Compartment syndromes from head to toe

Zsolt J. Balogh, MD, PhD, FRACS; Nerida E. Butcher, MD

Compartment syndrome is defined as the dysfunction of organs/tissues within the compartment due to limited blood supply
caused by increased pressure within the compartment. The aim of
this article is to introduce and discuss acute compartment syndromes that are essential for critical care physicians to recognize
and manage. Various pathophysiological mechanisms (ischemiareperfusion syndrome, direct trauma, localized bleeding) could
lead to increased compartmental pressure and decreased blood
flow through the intracompartmental capillaries. Although compartment syndromes are described in virtually all body regions,
the etiology, diagnosis, treatment, and prevention are best characterized for three key body regions (extremity, abdominal, and
thoracic compartment syndromes). Compartment syndromes can
be classified as either primary (pathology/injury is within the

he fixed-walled compartments
of the human body separate
and protect vital organs. The
walls of the compartments can
be fascia/connective tissue (muscle compartments, pericardium, and capsulated
visceral organs) or bone and connective
tissue (brain, spinal cord, and orbit).
Connective tissues with high collagen
content are less tensile than muscle or
skin and key determinants of the volume
of the compartments. In broad terms,
compartment syndrome is defined as the
dysfunction of organs/tissues within the
compartment due to limited blood supply
caused by increased pressure within the
compartment. Without timely intervention, compartment syndromes cause permanent and irreversible damage to the
tissues within the compartment. In the
case of vital organs, they cause rapid
physiologic deterioration and death. Prevention, timely recognition, and immediate intervention are the strategies of the
management of patients with potential

From the Department of Traumatology, John

Hunter Hospital and University of Newcastle, Newcastle, NSW, Australia.
The authors have not disclosed any potential conflicts of interest.
For information regarding this article, E-mail:
Zsolt.Balogh@hnehealth.nsw.gov.au
Copyright 2010 by the Society of Critical Care
Medicine and Lippincott Williams & Wilkins
DOI: 10.1097/CCM.0b013e3181ec5d09

Crit Care Med 2010 Vol. 38, No. 9 (Suppl.)

compartment) or secondary (no primary pathology or injury within

the compartment), and based on the etiology (e.g., trauma, burn,
sepsis). A recently described phenomenon is the multiple compartment syndrome or poly-compartment syndrome, which is
usually a complication of a severe shock and massive resuscitation. The prevention of compartment syndromes is based on
preemptive open management of compartments (primary syndromes) in high-risk patients and/or careful fluid resuscitation
(both primary and secondary syndromes) to limit interstitial
swelling. (Crit Care Med 2010; 38[Suppl.]:S445S451)
KEY WORDS: extremity compartment syndrome; abdominal compartment syndrome; acute compartment syndrome; organ/tissue
dysfunction; multiple compartment syndrome

compartment syndromes. The detrimental effects of increased pressure in the

skull (cerebral/cerebellar herniation),
pleural cavity (tension pneumothorax
and massive hemothorax), and pericardium (pericardial tamponade) are welldescribed, life-threatening conditions in
medical textbooks. The basic pathophysiology and definition of these conditions
are consistent with the ones of the compartment syndrome, but they are not regarded as compartment syndromes in
current medical terminology and are not
covered in this review. Without further
specification, the term compartment
syndrome refers to the extremity compartment syndromes (ECS); in the case of
other anatomical areas, the specific body
compartment must be defined (abdominal, thoracic, etc.). Considering the critical care focus, only acute compartment
syndromes are discussed in this article,
but many compartments can have subacute or chronic syndromes with a less
dramatic clinical picture. The aim of this
article is to introduce and discuss acute
compartment syndromes that are essential for critical care physicians to recognize and manage.

