clinical
ACUTE COMPARTMENT
Sharon Edwards RGN, DipN(Lon),
MSc, PGCEA is senior lecturer at
the department of nursing and
midwifery, University of
Hertfordshire
This article has been subjected to
double blind peer review
32
SYNDROME
SHARON EDWARDS explores the definition of acute compartment
syndrome, its aetiology, sites and causes
cute compartment syndrome is a com-
A mon but potentially life threatening con-
dition that occurs in the limbs and
abdomen, and that requires prompt recog-
nition and intervention.
Caused by high pressure in a closed fascial
space so that capillary perfusion is too low for
tissue viability, it is well recognised as a po-
tentially devastating complication of tibial
shaft fractures and many other common con-
ditions observed in emergency departments.
Diagnosis is usually made on clinical
grounds following a high index of suspicion,
with an excessive and unexpectedly dis-
proportionate pain response being one of
the key symptoms.
Avoiding delay in recognition requires
vigilance and repeated examination to avoid
significant complications.
A detailed understanding of the
pathophysiology involved in acute
compartment syndrome contributes to
understanding the seriousness of this
condition and the signs and symptoms that
are present. However, patients’ inability to
identify pain can mask its progression.
MUSCLE TISSUE
There are three types of muscle tissue:
skeletal, cardiac and smooth (Marieb 2004).
Compartment syndrome mainly involves
skeletal muscles.
Like all body cells, skeletal muscle fibres are
soft and fragile. The covering, or sheaths, of
connective tissue support individual cells,
reinforce muscle as a whole and provide it
with its natural elasticity. It also provides
entry and exit routes for blood vessels and
nerve fibres serving the muscle.
The normal activity of skeletal muscle is
absolutely dependent on a rich blood supply
and its nerve supply. Unlike other muscle
tissues, which can contract without nerve
stimulation, skeletal muscle fibres are
supplied with individual nerve endings that
control their activity
Muscle fibres use tremendous amounts of
energy when they contract so they need a
near continuous delivery of oxygen and nut-
rients by way of blood vessels. They also
produce large amounts of metabolic waste
that must be removed though the veins if
contraction is to remain efficient. In general
one artery and at least one vein serve each
muscle.
COMPARTMENT SYNDROME
The muscles of the leg are grouped into four
compartments that are formed by thick
layers of fairly inelastic tissue called fascia
(Fig. 1), and each compartment contains a
major nerve as well as blood vessels (Table 1).
Compartment syndrome is a serious
condition whereby trauma or haemorrhage
causes swelling within a muscle com-
partment. It is defined as ‘an elevation of the
interstitial pressure in a closed osseofascial
compartment that results in microvascular
compromise’ (Mubarak and Hargens 1983).
If this condition goes unrecognised, it can
be devastating, and delay in diagnosis can
affect patients’ future quality of life.
Compartment syndrome is fairly common
following soft tissue injury, and young men
are at particular risk especially if they have a
clotting disorder or are taking anticoagulant
therapy so that risk of intracompartment
haemorrhage following trauma is increased
(McQueen et al 2000).
SITES OF COMPARTMENT SYNDROME
The most common site of compartment
syndrome is the lower leg (Abramowitz and
Schepsis 1994), with the anterior com-
partment being the most frequently
affected, followed by the lateral com-
partment and the deep posterior com-
partment.
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Increase in volume of the contents of the

