+ − 2. (12)
H (2µ + λ) R H

For the completely saturated condition assumed in this study, κ = H = R and hence
N = (2µ + λ)−1 .
To solve equation (11) we need to specify the initial and the boundary conditions.
The initial condition P (r, t = 0) = P0 is the pressure in the compartment before injury
occurs. The boundary conditions at the inner and the outer surfaces are, respectively,
∂P
P (a, t) = Pa and ∂r
(b, t) = 0, where we introduced the subscript a on P to indicate
the ‘applied’ tibial artery blood pressure at the inner surface r = a. The condition at
the outer boundary r = b stems from the impermeability of the connective fascia. We
note that f (t) in equation (11) must vanish for t → ∞, and in this work we assume that
f (t) = 0 and solve this equation for P (r, t).
Next, it is convenient to additively decompose the function P (r, t) into time-dependent

7
and steady-state parts in the form

P (r, t) = P̃ (r, t) + P̄ (r). (13)

The expression of the time-independent function P̄ (r) is obtained by solving the ordinary
differential equation
d2 P̄ 1 dP̄
2
+ = 0, (14)
dr r dr
which has the form P̄ (r) = C1 ln r + C2 . From the conditions at the boundaries r = a
and r = b it follows that C1 = 0 and C2 = Pa , and we end up P̄ (r) = Pa . The time
dependent part of the pressure distribution satisfies equation (11) with P̃ (r, t) instead
of P (r, t) together with the the initial condition P̃ (r, 0) = P0 − Pa and the boundary
∂ P̃
conditions P̃ (a, t) = 0 and ∂r
(b, t) = 0.
Using separation of variables in the form P̃ (r, t) = ρ(r)T (t), we can write

d2 ρ 1 dρ
 
1 1 N dT
+ = = −β 2 , (15)
ρ dr2 r dr T k dt

where β is a constant. The resulting expressions for T (t) and ρ(r) are

2 kt/N
T (t) = A e−β , ρ(r) = B1 J0 (βr) + B2 Y0 (βr), (16)

where A, B1 and B2 are constants and J0 and Y0 are Bessel functions of the first and
second kind, respectively of the order zero. The boundary conditions become B1 J0 (βa) +
B2 Y0 (βa) = 0 and B1 J1 (βb) + B2 Y1 (βb) = 0. For a non-trivial solution the requirement
for a vanishing determinant, namely,

J0 (βa)Y1 (βb) − J1 (βb)Y0 (βa) = 0, (17)

gives the roots βi . In addition, from the condition at the inner boundary we obtain
B2 = − YJ00(βa) B.
(βa) 1
Finally, the expression for the pressure distribution in the compartment is
∞  
X J0 (βi a) 2
P (r, t) = Pa + Ai J0 (βi r) − Y0 (βi r) e−βi kt/N , (18)
i=0
Y0 (βi a)

where the constants Rb

a
r(P0 − Pa )R(βi r)dr
Ai = Rb , (19)
a
rR2 (βi r)dr

are found using the initial condition for P̃ and the orthogonality of the functions R(βi r).

8
3 Evolution of the ICP in the anterior compartment
We apply the theory to examine the ICP buildup in the anterior compartment of the
lower leg, following injury. As a representative geometry we take a = 1.41 mm (Deshatty
and Shubha, 2013) and b = 13.30 mm (McCreesh and Egan, 2011). The pressure in the
anterior tibial artery is Pa = 110 mmHg (Bollinger et al., 1976) and in the compartment,
before injury, P0 = 10 mmHg (Donaldson et al., 2014; Giannoudis et al., 2009). The
elastic Young’s modulus E = 2.12 kPa is taken from Chen et al. (1996), and the Poisson
ratio ν = 0.2 is approximated on the basis of Kallemeyn et al. (2006) analysis of the
cartilage. The corresponding Lamè coefficients are µ = 0.88 kPa, λ = 0.59 kPa and
the bulk modulus is κ = 1.18 kPa. Further, it is reasonable to consider the muscle
tissue as fully saturated and accordingly H = R = κ. Zakaria et al. (1997) report the
hydraulic conductivity of the abdominal wall muscle of a rat at different intra-peritoneal
pressures in the range between 0.7 and 8 mmHg. They report that for pressure differences
larger than 1.5 mmHg the permeability k increases linearly with the pressure P . Then,
extrapolating to P = 100 mmHg yields k = 6.54 mm4 /(N s). However, since immediately
after the onset of bleeding the pressure gradient is substantially smaller, the value k = 2
mm4 /(N s) is assumed. This value is in agreement with data of the permeability of the
tibialis anterior muscle of New Zealand White rabbits reported by Morrow et al. (2013).
We underline that the material and other parameters used in this study were taken from
independent sources and were not fitted to any clinical findings for CS.
Before proceeding we recall that differential pressure measurements are proposed to
obtain improved criteria to predict the onset of CS and to establish the need for fas-
ciotomy while taking into account the variability in the physiology and patient history
(Donaldson et al., 2014; McQueen and Court-Brown, 1996; White et al., 2003; White-
sides Jr et al., 1975). We follow this concept and define the normalized ICP

