3. Histor
yVolkmann 1881
Richard vonVolkmann published
an article in which he attempted to
describe the condition of
irreversible contractures of the
flexor muscles of the hand to
ischemic processes occurring in
the forearm
Application of restrictive
dressing to aninjured limb
4. Histor
yHildebrand 1906
First used the term Volkmann
ischemic contracture to describe
the final result of any untreated
compartment syndrome.
First to suggest that elevated tissue
pressure maybe related to ischemic
contracture.
5. Histor
yThomas 1909
Reviewed the 112 published cases of
Volkmann ischemic contracture and found
fractures to be the predominant cause.
Also, noted that tight bandages, an arterial
embolus, orarterial insufficiency could also
lead to the problem
6. Histor
yMurphy 1914
First to suggest that fasciotomy might
prevent thecontracture.
Also, suggested that tissue pressure and
fasciotomy wererelated to the development of
contracture
7. Histor
yEllis 1958
Reported a 2% incidence of compartment
syndrome withtibia fractures, and increased
attention was paid to contractures involving the
lower extremities
8. Histor
ySeddon, Kelly, and Whitesides 1967
Demonstrated the existence of 4
compartments in the leg and to the need to
decompress more than just the anterior
compartment. Since then, compartment
syndrome has been shown to affect many
areas of the body, including the hand, foot,
thigh, and buttocks
9. Types of compartment
syndrome
9
Compartment syndromes can be classified
as :
Acute compartment syndrome (ACS)
Chronic compartment syndrome (CCS)
depending on the cause of increased intra-
compartmental pressure and the duration
of symptoms
10. Sites of Acute Compartment
Syndrome
10
Acute compartment syndrome can develop
anywhere a skeletal muscle is surrounded by
a substantial fascia.
ACS may occur in foot, leg, thigh,
buttocks, lumbar paraspinous muscles,
hand, forearm, arm and shoulder.
11. Compartment
sFoot 9
Leg 4 (anterior,lateral, sup & deep
posterior )
Hand 4
Thigh 3 (anterior, posterior, medial )
Forearm 4 (sup &deep volar,dorsal,
mobile wad ofHenry)
16. Pathophysiology of
ACS
C S develops after prolonged elevated intra-
compartmental pressure , which results from
either externally applied or internally expanding
pressure forces.
Increased tissue pressure will decrease
capillary blood flow leading to local tissue
necrosis caused by O2 deprivation .
Local blood flow (LBF) =Pa-Pv/R.
17. Pathophysiology of
ACS
17
The elevated intra-compartmental pressure
increasesthelocal venous pressure leading to
narrowed arteriovenous perfusion gradient
and compartment tamponade, resulting -if
uncontrolled - in nerve injury and muscle
ischemia
18. Etiology of
ACS
External Restriction of
Compartment Size :
- casts
- tight dressings
- splints
- lying on limb for long period
- burn eschar
- closure of fascial defect
- lithotomy position
19. Etiology of
ACS
19
• Factures (the most common are) :
In adults --- closed and open tibial shaft
fracture , distal radial fracture
In children --- radial head or neck
fracture , supracondylar fracture ,
forearm fractures
20. Etiology of
ACS
20
Hemorrhage (e.g. due to vascular injury )
Coagulopathy (e.g. hemophilia , thrombolytics ,
sickle celldisease or trait )
Muscle edema (e.g. severe exercise , crush
injury, trauma with or without fx )
21. Etiology of
ACS
Surgically related(e.g. knee arthroscopy ,
tibial osteotomy without drainage , after
epidural anesthesia )
Massive crystalloid infusion
Ruptured Backer’s cyst
Muscle hypertrophy ( androgens )
22. Etiology of
ACSIntracompartmental fluid infusion
(interosseosus infusion)
Capillary leak syndrome
Intra-arterial injections of sclerosing
agents
Post –ischemicreperfusion
24. Compartment
SyndromePathophysiology
Normal tissue pressure
0-4 mm Hg
8-10 withexertion
Absolute pressure theory
3 0 mm Hg - Mubarak
4 5 mm Hg - Matsen
Pressure gradient theory
< 20 mm Hg of diastolic
pressure –Whitesides
McQueen, et al
26. Pai
nClassically out of portion to injury
Exaggerated with passive stretch of
the involved muscles in compartment
Earliest symptom
27. Paresthesi
aAlso earlysign
Peripheral nerve tissue is more
sensitive thanmuscle to ischemia
Permanent damage may occur in
75 minutes
Difficult to interpret
Will progress to anesthesia if
pressure notrelieved
33. Management of
ACS
33
Removal of the possible cause (release of
tight dressings or circular constrictive
bandages, splitting of casts)
Correction of
coagulopathy
Positioning of the limb at the level of
the heart
34. Management of
ACS
34
I f symptoms don’t resolve in 30 to 60
min after appropriate treatment
,pressure measurement should be
repeated,and,if equivocal, fasciotomy is
indicated
35.
36. Management of
ACS
The definitive treatment of acute compartment
syndrome is FASCIOTOMY
Procedure is done without a tourniquet,each
potentially limiting envelope is opened over the
entire length of the compartment, all muscle
groups should be soft to palpation at the end
of the procedure
Muscle debridement should be kept to a
37. FACIOTOMY OF LOWER
LIMB FOR THIGH
Make a lateral incision
distal to intertrochantric
line extending to the
lateral epicondyle.
Expose the iliotibial band & make aa
straight incision in line with skin incision
Reflect the vastus lateralis off the
intermuscular septum
41. Chronic Compartment
SyndromeAlso known as exertional CS, recurrent CS and
subacuteCS
Exercise –induced pain
Occur mainly in the lower limb
Typical patient is young (20-30s) athlete
(long distance runner)or military recruits
pushed past normal limits of functional
42. Pathophysiology of
CCS
42
Not yet fullyunderstood
Probably occurs from increased muscle
relaxation pressure during exercise ,
which causes decreased muscle blood
flow, leading to ischemic pain and
impaired muscle function
