Clinical evaluation and management

1. SUBJECT SEMINAR ON
“COMPARTMENT SYNDROME
AND VIC”
Moderator :
Dr GAURAV M
Asst proffesor ( Dept of orthopedics )
Presenter :
Dr NAGESH SHERIKAR
postgraduate ( Dept of orthopedics )
BANGALORE MEDICAL COLLEGE

2. OUTLINE - COMPARTMENT SYNDROME
 Definition
 Epidemiology
 Classification
 History
 Relevant anatomy
 Pathophysiology
 Etiology
 Clinical evaluation- History and examination
 Management- resuscitation , investigations, definitive treatment
 Complications
 Prognosis
 Prevention

3. A closed area of muscle groups, nerves and blood
vessels sorrounded by fascia
Muscles are arranged in different compartments and
sorrounded by one fascia , this arrangement is called
osteofascial compartment
Normal pressure : 5-15 mmhg
Intracompartmental pressure raises to 35-40 mmhg
WHAT IS COMPARTMENT ??

4. Acute compartment syndrome is defined as an elevation
in osteofascial compartment pressure to a level and for a
duration that without decompression will cause tissue
ischemia and necrosis.
 Volkmann ischemic contracture is a sequeal of
untreated or inadequately treated compartment syndrome
in which necrotic muscle and nerve tissue have been
replaced with fibrous tissue.
DEFINITION

5.  Is the elevation of intracompartmental pressure during exercise, causing
ischemia, pain, and rarely neurologic symptoms and signs
 It is characterized by resolution of symptoms with rest but may proceed to
acute compartment syndrome if exercise continues.
CHRONIC EXERTIONAL COMPARTMENT SYNDROME (CECS)

6. 1881: Richard von Volkmann - contracted state believed
due to ischemic muscle
1884- Lesser developed clinical model
1888- Peterson felt due to nerve compromise
1906- Hildebrand coined ' volkmans ischemic contracture '
1914- Murphy recommended FASCIOTOMY to prevent
contracture
1940- Griffiths 4p's
1967- Whiteside stressed 4 compartment FASCIOTOMY
HISTORY

7. Incidence- 3.1/ 100,000
Mean age was 32 years ; males - 30 years
Females - 44 years
M>F( 10 times )
Younger > older patients
Open = closed #
LEG IS THE COMMONEST SITE.
TIBIAL FRACTURE IS COMMONEST CAUSE AND ANTERIOR COMPARTMENT IS
MOST FREQUENTLY INVOLVED
FOREARM IS 2ND COMMONEST SITE, SUPRACONDYLAR FRACTURE IS THE
COMMONEST CAUSE WITH FLEXOR COMPARTMENT MOST FREQUENTLY
INVOLVED
EPIDEMIOLOGY

8. I. Acute compartment syndrome (ACS)
medical emergency
caused by a severe injury
can lead to permanent muscle damage.
II. Chronic compartment syndrome (CCS)
 known as exertional compartment syndrome
not a medical emergency
most often caused by athletic exertion.
Types of Compartment syndrome:

10. CAUSES

11. VISCIOUS CYCLE

12. PATHOGENESIS

13. A. BLEEDING
 FRACTURES
The most common reason for abnormally
increased tissue pressure.
In adults - closed and open tibial shaft
fracture , distal radial fracture
In children -radial head or neck fracture ,
supracondylar fracture
1. INCREASED IN VOLUME OF COMPARTMENT CONTENTS

14. SOFT TISSUE TRAUMA ( muscle rupture) rugby players , forestry
workers
SURGERY
Following surgical treatment by the knee arthroscopy , Hauser
operation, proximal tibia osteotomy without drainage and
intramedullary nailing of the tibia
Postoperative hematoma

15. B. EDEMA
 Venous stasis
Capillary leak syndrome
Exercise -Exercise-induced edema by marching and mountain
climbing may be another reason
Inflammation

