ACUTE COMPARTMENT

SYNDROM

BSNT HUNH QUANG TUYN

BSNT V NGC NAM

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 DEFINITION

Acute compartment syndrome is defined as an

elevation of intracompartmental pressure to a
level and for a duration that without urgent
decompression will cause tissue ischemia and
necrosis

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 HISTORY

The original description of the consequences of

unchecked rising intracompartmental pressures is
widely attributed to Richard von Volkmann
In 1881, He stated that paralysis and contractures
appeared after too tight bandaging of the forearm and
hand, were ischemic in nature, and were caused by
prolonged blocking of arterial blood
1906, Hildebrant,who first used the term
Volkmanns ischemic contracture, was the first to
suggest that elevated tissue pressure may be causally
related to ischemic contracture.
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 In 1909, Thomas, reviewing the literature of
Volkmanns ischaemic contractures found
fractures to be the main causative factor. Other
predisposing causes included arterial injury,
embolus, and tight bandaging.
Rowlands, in1910, suggested that reperfusion
of alimbafter a prolonged ischaemia could
result in the development of acute
compartment syndrome
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 1914, Murphy was the first to suggest that
fasciotomy, if done before the development
of the contracture, may prevent the
contracture from occurring
1922, Brooks concluded that the etiology of
CS and ischemic contractures was related to
venous outflow obstruction

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 Griffiths (1940) and Foisie (1942) felt that the true
etiology of Vokmanns ischemia was arterial spam
Griffiths had established the four Ps : pain with
passive stretch, painless onset, pallor and eventual
pulseleness.
During world war II The authors described how
crushed extremities with compartment syndrome
could cause systemic problems, renal failure
multiorgan system failure, and patient mortality

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 In the 1970s, investigators began to focus on the basic
science, clinical course, and treatment of
compartment syndrome
Rorabeck and Macnab recognized that either arterial
insufficiency or venous obstruction could lead to
compartment syndrome. They observed that blood
flow to a compartment was quickly restored
following fasciotomy. Further, they described
reperfusion injury after decompression
(Rorabeck CH, Macnab I: The pathophysiology of the
anterior tibial compartmental syndrome. Clin
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Orthop 113, 52-57, 1975)
 Whitesides et al noted the importance of duration of
ischemia.they found that fewer than 5% of muscle
cells were damaged after 4 hours of ischemia, while
nearly 100% of muscle cells were damaged after 8
hours of ischemia. Whitesides et al also introduced a
simple technique to measure tissue pressures by
needle manometry.
(Whitesides TE, Harada H, Morimoto K: Compartment
syndromes and the role of fasciotomy, its parameters
and techniques. Instr Course Lect 26:179-196, 1977)

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 Heppenstall et al has shown that muscle metabolism
in canine extremities is related to tissue pressures,
with normal cell activity if the difference between the
mean arterial pressure and the compartment pressure
was 30 mm Hg or higher in uninjured muscle and 40
mm Hg or higher in injured muscle
(Heppenstall RB, Sapega AA, Scott R: The
compartment syndrome. an experimental and clinical
study of muscular energy metabolism using phosphorus
nuclear magnetic resonance spectroscopy. Clin
Orthop 226:138-155, 1988)
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 Matava and colleagues reported similar findings, in
that increased tissue pressure for 8 hours was
associated with a higher percentage of cell death in
animals with compartment pressures that were within
20 mm Hg of the diastolic blood pressure.
(Matava MJ, Whitesides TE, Seiler JG III, et al:
Determination of the compartment pressure threshold of
muscle ischemia in a canine model. J Trauma 37:50-58,
1994 )

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 EPIDEMIOLOGY

The incidence of acute compartment syndrome

in a westernized population is 3.1 per 100,000.
The annual incidence for males is 7.3 per
100,000 compared with 0.7 per 100,000 for
females, a tenfold increase in risk for males
younger patients are at more risk of
compartment syndrome

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The annual age and gender specific incidence
of acute compartment syndrome

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 AETIOLOGY
Trauma
With fracture : open/closed fracture
Fractures account for approximately 75 percent of cases of
ACS. Risk increases with comminuted fractures, The tibia is
involved most often, with ACS developing in approximately
2,7 to 11 percent of such fracture and with the anterior and
deeposterior compartments being most commonly affected
Among children, supracondylar fractures are a common
cause.