P − P0
, (20)
Pa − P0

where P is the absolute value of the ICP. Before injury, this ratio vanishes, but increases
asymptotically with increasing ICP afterwards, approaching a unit value when P = Pa . In
addition, to account for the variability in the compartment size, we define the normalized
radial distance
r−a
. (21)
b−a
This ratio vanishes at the arterial surface r = a and becomes unity at the impermeable
fascia at which r = b.
Fig. 3 shows the distribution of the normalized ICP as a function of the normalized ra-
dial distance for different times. To highlight the clinical significance of the change in the

9
 1.0

0.8
Normalized ICP

Pdnorm
0.6

0.4 300 min

Pthnorm

0.2
6 min  120 min
20 min
45 min
0.0
0.0 0.2 0.4 0.6 0.8 1.0
Normalized radial distance
Figure 4: Distribution of the normalized ICP as a function of the normalized
Figure 3: Distribution of the
radial distance normalized
at different times. The ICP as alines
horizontal function oftothe
correspond the normalized radial
normalized diastolic pressure and to the normalized threshold ICP proposed
distance at different times. The horizontal lines correspond to the normalized diastolic
in White et al. (2003); McQueen and Court-Brown (1996); Donaldson et al.
pressure and to (2014)
the normalized
and Whitesides Jr threshold
et al. (1975).ICP (Donaldson et al., 2014; McQueen and
Court-Brown, 1996; White et al., 2003; Whitesides Jr et al., 1975).
divide the compartment into micro-vascular units. These are representa-
tive control elements of muscle fiber perfusion that include an arteriole with
ICP we include thethe group of the capillaries
normalized it supplies
diastolic (EmersonPand Segal,
pressure 1997; Fuglevand
dnorm and the normalized ICP thresh-
and Segal, 1997). Following (Emerson and Segal, 1997; Fuglevand and Segal,
old Pthnorm , both1997;
shown
Blochasandhorizontal lines.
Iberall, 1982), we Fig.
take the 3 suggests
characteristic lengththat
of the ischemic
micro- processes may
vascular units to be 2 mm and use vertical lines to schematically divide the
occur in any region whereinto
compartment thesuchnormalized
micro-vascularpressure is 4.higher than normalized threshold
units, see Fig.
Figs. 3 and 4 show a highly nonlinear distribution of ICP. Specifically,
Pthnorm . To gainFig.
further understanding
4 indicates that in the first fewwe divide
minutes therises
pressure compartment
only in the vicinityinto micro-vascular
of the damaged artery. 45 minutes afterwards the ICP exceeds the critical
units. These are representative control elements of muscle fiber perfusion that include an
arteriole with the group of the capillaries it17supplies (Emerson and Segal, 1997; Fuglevand
and Segal, 1997). Following Emerson and Segal (1997); Fuglevand and Segal (1997), we
take the characteristic length of the micro-vascular units to be 1 mm. For convenience,
the vertical lines in Fig. 3 schematically divide the compartment into sections the size of
two micro-vascular units.
We recall that at time zero the normalized pressure throughout the compartment is
0, and as blood from the artery perforates into the compartment the ICP rises. Fig. 3
shows a highly nonuniform distribution of the ICP, in agreement with experimental
observations reported by Olson and Glasgow (2005). Specifically, we observe that in
the first few minutes pressure rises only in the vicinity of the damaged artery. Roughly
45 minutes afterwards the ICP exceeds the critical pressure Pthnorm in a region the size
of almost 3 micro-vascular units. Note that at the same time the ICP in the vicinity
of the fascia hardly changes from the pressure in a healthy compartment. Even 120
minutes after the edema initiates the pressure in most of the compartment is still lower
than the threshold pressure. Thus, a pressure gauge used to monitor the ICP will not