16. A. EXTERNAL COMPRESSION
 All induce a postischemic
reperfusion injury to the
capillary bed. Tissue hypoxia
induces dysfunction of the
endothelial cells of the capillary
bed, which may leak plasma and
water into the interstitial space.
2.PROLONGED ISCHEMIA

17. External compression by tight
bandages such as orthoses, plaster
cast, or elastic stockings increases
intramuscular pressure.
A tight plaster cast decreases the
compliance of compartment tissues. A
normal swelling of a limb may
therefore create pathologically
increased intramuscular pressure

18. B. ARTERIAL OCCLUSION
if exceeds 6 hours of complete
ischemia, the endothelial
cells most likely will be damaged
and leak plasma into the interstitial
space
C. LIMB ELEVATION
Patients with arteriosclerosis and
diabetes --- increased risks for
insufficient blood perfusion and
development of ischemia.

19. A.FASCIAL DEFECT
B. BURN INJURY
◼ The constrictive effects of circumferential burns may cause acute compartment
syndromes which may be relieved by long, linear incisions through the skin along
the axis of the extremity.
3. DECREASED SIZE OF THE COMPARTMENT

20. Prolonged anesthesia
Viper bite
Infections
intraosseous infusion
coagulopathy ( hemophilia, sickle cell anemia)
Conditions causing rhabdomyolysis
Drug overdose
OTHER CAUSES

21. 1. Arteriovenous Gradient Theory : Rowland
The increase in local tissue pressure reduce the local arteriovenous
pressure gradient and thus reduce blood flow . When flow diminishes to less
than the metabolic demands of the tissue ( not necessarily to zero ) , then
functional abnormalities result
The relationship between AV gradient and local blood flow ( LBF) is
summarised as
LBF = PA-PV ×R
THEORIES

22.  The ultimate result of reduced blood flow to skeletal muscle is
Ischemia followed by necrosis , with increasing periods of complete
Ischemia produce increasing irreversible change .
The duration of muscle Ischemia dictates the amount of necrosis
Examples
EFFECT OF RAISED TISSUE PRESSURE ON MUSCLE

23. There is little dispute about the effects of raised tissue pressure on
neurologic function.
EFFECTS ON NERVE
EFFECTS ON BONE
Non union

24. Muscle
– 3-4 hours - reversible changes
– 6 hours - variable damage
– 8 hours - irreversible changes
Nerve
– 2 hours - looses nerve conduction
– 4 hours - neuropraxia
– 8 hours - irreversible changes
TISSUE SURVIVAL

25. CLINICAL PRESENTATION
Pain out of proportion
Pallor
Paresthesia/hypoesthesia
Paralysis
Pulselessness
These are signs of an ESTABLISHED
compartment syndrome where ischemic
injury has already taken place
5P's

26.  Earliest symptom
 Classically out of portion to injury
 Severe pain with passive stretch
 Pain that is not responsive to the normal dosage of pain
medication
 sensitivity -19% ,
 specificity of 97% (i.e., a high proportion of false-
negative or missed cases but a low proportion of false-
positive cases)
PAIN

28. PARESTHESIA
First sign of nerve Ischemia
Followed by hypoesthesia, anesthesia , paresis , paralysis
Peripheral nerve tissue is more sensitive than muscle to ischemia
Permanent damage may occur in 75 minutes
sensitivity -13%
specificity - 98%

29. PARALYSIS
Very late finding
Irreversible nerve and muscle damage present
it is recognized that if a motor deficit develops, full recovery
is rare

30.  Rarely present
 Indicates direct damage to vessels rather than compartment syndrome
PALLOR AND PULSELESSNESS
(presence of a pulse does not exclude the diagnosis)

31. • Compartment pressure - objective
parameters
• Lab tests : Pulse CPK, Urine myoglobin
• Pulse oximetry :
• Is helpful in identifying limb hypoperfusion
• Is not sensitive enough to exclude
compartment syndrome.