Other causes include treatment of fractures

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 In 1986, Bliss and al reported that acute open fractures of the
tibial shaft and were admitted to a multipletrauma referral
center over a three-year period revealed an incidence of
accompanying compartment syndrome of 9.1%. this
complication occurred most often in association with a
comminuted, grade-III open injury to a pedestrian.
JESSE c. and al. In a series of 104 open tibia fractures, six
patients developed compartment syndromes involving all four
compartments of the lower leg, four of which developed after
initial debridement and reduction. The presence of an open
tibia fracture with a displaced, comminuted, fibula fracture
should suggest the possibility of a developing compartment
syndrome
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 Without fracture
Trauma to a tissue
The authors found that cases of ACS without a fracture were at
significantly greater risk for delayed diagnosis and treatment. At
fasciotomy, 20 percent of patients without a fracture had muscle necrosis
requiring debridement, compared with 8 percent of patients with a fracture

Burns
Gunshot wounds
Arterial and Venous injury
Minor trauma in patients taking anticoagulants or
bleeding diathesis 15
 Conditions Associated with Injury Causing
AcuteCompartmentSyndrome Presenting to an
Orthopaedic Trauma Unit
Underlying Condition % of Cases
Tibial diaphyseal fracture 36
Soft tissue injury 23.2
Distal radius fracture 9.8
Crush syndrome 7.9
Diaphyseal fracture forearm 7.9
Femoral diaphyseal fracture 3.0
Tibial plateau fracture 3.0
Hand fracture(s) 2.5
Tibial pilon fractures 2.5
Foot fracture(s) 1.8
Ankle fracture 0.6
Elbow fracture dislocation 0.6
Pelvic fracture 0.6
Humeral diaphyseal fracture 0.6 16
 AETIOLOGY
Nontraumatic causes
Ischemia reperfusion injury
Revascularization procedures and treatments
Prolonged limb compression
Bleeding disorders
Snakebite
Infection
Tight cast, cirular dressing
Intensive muscle use
Use of a pump for infusion of fluids into the joint during an
arthroscopic procedure,........
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 causes of ACS
I. Decreased compartment size
A. Closure of fascial defects
B. Tight dressings
C. Localized external pressure
II. Increased compartment content
A. Bleeding
1. Major vascular injury
2. Bleeding disorder
B. Increased capillary permeability
1. Postischemic swelling
2. Exercise
3. Seizure and eclampsia
4. Trauma (other than major vascular)
5. Burns
6. Intra-arterial drugs
7. Orthopaedic surgery
C. Increased capillary pressure
1. Exercise
2. Venous obstruction
3. Long-leg brace
D. Muscle hypertrophy
E. Infiltrated infusion 18
F. Nephrotic syndrom
 Risk Factors for Development or Late
Diagnosis of Acute Compartment Syndrome
Demographic Altered pain perception

Youth Altered conscious level

Tibial fracture Regional anesthesia

High energy forearm fracture Patient controlled analgesia

High energy femoral diaphyseal fracture Children

Bleeding diathesis/anticoagulants Associated nerve injury

Polytrauma with high base deficit, lactate levels, and

transfusion requirement

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 Pathophysiology
Compartment syndrome occurs when the pressure
within a closed osteo-fascial muscle compartment rises
above a critical level. This critical level is the tissue
pressure which collapses the capillary bed and prevents
low-pressure blood flow through the capillaries and
into the venous drainage. Normal tissue pressure is 0-
10 mm Hg. The capillary filling pressure is essentially
diastolic arterial pressure. When tissue pressure
approaches the diastolic pressure, capillary blood flow
ceases. A number of studies have shown that
if diastolic arterial pressure is not more than 30 mm
Hg above tissue pressure, compartmental capillary
blood flow is significantly obstructed and severe
hypoxia occurs in muscle and nerve tissue. 20
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 skeletal-muscle necrosis in ACS

Hazen and co reported Significant muscle necrosis associated

with an impending compartment syndrome occurs at a
threshold intracompartmental pressure of thirty millimeters of
mercury after eight hours. Fasciotomy is recommended when
intracompartmental pressure exceeds thirty millimeters of
mercury in a patient with normal blood pressure
Matava and colleagues reported similar findings, in that
increased tissue pressure for 8 hours was associated with a
higher percentage of cell death in animals with compartment
pressures that were within 20 mm Hg of the diastolic blood
pressure

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 In study evaluated DNA degradation in nuclei of
muscle cells during ischemia in a rabbit limb
amputation model. The results showed that the DNA
content in muscle cell nuclei was slightly decreased at
4 and 8 h of global ischemia. At 12 h after global
ischemia, the DNA content was found to be
significantly decreased