Fig. 1. Lower leg compartments
compartment can be caused by bleeding,
infiltration of intravenous fluid or post-
traumatic or ischaemic swelling.
However, compartment syndrome can also
occur in either of the two compartments of
the forearm, and any of the three
compartments of the thigh (Tiwari et al
2002) (Table 2).
It can also occur in the abdomen after
laparotomy for major trauma and can
render the abdomen difficult or impossible
to close (Ertel et al 2000).
Compartment syndrome can occur in an
open wound if the skin laceration is
insufficient to decompress the oedema or if
there is haemorrhage. Even if the wound
does not involve the compartment fascia,
compartment syndrome is still possible. Tibia Anterior muscle
compartment
Compartment syndrome can also be seen
elsewhere: the feet of patients with diabetes
(Lee et al 1995) and the lower limbs after
Lateral muscle
malignant hyperthermia (Johnson et al compartment
1999).
Deep posterior,
or medial,
CAUSES AND PATHOPHYSIOLOGY OF muscle Fibula
COMPARTMENT SYNDROME compartment
Tiwari et al (2002) describe several ways that
compartment size can be reduced (Table 3).
The initial injury, whether traumatic, Superficial
haemorrhagic, surgical, vascular or a com- posterior
PETER GARDINER

Blood vessels muscle

plication of another condition, leads to local- and nerves compartment
ised swelling in the muscle compartments
due to the stimulation of the inflammatory
response (IR) (Huddleston 1992).
Table 1. The four compartments of the leg and their nerve supplies
INFLAMMATORY RESPONSE
The IR is a systemic response that produces Compartments of the leg Nerve supply
extensive inflammation by attracting
> anterior deep peroneal
nutrients, fluids, clotting factors and large
numbers of neutrophils and macrophages > deep posterior, or medial tibial

to a damaged site. > lateral superficial peroneal

To attract these, damaged tissue releases > superficial posterior saphenous
mediators that are part of a chemotaxic
signalling system. These mediators include
histamine, prostaglandins and cytokines but Table 2. The compartments of the forearm and thigh
the list is immense and is rapidly growing
(Zuccarelli 2000). Compartments of the forearm Nerve supply
They cause a localised increase in capillary > volar (anterior) musculocutanous nerve
permeability, which leads to swelling,
oedema and pain, and vasodilatation, which
> dorsal (posterior) radial nerve

leads to redness and heat, the signs often Compartments of the thigh Nerve supply
observed at the site of inflammation (Fig. 2). > anterior femoral
The stimulation of the inflammatory
process damages the endothelium of the
> posterior sciatic

blood vessels, which is a major contributor > medial obturator

to the activation of the IR.