10
 0.7

Pdnorm
0.6

0.5 rnorm = 0.2

Normalized ICP

0.4

0.3 Pthnorm

rnorm = 0.4
0.2 rnorm = 0.6

0.1 rnorm = 1

0.0
0 50 100 150
Time [min]
Figure 5: The distribution of the normalized ICP as a function of time at
Figure 4: The different locations.
distribution ofThe
thedotted and the dashed
normalized ICP linesas
correspond to the nor-
a function of
time at different
malized diastolic pressure and the differential threshold ICP, respectively.
locations. The horizontal lines correspond to the normalized diastolic pressure and the
differential threshold ICP,
In this respectively.
work, in view of the mechanical nature of the ICP buildup, we
present a quantitative analysis of the CS induced by internal bleeding of a
blood vessel. We exploit the widely used theory of poroelasticity and treat
record significantthepressure increase
muscle tissue as a fullyunless
saturatedthe recording
poroelastic is done
material. closeanto the source (the
We consider
axisymmetric model of an artery surrounded by muscle tissue which, in turn,
damaged artery in this case).
is enveloped Approximately
by an inextensible 5 hours
and impermeable from
fascia. the with
Starting onset
the of the edema the
governing equations of poroelastic materials, we prescribe the appropriate
pressure in the entire compartment
displacement, pressure and rises above at
flow conditions thethecritical value
arterial wall Pththenorm . Thus, only at
and at
fascia, together with the appropriate initial conditions. A closed-form ana-
this relatively latelytical
stage anyispressure
solution determinedrecordings in the compartment
for the initial boundary value problem, whichwill provide definite
is reminiscent of the one developed by Armstrong et al. (1984).
indication for CS and the need for fasciotomy. These findings are in good agreement with The values
of the material parameters are extracted from independent sources and the
clinical results reported by Goaley et al. (2007).
19
Changes of the normalized pressure as a function of time, for different distances from
the artery, are depicted in Fig. 4. For example, following the curve rnorm = 0.2 we find
that the ICP, at this distance from the artery, increases beyond the threshold value within
15 minutes. Similarly, the figure shows that after approximately 120 minutes the ICP
is above the critical value in a region that extends halfway through the fascia. As time
passes the region in which the ICP is above the critical value expands, and concurrently
the pressure magnitude increases everywhere throughout the compartment.

4 Conclusions
The CS of the limb refers to an increase of the ICP in a muscle compartment, which is
accompanied by intensive pain. Different mechanisms, such as internal bleeding, among
others, may increase the tissue volume in the confined compartment and thus generate
changes to ICP. Early diagnosis of the syndrome can be difficult since the associated

11
symptoms are common with other diseases. Therefore, the CS is frequently diagnosed
only after ischemia and other irreversible damage processes have taken place. While a
few conservative treatments are possible, it is widely agreed that fasciotomy is required
for an instantaneous release of the excess pressure.
In this work, in view of the mechanical nature of the ICP buildup, we present a
quantitative analysis of the CS induced by internal bleeding of a blood vessel. The
results show that CS is characterized by a highly nonuniform pressure distribution in the
compartment. We found that the region adjacent to the damaged artery is subject to
a pressure substantially higher than a critical value, indicating the need for fasciotomy.
At the same time, even two hours after initiation of the edema, the ICP in regions far
from the bleeding artery is substantially lower than the threshold value. Accordingly,
soft tissues in the compartment may be permanently damaged before any symptoms of
CS are properly diagnosed (Frink et al., 2010; Vaillancourt et al., 2004). In order to
develop a trustworthy diagnostic procedure there is a need for improved constitutive
models for the muscle in the compartment. More realistic geometries, boundary and
initial conditions can be considered once these constitutive laws are implement. Such
a development will improve the understanding, prevention and timely diagnosis of the
compartment syndrome.

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