General Pathophysiology
The underlying pathophysiology of all
compartment syndromes is the inadequate perfusion and oxygenation of the
organs/tissues within the confined space

(1). Pressure in the microcirculation determines the adequacy of nutrient blood

flow in the capillaries, and this pressure
is opposed by both venous and tissue
pressures.
Although authors agree that cellular
anoxia is the final common pathway, several explanations (2) have been proposed
to account for the complex pathophysiology resulting in compartment syndrome.
The two generally accepted theories are:
1) the ischemia-reperfusion syndrome
(3); and 2) the arteriovenous pressure
theory (4). Although the two theories are
complementary and not contradictory,
the most recognized explanation is the
arteriovenous pressure gradient theory.
The perfusion of the intracompartmental tissues is hindered by the elevation of the interstitial fluid pressure
above the level of the pressures in the
capillaries. The interstitial pressure in
loose connective tissue spaces is reported
to be subatmospheric, whereas in tightly
encased tissues, it is positive pressure
10 mm Hg (5). The capillary pressures
on the arterial and the venous ends are
30 mm Hg and 10 mm Hg, respectively. Depending on the organs normal
interstitial pressure and potential for autoregulation, the compartment pressure,
which causes organ dysfunction, is between 15 and 25 mm Hg. In most compartments, pressure of 30 mm Hg critically compromises organ perfusion.
S445

More recently, it has been recommended

that compartment pressures be interpreted in the context of the difference of
diastolic or mean arterial pressure (P
diastolic pressure compartment pressure) rather than absolute pressures (6,
7). This approach helps to consider the
compartment pressure in context of the
arterial inflow. Once the compartments
perfusion is compromised, a vicious cycle
of hypoxia, anaerobic metabolism,
edema, further pressure increase and further decrease of capillary flow takes place.
This process is irreversible without intervention.
The increased pressure in the compartment can be due to the increased
content within the fixed volume space
(bleeding, edema) or due to the decreased
volume of the compartment (external
compression, bandage, cast), or both.
Compartments can be in relative ischemic state due to higher oxygen demand
(exercise, trauma, sepsis) but peripheral
vasoconstriction (vasopressor medication) also can further limit their perfusion. This absolute or relative ischemia
can lead to massive tissue edema and
consequent compartment syndrome after
reperfusion. The symptoms of the specific
compartment syndrome are dependent
on the function of the enclosed organs.
Compartment syndromes, in general, can
be classified as primary (the pathology/
injury is within the compartment) or secondary (no primary pathology or injury
within the compartment).

Individual Compartments
Thoracic/mediastinal
compartment syndrome
A syndrome of tight mediastinum
after prolonged cardiac surgery was described by Riahi et al (8) in 1975. The
condition, known as thoracic or mediastinal compartment syndrome, has been
described in almost 200 reported cases of
adult and pediatric patients undergoing
cardiac surgical procedures. Open chest
management has gained acceptance as a
technique in the management of hemodynamically unstable patients where cardiac compression by sternal closure is not
tolerated. Early concerns to use this technique were related to the potential increased risk of mediastinitis after prolonged open sternotomy; however,
infectious complications and sternal
morbidity have been less frequent than
first anticipated in the late 1970s (9 12).
S446

Although thoracic compartment syndrome is well known in the cardiac surgical literature, it is hardly mentioned in
the noncardiac surgical and trauma literature (13).
Etiology. Research into cardiac function after cardiac surgery has found that
restriction of diastolic filling is the main
point at which compression or tamponade
develops in the thoracic cavity. Both the
pericardium and the sternum act to increase diastolic stiffness; however, a larger
decrease in cardiac output noted after sternal closure suggests that the latter may
exert a greater effect than pericardial closure, particularly in patients with fluid
overload (14). The decrease in blood
pressure and the increased end-diastolic pressure can result in subendocardial ischemia, leading to a cycle of
progressive deterioration (13). Low cardiac output can be improved by opening
the sternum (15).
Thoracic compartment syndrome is
an infrequent occurrence, even in the
busiest cardiac and trauma centers. Prolonged open sternotomy with delayed
sternal closure has been illustrated as
useful after cardiac surgery in the setting
of severe myocardial dysfunction, marked
myocardial edema, coagulopathy with
uncontrolled bleeding, and relentless arrhythmias (16 18). Patients with decreased lung compliance, acute pulmonary edema, or congestive cardiac failure
are also at a significant risk for a delayed
sternal closure.
There are two case reports in the literature describing thoracic compartment
syndrome after noncardiac thoracic procedures (13, 19).
With regard to the trauma patient,
Kaplan et al (20) reported a patient with a
gunshot wound causing thoracic and cardiac injuries that was treated with delayed sternal closure. This is the only case
reported in the literature of thoracic
compartment syndrome with the etiology
of trauma. The lack of further data to
support prolonged open sternotomy in
trauma patients (more than anecdotal evidence) is due largely to the limited survival of patients whose injuries are significant enough to result in massive tissue
edema after resuscitation from thoracic
trauma. In this context, it is important to
note that thoracic compartment syndrome can also occur after thoracotomy
with packing for trauma.
Diagnosis. In the poststernotomy
state, massive resuscitation and acute
mediastinal swelling/bleeding should