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Table 3. Ways that compartment size can be reduced
> fracture (tibia or fibula fractures, usually in the middle or distal third of the leg,
or supracondylar fracture of the humerus)
> crush injury
> excessive exercise of a muscle group
> surgical procedures including closure of fascial defects
> major vascular surgery
> bleeding disorders
> compression bandages
> constrictive devices such as a tight cast
> insect sting or snake bite
> burns
> IV drug use
> weightlifting
> post-ischaemic swelling
All of the above generally lead to ischaemia due to the swelling in the compartment.
Prognosis depends directly on the time interval between the onset of the
intracompartment ischaemia and the start of effective treatment
The endothelium is not just an inert barrier
between the blood and the substructure of
the blood vessels and tissue (Edwards
2002a). It is an active metabolic organ and,
when damaged, is responsible for stim-
ulating anticoagulation pathways.
Stimulation of the clotting cascade always
accompanies injury and is closely linked to the
IR. This serves to prevent excessive blood loss
and isolate the injured site (Huddleston 1992).
Increased capillary permeability leads to
swelling and an increase in intracom-
partmental pressure (ICP). Compartments
have relatively fixed volumes so introducing
fluid or constricting them increases pressure
and decreases tissue perfusion. This results
in hypertension, or an increase in hydrostatic
pressure (HP), at the venous end of the
capillary bed (Tiwari et al 2002).
But further oedema occurs when there is
an increase in HP at the arterial or venous
end of the capillary bed (Edwards 2003a ).
This raises the pressure of blood in the
capillary and cause an increase in filtration
rate. Larger than usual amounts of fluid
then move into the interstitial space and
causes the collection of even more fluid in
the compartments (Fig. 3).
INCREASED PERFUSION PRESSURE
Elevated perfusion pressure is the physio-
logical response to rising ICP. As ICP rises,
autoregulatory mechanisms are over-
34
whelmed and a cascade of injury develops.
A normal resting intramuscular pressure is
0-8mmHg. Pain and paraesthesia occurs at
20-30mmHg (Tiwari et al 2002).
An ICP of 30mmHg is often used as a
basis for performing a fasciotomy (Cooper
1992).
Whitesides et al (1975) and later McQueen
and Court-Brown (1996) however use a
differential between diastolic pressure and
ICP of 10-30mmHg as the threshold for
doing so. Using this method severely reduces
the number of patients that undergo this
procedure without endangering those who
do not (Ovre et al 1998).
Tiwari et al (2002) suggest that fasciotomy
should be performed when the difference
between mean arterial pressure and ICP –
the so-called b pressure – is 40-50mmHg.
But the ideal b pressure threshold for
performing a fasciotomy remains unknown.
If ICP exceeds 30mmHg and observations
are compatible with compartment syn-
drome, prompt therapies to decrease the
pressure such as removal or opening of
casts, skeletal fixation of unstable fractures,
maximising local arterial pressure, placing
the limb at a level with the heart or in some
instances anticoagulation to prevent
complications, are necessary. If ICP exceeds
40mmHg, emergency treatment is needed
because blood flow through the capillaries
and therefore oxygen delivery will cease.
HYPOXIC INJURY
Eventually blood flow is so reduced that
tissue is no longer viable (Phillips 1992).
Increased interstitial pressure overcomes
intravascular pressure of the microcirculation,
causing the vessel walls to collapse and
thereby impeding blood flow still further.
This results in local tissue ischaemia and
intracellular oedema, which in turn further
increases ICP (Jobe 1992).
Meanwhile, the interrupted supply of
oxygenated blood results in anaerobic
metabolism, loss of adenosine triphosphate
(ATP) and cellular membrane disruption
(Edwards 2002b) (Fig. 4).
High intracellular potassium and low
intracellular sodium and calcium concen-
trations are maintained by active transport
systems. Without sufficient ATP, the plasma
membrane of the cells can no longer
maintain normal ionic gradients, and the
sodium and potassium, and calcium, pumps
can no longer function.
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Potassium leaks into the extracellular

Fig. 2. The inflammatory response (IR)
space, while calcium and sodium followed
by water move into the cells. This causes
Insult or injury
cellular oedema and increased intracellular
osmotic pressure (Edwards 2003b), which
can eventually cause the cells to burst.
Muscle contraction relies on the passage of IR, sympathetic nervous system stimulation, endothelial damage
electrochemical impulses down specialised
pathways and require the movement of
sodium, potassium and calcium ions in and
out of cells to produce action potentials. Release of histamine, complementary proteins, kinins
These action potentials may limit movement and prostaglandins
and contraction of muscle but these changes
are reversible if oxygen supplies are restored.
If interventions such as fasciotomy and
oxygen administration are not started, Attraction of
neutrophils,
intracellular acidaemia and cellular dys- Increased
Vasodilatation monocytes and
function become extreme. This can lead to capillary
of arterioles lymphocytes to
permeability
intracellular lysosome membrane disruption, site of insult or
an accumulation of intracellular calcium and, injury
if allowed to continue, irreversible cell
damage, loss of limb and death.
Necrotic muscle never recovers so the
Local hyperaemia Leakage of fluid from capillaries Clotting cascade
seriousness of this condition and the (excess blood) (exudate formation) stimulated
importance of recognising the warning signs
should not be underestimated.
The surrounding tissue suffers further
damage because of increased pressure with- Heat Redness
in the compartment, leading to injury,
stimulation of the IR and reduced blood
supply. This leads to further hypoxic dam-
age, which stimulates the release of IR med- Leakage of
Increased oxygen Leakage of
iators, thereby developing a vicious cycle. protein rich fluid
and nutrients clotting proteins
into tissue spaces