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 Classification
Type and Stage
Incipient compartment syndrome
Acute compartment syndrome
Early stage
Late stage
Volkmann's ischemic contracture
Chronic, recurrent compartment syndrome
Characteristics
Early period of limb edema, Intolerable pain can
be present, but tissue pressure measurements
may not be diagnostic
Excessive compartment pressure has occurred.
Ischemia, edema, and cell death cascade has
begun. Extensive muscle and nerve necrosis is
not yet present. Usually <8 hours from onset of
conditions that caused compartment syndrome.
Extensive muscle and nerve death has occurred.
Fibrous replacement of compartment contents or
limb loss is likely. Usually >8 hours from onset of
conditions that caused compartment syndrome.
End stage of compartment syndrome.
Characterized by muscle death and replacement
of compartment with fibrous tissue. Patients have
significant contractures and loss of function.
Condition occuring in athletes during exercise
(usually in lower extremity) characterized by
increased compartment pressurization during 26
exercise, loss of strength or sensation during
 CLINICAL FEATURES
The mechanism of injury is the first indication that a
patient may be at risk of developing compartment
syndrome
The signs and symptoms of acute compartment
syndrome generally appear in a stepwise fashion.
Compartment syndromes requires having and
maintaining a high index of suspicion, performing
serial examinations in patients at risk, and carefully
documenting changes over time.
(Acute compartment syndrome in lower extremity
musculoskeletal trauma.AU,Olson SA, Glasgow
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RR,SO, J Am Acad Orthop Surg. 2005)
 Diagnosis is primarily clinical, supplemented
by compartment pressure measurements.
Certain anesthetic techniques, such as nerve
blocks and other forms of regional and
epidural anesthesia, reportedly contribute to a
delay in diagnosis

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 CLINICAL ASSESSMENT
Symptoms
Pain
Pain is considered to be the first symptom
Pain has been shown to have a sensitivity of only 19%, a specificity of 97%
Pain is usual disproportionate to the pain expected from the initial injury
Persistent deep ache or burning pain
Pain is unrelenting and not improved by immobilisation or different
positions
Pain companion with a tense, swelling compartment, is increased with
passive stretch of muscles in the affected compartment (early finding)
Pain is not easily assessed in the sedated, intoxicated, or head injured
patient or in patients after regional anaesthesia, never injury
Pain may be absent in an established compartment syndrome
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 Paraesthesia
Paraesthesia are also a significant diagnostic sign and a
valuable indicator for fasciotomy.Neurological symptoms in
the early stages (onset within approximately 30 minutes to two
hours of ACS; suggests ischemic nerve dysfunction)
Paraesthesia and hypoesthesia may occur in the territory of the
nerves traversing the affected compartment
Include reduced vibratory sensations, increased two-point
discrimination, paraesthesia, numbness or tingling
Sensitivity of 13% and specificity of 98%

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 Paralysis
Paralysis of muscle groups affected by the acute compartment
syndrome is recogni
The difficulty of interpreting the underlying cause of the
weakness, which could be inhibition by pain, direct injury to
muscle, or associated nerve injuryzed as being a late sign.
Pulse
The pulse status has a restricted diagnostic value, since pulses
are usually palpable until the late stages of ACS, their absence
should raise suspicion for an Compartment Syndromes
underlying arterial injury
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Symptoms
Pain
Pain with passive range of motion
Pain out of proportion to injury
Numbness
Paresthesias
Weakness
Signs
Pallor
Altered perfusion

Diminished pulses or pulselessness

Altered capillary refill

Palpable fullness or tenseness of a compartment, the forgotten "P"

Altered sensibility

Increased threshold density (monofilament testing)

Increased innervation density (2-point discrimination)

Pain on passive muscle stretch

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Muscle weakness
 MEASUREMENT OF COMPARTMENT
PRESSURES

The normal pressure of a tissue compartment falls between 0

and 8 mmHg
Capillary blood flow becomes compromised when tissue
pressure increases to within 25 to 30 mmHg of mean arterial
pressure
Pain may develop as tissue pressures reach between 20 and 30
mmHg.
Ischemia occurs when tissue pressures approach diastolic
pressure

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 MEASUREMENT OF COMPARTMENT
PRESSURES
a threshold based upon the difference between
systemic blood pressures and compartment
pressures to confirm the presence of ACS.
ACS delta pressure
diastolic blood pressure measured compartment pressure
ACS delta pressure <20 to 30 mmHg indicates
need for fasciotomy ( use <30 mmHg)

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TABLE 27-4 Recommended Catheter
Placements for Compartmental
Pressure Monitoring

Anatomic Area Catheter Placement

Thigh Anterior compartment
Leg Anterior compartment
Deep posterior if clinically suspec
Foot Interosseous compartments
Consider calcaneal compartment i
hindfoot injuries

Forearm Flexor compartment

Hand Interosseous compartment
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 Three methods have been used most
frequently:
A simple needle manometer system
A handheld manometer (eg, Stryker device)
The wick or slit catheter technique

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Thank you 37