alert critical care physicians. Rising peak

inspiratory pressure during thoracic wall
closure may serve as an early warning
that the patient is at risk for thoracic
compartment syndrome (20). Since the
rest of the symptomslike falling cardiac
output and worsening acidosisare nonspecific, clinical suspicion remains a crucial component in the diagnosis of thoracic compartment syndrome. The
syndrome may not develop until hours
and possibly days postclosure when ventilation pressure monitoring has ceased.
Treatment. Immediate decompression
of the chest and open chest management
with delayed sternal closure is the key in
thoracic compartment syndrome where
thoracic closure precipitates hemodynamic collapse. Open sternotomy involves leaving the sternum and subcutaneous layer open after surgery. The skin
can be left open and packed, or closed
directly or with an interposed synthetic
material. Several approaches have been
illustrated in the literature (13, 20).
Maintenance of the open chest must
continue until the patient demonstrates
correction of the hemodynamic instability. There must be evidence of increased
cardiac output, decreased filling pressures, and improved lung function before
closure, with the average time to closure
reported from 2 to 7 days (21). Aggressive
diuresis to achieve this has been suggested; however, this may be difficult and
potentially detrimental in patients undergoing acute traumatic shock resuscitation.

Abdominal compartment
syndrome
Abdominal compartment syndrome
(ACS) is the most frequently cited compartment syndrome after ECS. The clinical consequences of elevated intraabdominal pressure (IAP) were described
as early as the mid-19th century (22).
Pediatric surgeons became aware of the
catastrophic consequences of attempted
closure of omphaloceles, and vascular
surgeons described the problem after surgical management of ruptured abdominal
aortic aneurysms (23, 24). Damage control surgery improved the chances of survival of patients with hemorrhagic shock
and severe abdominal trauma. The fact
that the patients survived and some of the
practices of damage control (abdominal
packing and aggressive fluid resuscitation) led to the emergence of the epidemic of postinjury ACS (25). The expoCrit Care Med 2010 Vol. 38, No. 9 (Suppl.)

nential increase of scientific publications

on the topic and the regular monitoring
of IAP increased the awareness of the
syndrome. During the last decade, the
consequences of intra-abdominal hypertension (IAH) and ACS were described by
most surgical specialties and also recognized as prevalent conditions among
nonsurgical intensive care unit (ICU) patients.
Classification, definitions. The World
Society of the Abdominal Compartment
Syndrome (WSACS, founded in 2004) was
fundamental to establish consensus definitions driven by a multidisciplinary
group of experts. The WSACS recommends the intravesical (bladder) route for
IAP measurement, and among many, it
established the following definitions (26):

Intra-abdominal hypertension (IAH) is

defined as IAP of 12 mm Hg without
pathophysiology of ACS. IAH is graded
from I to IV based on the IAP value
(grade I: 1215 mm Hg; grade II: 16 20
mm Hg; grade III: 2125 mm Hg; grade
IV: 25 mm Hg.
ACS is defined as a sustained IAP of
20 mm Hg that is associated with
new organ dysfunction/failure defined.

Primary ACS is a condition associated

with injury or disease in the abdominopelvic region that frequently requires early surgical or interventional
radiologic intervention.
Secondary ACS refers to conditions
that do not originate from the abdominopelvic region.

The clinically most relevant classification is to describe the acuity of the syndrome (acute, subacute, or chronic), the
etiology (e.g., postinjury, sepsis, burn, abdominal aortic aneurysm), and the primary or secondary nature of the problem.
Etiology. The acutely increased IAP,
the IAH, and the ACS can be due to a
variety of abdominal and extra-abdominal
factors (Table 1) (27). Considering the
size of the abdominal cavity, its central
location in the body, and the number of
vital organs located within, it is not surprising that ACS has symptoms related to
extra-abdominal organs (Table 2) (28,
29). In patients with already marginal
organ function, the characteristic IAH/
ACS-related organ dysfunctions tend to
be apparent at lower IAP.
ACS can be caused by many pathologic
conditions but the high-risk patients al-