MYOGLOBINURIA
When muscle tissue suffers necrosis, it
releases the intracellular muscle protein,
myoglobin. Excess myoglobin after major
muscle trauma appears in urine as a dark
Pain Swelling
reddish brown colour.
Myoglobinurea, often known as rhab-
domyolysis, is indicative of severe, life threat-
ening muscle trauma. Increased Walled-off
temperature, process
The renal threshold for myoglobin is low, leading to (blood clots
about 0.5mg/100ml urine, so that only increase in prevent injury to
200g of muscle need be damaged to cause metabolic rate surrounding area)
visible changes in the urine (McCance and
Huether 2003).
Priorities on observing myoglobinurea Temporary fibrin
Temporary limitation of joint
include identifying and treating com- patch forms
movement that can lead to hypoxic
partment syndrome and preventing life scaffolding for
injury if severe
repair
threatening renal failure.
Myoglobinurea from muscle death, as well
as causing acidosis and renal failure, can also
result in amputation of the involved extremity, IR prevents infection and promotes healing
sepsis and death. Early diagnosis of com-
partment syndrome is therefore essential.

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PATIENT MANAGEMENT
Fig. 3. Oedema formation due to high hydrostatic pressure
Ischamia is a major feature of compartment
syndrome but blood pressures are only rarely
Capillary
low enough to occlude arterial blood flow
Arterial end Venous end (Fig. 5). For early recognition, more subtle
HP = 43mmHg HP = 21mmHg skills and knowledge are required.
OP = 25mmHg OP = 25mmHg

EARLY RECOGNITION
Recognising compartment syndrome early is
imperative (Middleton 2003a). Early
symptoms are pain that is disproportionate
HP = 1mmHg HP = 1mmHg to the apparent injury and paraesthesia. If
OP = 0mmHg OP = 0mmHg present, they are signs of severe involvement.
NFP = 42 - 25 = 17mmHg NFP = 20 - 25 = -5mmHg Pulselessness is uncommon and rarely
noted as an early symptom; it appears at a
Cell much later stage and generally implies
NFP = 17 - 5 = 12mmHg deficit vascular injury.
leading to oedema formation Nerves that traverse the area of decreased
perfusion are affected and paresthesias
HP = hydrostatic pressure, OP = opposing pressure to the HP, develop in their distribution. They may be an
NFP = net filtration pressure
early complaint but, if allowed to persist, can
If hydrostatic pressure at the arterial end of the capillary increases by 5mmHg, be irreversible. Unfortunately, paresthesias
from 38 to 43mmHg, and at the venous end from by 5mmHg, from 16 to are also seen after contusions that affect
21mmHg, filtration increases, absorption reduces and fluid accumulates in the nerves and after vascular damage.
interstitial space (oedema).
Nevertheless, the most reliable physical
finding in compartment syndrome is sensory
deficit (Moore and Freidman 1989). The loss
of two-point discrimination is a sensitive sign
Fig. 4. Cellular changes following hypoxic or ischaemic injury
(Tiwari et al 2002) and the distribution of
Ischaemia and impaired tissue perfusion causing generalised cellular damage
sensory changes can help differentiate which
compartments are affected.
However, all of these signs of vascular
injury can only be identified in fully conscious
Anaerobic cellular metabolism causes the formation of lactic acid and oxygen
free radicals patients. Emergency nurses must therefore
be vigilant in clinical observation and
examination.
Depletion of ATP and Water and sodium influx
The formation of INTRACOMPARTMENT PRESSURE
failure of sodium/ causes cellular swelling
nitric oxide MEASUREMENT
potassium pumps and metabolic acidosis
Patients with ICPs of 10-30mmHg should be
admitted and followed closely with repeated
pressure measurements (Table 4).
Lysosome membranes damaged,
Mitochrondrial calcium further impairs If the pressure continues to increase,
releasing toxic enzymes into the
cellular functions
cytoplasm treatments are indicated. Due to the effect
of blood pressure on the development of
compartment syndrome, it may be more
Endothelial damage, cytotoxic vasodilator mediators released into the circulation
appropriate to monitor differential pressures
such as that between diastolic pressure and
ICP rather than absolute ICP (McQueen and
Court-Brown 1996, Tiwari et al 2002,
Progressive vasodilatation, myocardial Release of mediators such as kinins, Whitesides et al 1975).
depression, increase in capillary serotonin, lysosomal enzymes and
permeability and intravascular histamine leads to stimulation of the
coagulation inflammatory immune response ADMINISTERING ANALGESIA
Drug overdose and pain deserve a special
mention because they can rival or surpass
limb trauma as major causes of com-
Cellular damage leading to tissue and organ death and failure
partment syndrome.

