Jasreena Kaur Sandal
COMPARTMENT
SYNDROME
Definition
condition
characterised by raised
pressure within a closed space with a
potential to cause irreversible damage
to the contents of the closed
compartment
Acute compartment syndrome
Chronic exertional compartment
syndrome
Acute Compartment Syndrome
pressure within an osseofascial
compartment rises to a level that
decreases the perfusion gradient
across tissue capillary beds, leading
to cellular anoxia, muscle ischemia,
and death.
Chronic Exertional Compartment
Syndrome
is an exercise-induced
neuromuscular condition that causes
pain, swelling and sometimes even
disability in affected muscles of the
legs or arms
can occur in both beginning and
seasoned athletes in sports that
involve repetitive movement
Where does it occur?
Lower Extremity
Gluteal
Thigh
Lower Leg
Foot
Upper Extremity
Deltoid
Arm
Forearm
Hand
Muscle
compartments of the
forearm.
The forearm consists of three major
compartments: the volar, dorsal, and
mobile wads.
Compartments
of the leg
Etiology
Conditions
that
1. Reduces the volume of a
compartment
2. Increases the content of the
compartment
Reduce the Volume
Cast or Splint
Circumferential constricting dressing
Closure of fascia
Military antishock trousers (MAST)
3rd degree Burns (circumferential)
Malfunctioning sequential
compression devices (SCDs)
Tight ski boots
Increase the Content
Fractures, direct tissue trauma
Hemorrhage: vascular injury, coagulopathy, anti-coagulation
Increased capillary permeability after burns
Infusion or injection (infiltrated line)
Reperfusion after period of ischemia
Gunshot wound to thigh
Drug/alcohol abuse and coma
Compartment fluid injection
Crush injuries
Gastronomies or peroneus muscle tear
Androgen abuse/muscle hypertrophy
Ruptured Baker cyst
High risk Injuries causing
compartment syndrome
Fractures of elbow (supracondylar
fractures)
Fractures of forearm bones
Fractures of proximal third of tibia
Multiple fractures of the foot and
hand
Crush injuries
Burns
Pathophysiology
Pathophysiology
Compartment Pressures Rise
Venous obstruction occurs, causing further pressure
escalation
Low intramuscular arteriolar pressure is exceeded
MUSCLE AND NERVE ISCHEMIA
14
Decreased tissue perfusion
tissue death
Muscle
reversible damage after 4 hours; irreversible after
8 hours
Nerve damage irreversible after 8 hours
Episodes
of hypotension will therefore increase the extent
of irreversible muscle damage
In tissue damaged by injury, resistance to ischemia is
decreased. A pressure of 20mm Hg below diastolic shown to
cause ischemia
15
Ischaemic fibrotic contracture
Areas of muscle infarction
Hypovolumia +
myoglobulinaemia
Hyperkalamia
Rabdomyolysis
Hypovolumia
Hyperkalamia
Increase uric acid
Metabolic acidosis
Acute renal
failure
Cardiac arrest
16
Clinical Manisfestations
6 Ps of compartment syndrome
Parasthesi
a
Pulselessn
ess
Pain
Paralysis
Pressure
Pallor
1.Paresthesia
Subtle first symptom Compartment
Syndrome
Best elicited by direct stimulation
Complaints of tingling or burning
sensations
Loss of 2 point discrimination
Can lead to numbness
2. Pain
Out of proportion to the injury
Elicited by passive stretching of the involved
compartment
Described as throbbing or deep localized or diffuse
Increases with the elevation of the extremity
Unrelieved by narcotics
May not be present if central or peripheral sensory
deficits are also present
Pain will diminish after pressure-induced ischemia
affects the conductivity of the nerves in the
compartment.
3. Pressure
Involved compartment or limb will feel tense and warm on
palpation
Skin is tight and shiny
Skin may appear cellulitic
Direct compartment pressure of 30-40 mmHg as measured
by a wick, continuous infusion, or injection method such as
the Stryker monitor normal intracompartmental tissue
pressure is
0-10 mmHg.
Differential pressure of greater than 30 mmHg diastolic
blood pressure minus compartment pressure as long as
diastolic pressure remains high enough or at least 30 mmHg,
the compartment will be perfuse
4. Pallor
Late sign
Pale, grayish or whitish tone to skin
Prolonged capillary refill (>3
seconds)
Cool feel to skin upon palpation due
to lack of capillary perfusion
5. Paralysis
Late sign
May start as weakness in active
movement of involved or distal joints
Leads to inability to move joint or
digits actively
No response to direct neural
stimulation due to damage
6. Pulselessness
Late sign
Very weak or lack of palpable or
Doppler audible pulse
Due to lack of arterial perfusion
Other warning signs :
Fractured blisters: represent areas of necrosis of the
epidermis and separation of the skin layers-body
attempts to relieve the pressure in the
compartment.
elevated
temperature due to ischemia/necrosis of
tissue and possible infectious response.
stretch
pain or pain on passive extension or
hyperextension of digits (toes or fingers, depending
on the site)
Investigation
Tissue
Pressure Measurement
Lab Studies
Hematology/chemistry laboratory studies Serum
myoglobin and CK measurements should be obtained
to determine the degree of muscle necrosis.
Serial CK levels may show increases indicative of
a developing CS.
High CK levels should alert to possible
rhabdomyolysis.
Complete blood cell count (CBC) and coagulation studies
elevated WBC (white blood cell count) and ESR
(erythrocyte sedimentation rate) levels -severe
inflammatory response
elevated
Serum Potassium due to cell damage
lowered
Serum pH levels due to acidosis
anemia
worsens muscle ischemia
look
for disseminated intravascular coagulation (DIC),
which is rare.
Imaging Studies
Plain
radiographs of the affected extremity are used to determine
fracture pattern, soft-tissue injury, and radiographic clues that may
indicate occult fractures.
MRIs
may show increased signal intensity in an entire compartment
on T2-weighted, spin-echo sequences.
Computed
tomography (CT) scanning is especially useful if pelvic or
thigh CS is in the differential diagnosis.
Lower
extremity venous Doppler or arterial ultrasonography (US) is
performed as needed to address possible DVT or arterial occlusion.
Management
Medical Theraphy
Place
the affected limb(s) at the level of the heart.
Elevation
is contraindicated because it decreases arterial blood
flow and narrows the arteriovenous pressure gradient and thus
worsens the ischemia.
Remove
cast, bandages and any dressing.
Correct
hypo perfusion with crystalloid solution and blood
products.
Mannitol
may reduce compartment pressures and lessen
reperfusion injury
Surgical Theraphy
emergency fasciotomy
-should be done in less than 6 hours and no
later than 12 hours after onset
-usually left open protected by suitable sterile
dressings
-Inspection of the wound after 48 hours may
necessitate further necrotic tissue excision.
-delayed skin closure or skin grafting may
become treatment options
subsequent orthopedic reductionor fracture
stabilization and vascular repair
Prognosis
Depends upon the timeliness of diagnosis and treatment
Dependent upon etiology and age of patient
If recognized and treated before my necrosis, >90% recover
function
May have some loss of muscle power due to the fasciotomy