Table 1. Frequent causes of abdominal compartment syndrome

Primary

Secondary

Ascites
Abdominal trauma
Damage control laparotomy
Ruptured abdominal aortic aneurysm
Abdominal aortic cross-clamping
Intestinal obstruction
Ileus
Severe constipation
Major abdominal surgery
Abdominal sepsis
Large abdominal tumors
(especially ovarian)
Pancreatitis
Liver transplantation

Whole-body ischemia/reperfusion injury

Hemorrhagic shock
Septic shock
Major burns

Table 2. Organ dysfunctions caused by increased intra-abdominal pressure

Organ/Body Part
Brain
Lungs
Chest
Heart/circulation
Visceral organs
Kidneys
Lower extremities

Symptoms/Signs
Increased intracranial pressure
Increased airway pressures, decreased compliance, poor oxygenation,
CO2 retention
Increased intrathoracic pressure, elevated diaphragms
Elevated filling pressures, decreased cardiac output, increased systemic
vascular resistance
Decreased intestinal pH, intolerance of enteral nutrition, bowel edema,
compromised intestinal barrier function, ileus
Decreased urine output, decreased glomerular filtration rate
Venous congestion, edema, increased risk for deep vein thrombosis
and extremity compartment syndromes

Crit Care Med 2010 Vol. 38, No. 9 (Suppl.)

ways have some abdominal mass effect

(fluid, blood, packs, intraluminal contents, tumor) and/or requirement for
massive fluid resuscitation (traumatic
shock, septic shock, ischemia-reperfusion
injury, burns). With regard to the patient
with burns, they are a specifically high
risk of secondary ACS due to the common
situation of free fluid accumulation after
massive burn resuscitation. Considering
the multitude of etiologies, most ICU patients have at least one risk factor to
develop ACS (30).
Diagnosis. The measurement of the
IAP is essential for the monitoring of the
high-risk patients, as the clinical examination has been repeatedly shown to be
inaccurate to detect ACS and to estimate
IAP (31, 32). The accepted method to
measure IAP is via the urinary catheter,
using the bladder as a conduit of the
abdomen (bladder pressure and urinary bladder pressure/UBP are frequently used synonyms of IAP). Kron et
al (24) originally described the technique,
and today numerous modifications exist
in the literature. The measurement can
be performed with a homemade kit of a
Foley catheter, a three-way stopcock, and
a pressure transducer connected to the
bedside monitor, but several proprietary
devices are also available. The main principles are to use a closed system, fixed
reference point (midaxillary line), standard instillation volume (25 mL), and
standardized recording (respiratory
phase, body position). Most ICUs practice
an initial screening among patients who
have at least one risk factor, and later,
2 8 hourly monitoring in high-risk patients or in patients with initially abnormal measurements.
The normal IAP is considered 10
mm Hg among nonlaparotomy, nontrauma hospitalized patients (33). Postlaparotomy patients and morbidly obese
patients have a higher baseline IAP value.
Traumatic shock patients requiring hemorrhage control and resuscitation typically have grade IIIII IAH during the
first 24 hrs of resuscitation (34). The effect of this transient IAH on the outcome
is largely unknown. After damage control
surgery (both trauma and emergency
general surgery) and during shock resuscitation (regardless of the etiology), frequent monitoring is recommended. In
shocked multiple trauma patients, ACS
can develop within 6 hrs of ICU admission, presenting with oliguria, increased
airway pressures, inability to oxygenate,
and no response to preload driven resusS447