36 emergency nurse vol 12 no 3 june 2004


Patients who self administer morphine
regularly, for example those who use patient
controlled analgesia (PCA), do not at first
perceive pain, so diagnosis of compartment
syndrome can be delayed.
Pain is a vital protective response; it can
warn of a tight cast, or of underlying haem-
atoma, infection, ulceration, subluxation or
slipping of fixation. Conditions that mask a
pain response can result therefore in deva-
stating consequences.
Patients with compartment syndrome can
present with no pain response because of
high blood morphine concentrations admin-
istered in hospital for pain relief.
Nevertheless, the first symptom of com-
partment syndrome is usually pain, which
often appears late and out of proportion to
initial injury. Because of the seriousness of
the condition, therefore, a low level of pain
or discomfort should be advocated where
the risk of compartment syndrome is high.
This is difficult because pain is what
patients say it is, but it can be determined
by pain assessment.
TREATMENT
Full recovery from compartment syndrome
is probable when treatment is started within
between four and eight hours of the onset
of symptoms, such as swelling or pain.
Intracompartment pressure measurement
(Table 4) should be considered immediately
when compartment syndrome is suspected.
If the ICP is not relieved by decompression
of cast or temporary elevation of limb,
fasciotomy is indicated to decompress the
compartment and allow reperfusion of the
muscle.
Fasciotomy has a high complication rate
because it transforms a closed lesion into an
open wound (Fitzgerald et al 2000). The
open wound can be allowed to heal by
second intention, where for example the
skin is left open after the fasciotomy and
allowed to granulate from the outside in, or
undergo skin closure within four days, skin
grafting or flap coverage.
However, the combination of an open
wound and necrotic muscle can contribute
to the development of life threatening
infection and other complications such as
acidosis, renal failure and loss of limb.
CONCLUSION
Compartment syndrome simply cannot
afford to be overlooked. If it is confirmed or
vol 12 no 3 june 2004 emergency nurse
clinical
Fig. 5. Managing acute limb compartment syndrome
Suspected compartment syndrome
(less than 30mmHg difference between diastolic pressure and ICP)
Conscious patient Unconscious, obtunded patient
Obvious signs Signs that may Measure ICP
such as severe be masked by
pain, swollen analgesia,
and tense pulse remains
compartment, present
paraesthesia,
pallor, paralysis
Normal ICP
Raised ICP
ICP monitoring, clinical assessment
Fasciotomy ICP measuring catheter removed
when ICP and clinical situation is
normal
suspected, prompt consultation with an
orthopaedic or vascular surgeon is warrant-
ed. If left unchecked, the cycle of oedema
and ischaemia results in muscle infarction,
nerve injury and permanent loss of function
in the extremity.
Diagnosis of compartment syndrome in the
leg can be delayed because patients fail to
show a pain response. This ultimately results
in an emergency fasciotomy and possible
shock. This should prompt health practitioners
to question the use of PCA in any trauma-
tised limb.
It is suggested that ICP monitoring of the
anterior compartment of the leg be carried
out when analgesic manoeuvres can have
masked early clinical features of the
syndrome. Nurses must be ever vigilant when
caring for patients with limb injuries and be
aware of the physiology, signs and symptoms
indicating the development of compartment
syndrome, and there is clearly a need for
prompt diagnosis and intervention, without
which limbs and lives can be lost.
There is a need for further nursing
literature, better evaluation of the syndrome
and the development of nurses’ skills in
recognising the syndrome early and using
the appropriate measuring techniques.
37
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