citation. When the abdominal compartment is already on the steep phase of its
pressure-volume curve, a decrease in
compliance and even small increases in
volume can lead to sharp elevations
in IAP. In most critically ill patients, continuous IAP monitoring is recommended
via the irrigation port of the previously
inserted three-way catheter (35). The diagnosis of ACS is confirmed if the deteriorated organ functions improve after
the IAP is decreased by either operative or
nonoperative means.
Based on a retrospective study,
Cheatham et al (7) have recommended
abdominal perfusion pressure (abdominal
perfusion pressure mean arterial pressure IAP) as a potentially superior and
more physiology-oriented definition of
IAH and ACS. Abdominal perfusion pressure was recommended to be kept at 60
mm Hg; however, this therapeutic goal
remains to be proven by higher-level evidence.
Treatment. The treatment of ACS entails the resolution of the underlying
problem simultaneously with measures
to decrease IAP. The authors believe that
medical methods to decrease IAP (diuretics, skeletal muscle paralysis, motility
agents, gastric and colonic decompression) can have a role in less acutely developing IAH, especially without surgical
causes (36). In the acute setting, especially postinjury, ACS deteriorates the already critically ill patients physiology to
organ failure within hours. This fulminant process prevents the opportunity to
reassess and titrate medical treatment before the condition becomes irreversible.
Thus, in the acute ACS, abdominal decompression is recommended. In cases of
primary ACS, this means usually abdominal reexploration in the operating room
for continued bleeding or for major septic
source. In secondary ACS, decompressive
laparotomy can be performed at the bedside as a lifesaving measure, because no
further surgical intervention is necessary
within the abdomen (37).
There are promising preliminary reports on percutaneous drainage of the
intraperitoneal fluid (especially in burns)
and subcutaneous linea alba fasciotomy
(pancreatitis) (38 40). However, these
techniques always require careful reassessment of the potential need for formal
decompression (full midline laparotomy).
The limitation of percutaneous decompression is the fact that, apart from burns
injury, secondary ACS is rarely caused by
free intraperitoneal fluid alone and withS448

out associated significant bowel edema.

Although the subcutaneous linea alba decompression could prevent two potential
morbid consequences of the open laparotomy (peritonitis, fistula formation), its
decompressive effect may not be sufficient in all cases. It is important to emphasize that the previously recommended
fluid boluses to overcome the IAH-related
organ dysfunctions are usually inefficient
and can lead to full-blown ACS (41).
Some early reports (42) described sudden circulatory collapse in cases that decompressed late, but in general after abdominal decompression, there is a
prompt improvement in blood pressure,
filling pressures, vascular resistance, oxygenation, and airway pressures. Although these improvements show the effectiveness of decompression, they are
unfortunately not necessarily associated
with better outcomes. Survivors respond
with consistently improved cardiac output and urine output (34).
Prevention. Outcomes of ACS are poor
even with timely decompression because
the maintenance of an open abdomen is
also a condition with significant morbidity and mortality. For this reason, primary prevention is the most rational approach. To date, postinjury ACS is the
best characterized form of the syndrome
with statistically validated predictors
(34). Primary ACS can be predicted by the
damage control physiology and management pattern (rapid transport to the operating room, hypothermia, acidosis, hypotension and massive transfusion).
Primary postinjury ACS is largely preventable with the liberal use of open abdomen and limiting the number of laparotomy packs left in the abdominal
cavity. It is important to emphasize that
ACS can also develop in the open abdomen (recurrent ACS).

Secondary ACS is always associated

with shock and massive resuscitation, regardless of the etiology (trauma, sepsis,
burn). Aside from the commonality of no
abdominal surgery, independent predictors for the development of secondary
ACS include: metabolic acidosis, administration of 7 L of crystalloid over the
first 6 hrs and lengthy pre-ICU diagnostics. The prevention of secondary ACS
relies on timely elimination of the cause
of shock and avoidance of uncontrolled resuscitation with repeated crystalloid boluses. The importance of understanding the
quality and magnitude of fluid resuscitation is further emphasized by the fact that
shock resuscitation aimed at supranormal
oxygen goals has been found to result in
more ACS and organ failure than resuscitation aimed at normal oxygen delivery
goals and the use of significantly less crystalloid infusions (43).

Skeletal muscle compartments

Etiology and risk factors. Any condition that increases the content or reduces
the volume of a compartment can produce a compartment syndrome (Table 3).
ECS most often develops in the context of
significant trauma, commonly long-bone
fractures; however, it may also develop
from both minor trauma and nontraumatic causes, such as exertion (44, 45).
Fractures account for approximately
75% of all ECS. Although the condition is
more frequent in closed fractures, limbs
with open fractures can also develop
compartment syndrome because the
open wound does not necessarily result in
adequate decompression of all compartments (1, 46). Comminuted, displaced
fractures (large area for potential bleeding, high energy transfer) of the proximal
tibial shaft and proximal forearm (more

Table 3. Causes of extremity compartment syndrome

Increased Content of Compartment
Fracture-related swelling, bleeding
Vascular injury, bleeding
Hemorrhage into compartment
Bleeding diathesis
Anticoagulation
Bleeding disorders
Increased vascular permeability
Burns, shock
Venomous bites
Edema
Postischemic reperfusion
Unusual exertion
Decreased serum osmolarity
Extravasation of intravenous fluids

Reduced Volume of Compartment

Direct compression by fracture fragments
Constriction via casts, dressings, clothing
Constriction via surgical closure of fascia
Constrictive pressure via burns eschar
Obtunded/sedated patients positional pressure
Excessive traction of fractures

Crit Care Med 2010 Vol. 38, No. 9 (Suppl.)

muscle bulk and thick, nontensile fascia)

are the most dangerous patterns. In the
pediatric population, supracondylar humerus fractures are frequent causes of
excessive swelling, but in these fractures
direct arterial and nerve injury/compromise often dominate lead the clinical picture. The involvement of the foot, thigh,
and gluteal region is also now well recognized, in particular, in multiple trauma
patients (47 49).
Closed fracture reduction theoretically decreases the blood loss into the
compartment and the ongoing traumatization of the soft tissues, but tight circumferential bandages or casts can further compromise the limb. Operative
fracture fixation, especially intramedullary reaming/nailing and prolonged tourniquet use, may also cause increases in
compartment pressures. McQueen et al
(50) showed that pressures during intramedullary nailing of the tibia peaked
during the procedure but fell again over
the next 36 hrs. The risk of compartment
syndrome also increases in proportion to
the length of the procedure.
Thermal injuries, in particular, fullthickness burns, cause secondary tissue
constriction, eschar, edema, and large
fluid shifts associated with major burns
adding to extra volume pressure. The obtunded patient with prolonged limb compression, either during surgery or postoperative sedation, is at particular risk for
development of a extremity compartment
syndrome, which may go unnoticed. Prolonged positioning of a limb, especially in
traction or lithotomy position can also
place compartments at risk, in particular,
if there is ongoing bleeding related to
injury (51). Victims of penetrating extremity trauma can also develop a compartment syndrome (52).
Diagnosis. The diagnosis of compartment syndrome depends on close attention to clinical history and symptoms.
Multiple studies have shown that, on its
own, clinical examination is insufficient
to accurately assess compartment pressures and to differentiate between generalized swelling and a tight compartment.
Compartment pressure monitoring is
now an established method of managing
at-risk patients; however, there is a lack
of consensus on which patients are indicated for monitoring and the threshold
pressures that should be used to guide
fasciotomy. In terms of the role of increasing creatine kinase levels, myoglobinuria, or rhabdomyolysis, these are
nonspecific signs of muscle necrosis and,
Crit Care Med 2010 Vol. 38, No. 9 (Suppl.)

thus, are late signs of untreated irreversible compartment syndrome. Although

creatine kinase is helpful for monitoring
ongoing muscle necrosis, it is probably
not specific enough to diagnose ECS.
Clinical signs. The diagnosis of compartment syndrome in alert patients relies on clinical suspicion. The classic 5 Ps
(pain, pallor, pulselessness, paresthesias,
paralysis), associated with arterial insufficiency, are often mistakenly described
as signs of compartment syndrome (53).
Of the five classic signs, only pain and
perhaps paresthesia are associated with
reversible compartment syndrome. Any
nerve running through the involved compartment will become ischemic, often resulting in sensory deficit in the nerve
distribution. Pulselessness and paralysis
are late signs and the result of extreme
pressures invariably associated with loss
of function. The most important sign to
emphasize is pain out of proportion to
injury and pain felt on passive stretching
of the muscles within the compartment.
These symptoms are hard to differentiate
from the acute fracture-related pain but
compartment syndrome pain is typically
a dull pressure (ischemic pain), which
does not respond to pain relief. In summary, in a conscious patient, whose perception or response is not changed by
distracting injury, alcohol, or drugs, the
diagnosis of a compartment syndrome is
usually made by the clinical manifestation of unrelenting ischemic pain that
fails to respond to the expected amount of
analgesia. Later, pain may become a
much less reliable indicator of significant
pressure elevation after muscle necrosis
has occurred.
It is important to highlight that, although capillary refill may be slowed, palpable pulses are always present in ACS unless there is an associated arterial injury.
Pressure within the compartment (assuming the patient is normotensive) is unlikely
to increase sufficiently to totally obstruct
the systolic pressure in the major artery
traversing the compartment (54).
Measurement. Since 1975 compartment pressure monitoring has been advocated for early diagnosis of compartment syndrome (55, 56). There is,
however, no consensus about the clinical
indications for monitoring compartment
pressures or about the threshold value for
diagnosis and treatment. A single normal
compartment pressure reading, which
may be performed early in the course of

the disease, does not rule out a compartment syndrome; thus, serial or continuous measurements can be important in
high-risk patients, especially in conditions where clinical examination is unreliable. The normal pressure of a tissue
compartment falls between 0 and 8
mm Hg, with symptoms and signs of
compartment syndrome developing with
pressures above approximately 20
mm Hg. However, the pressure necessary
for permanent damage varies. McQueen
and Court-Brown (57) performed a prospective cohort study of continuous monitoring of the anterior compartment pressure in 116 diaphyseal tibia fracture
patients. Forty-three percent and 23%
patients had compartment pressures of
30 mm Hg and 40 mm Hg, respectively.
The authors decompressed only those
who had a pressure (diastolic blood
pressure compartment pressure) of
30 mm Hg. This strategy resulted in
only three fasciotomies but prevented 50
unnecessary decompressions. No patients
had missed compartment syndrome. This
study highlights the need to consider the
general condition of the individual patients and questions the need for extensive monitoring, especially in awake oriented patients.
Compartment pressures can be measured with proprietary handheld devices
or with a simple ICU pressure transducer
set-up connected to the bedside or operating room monitor. Pressures should be
measured in all compartments of the
limb by inserting a needle, which is connected to the pressure measuring device.
The manometer needs to be zeroed at the
level of the measured compartment.
Treatment. The treatment of an ECS
is dermatofasciotomy (fasciotomy). Subcutaneous fasciotomy is not recommended in trauma/critical care scenarios.
Fasciotomy is performed preferably in the
operating room but, in critically ill patients, it should not be delayed because of
lack of operating room access or a patients general condition. Apart from its
therapeutic role, fasciotomy may also be
preventive in situations that are known to
be high risk for compartment syndrome.
In this case, avoiding the procedure carries a higher risk than managing the
complications of the fasciotomy itself.
These scenarios include major (proximal)
reimplantation, arterial repair with long
ischemic time, and combined arterial and
venous repair on the ipsilateral limb.
Prevention. Prehospital atraumatic
splinting and timely reduction (open or
S449

closed), followed by stabilization, can prevent compartment syndrome in low-risk

injury patterns. The avoidance of tight
bandages, splints, and casts is mandatory.
Some of the patients (entrapment, difficult extraction, long prehospital time,
and prolonged compression to the compartments) may present with full-blown
compartment syndrome where these preventive measures are no longer feasible.
In high-risk situations (typical injury patterns, inability to reexamine the patient
clinically owing to head injury or intoxication), preventive fasciotomy must be
considered. The fasciotomy wounds
themselves require planned reassessment
and gradual skin closure or skin grafting.
The secondary limb compartment syndromes can be prevented by careful shock
resuscitation (hemorrhagic, burn, and
septic) without crystalloid overload, with
simultaneous monitoring of the compartment pressures.

Polycompartment syndrome
More recently, the multiple compartment syndrome or poly-compartment syndrome was described as a result
of a futile attempt to optimize critical
trauma patients circulation with preload-driven resuscitation with crystalloid
solutions. The authors described a vicious cycle of increasing intracranial
pressure, intrathoracic pressure, and IAP
secondary to fluid therapy to optimize
cerebral perfusion and the aggressive
ventilatory management to treat acute
lung injury (58). Simultaneously, other
researchers (59) described the potential
interactions among different compartments. We believe most of these complications, including the secondary ECS, are
results of the previously described salty
water vicious cycle of futile crystalloid
loading.

CONCLUSIONS
Compartment syndromes are serious
limb, organ, or life-threatening conditions.
Clinicians need to be familiar with their
etiology and the frequently elusive presentation (especially secondary compartment
syndrome) in critically ill patients. Prevention of compartment syndrome with preemptive open management of compartments (primary syndromes) in high-risk
patients and/or careful resuscitation (both
primary and secondary syndromes) is the
recommended approach.
S450

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