32. • Cellulitis
• DVT
• Gas gangrene
• Peripheral nerve injury
• Muscle rupture
• Necrotizing fasciitis
DIFFERENTIAL DIAGNOSIS

33. Raised tissue pressure is primary event in compartment syndrome
and changes in ICP precede the clinical signs and symptoms.
 When to monitor ?
Where to monitor ?
Threshold for diagnosis of Compartment syndrome and
fasciotomy ?
PRESSURE MONITORING

34. Suspected compartment syndrome
 Equivocal or unreliable examination findings
Unconscious patient with tight compartments
 Vascular injury
Regional anesthesia
WHEN ??????

35. INDICATIONS :
◼High risk
TECHNIQUE : performed each compartments at close to the
fracture site as possible ( highest pressure ) or maximal swelling
area

38. 1.Needle manometer method/ WHITESIDES saline infusion technique
Performed by using a needle introduced into the compartment and connected to a column filled
partly with saline and partly with air .To this column a syringe filled with air is attached , as is a
pressure manometer or transducer .
Advantage -simple and inexpensive
Disadvantage –
1.Not suitable for continuous monitoring
2. Required injection of saline into the compartment and in this way could aggravate impending
syndrome
3. Least accurate
4. Needle with only one perforation at its tip also can become easily blocked.
METHODS

40. 2. The wick catheter-Mubarak et al
 modification of the needle technique, in which fibrils protrude from the bore of
the catheter assembly. This allows a large surface area for measurement and
prevents obstruction of the needle
Advantage - Ideal for continuous measurement
 Disadvantage –
1. Blood clot blocking the tip or air in the column of fluid between the catheter and
the transducer, which will dampen the response and give falsely low readings.
2. retention of wick material in the tissues.

41. 3. slit catheter- Rorabeck et al.
same principle as the wick catheter in that it is
designed to increase the surface area at the tip of
the catheter by means of being cut axially at the
end of the catheter.The interstitial pressure is
measured through a column of saline attached to
a transducer .
The slit catheter is more accurate than the
continuous infusion method
as accurate as the wick catheter

43. 4. solid state transducer intracompartmental catheter (STIC)

47. THRESHOLD FOR DECOMPRESSIVE FASCIOTOMY
Mubarak -- Fasciotomy when >30-40mmHg
Matsen -- >45 mmHg developed ACS
Whitesides -- Fasciotomy when within 20mmHg of DBP
McQueen -- Fasciotomy when within 30mmHg of DBP
Heppenstall – within 40mmHg MAP

48. Also known as exertional CS, recurrent CS and subacute CS
 Exercise –induced pain
Bilateral in 80-95% of patients
Occur mainly in the lower limb
 Incidence is equal among male nd female young athletes
Typical patient is young (20-30s) athlete
Pathophysiology of CCS
Probably occurs from increased muscle relaxation pressure during exercise ,
which causes decreased muscle blood flow, leading to ischemic pain and
impaired muscle function
CHRONIC COMPARTMENT SYNDROME

49. ◼Exercise can increase muscle volume by 20% , causing an increase in
pressure in a noncompliant Compartment

52. One or more among the following:
1.Pre-exercise pressure >=15mmHg
2.Post-exercise pressure at 1 minute >=30 mmHg
3. Post exercise pressure at 5 min >= 20mmHg
DIAGNOSIS

53. Conservative-
◼ Cessation of causative activity
◼ Rest.
◼ Ice
◼ Physical therapy
◼ FASCIOTOMY IS THE ONLY PROVEN SUCCESSFUL TREATMENT
MANAGEMENT

54. DIFFERENTIAL DIAGNOSIS

56.  COMPLETELY remove the cast , bandages and dressings
 The limb should be NURSED FLAT
 (DO NOT ELEVATE as elevation reduces the arterial inflow and the arterio-venous
pressure gradient on which perfusion depends )
 Ensure patient is normotensive as hypotension reduces perfusion pressure and
fascilitates further tissue injury
 Oxygen administration
 Correct hypoperfusion with iv fluids and blood products
EMERGENCY TREATMENT

57.  Fasciotomy - prophylactic release of
pressure before permanent damage occurs.
Will not reverse injury from trauma.
 Fracture care – stabilization with
– Ex-fix
– IM Nail
SURGICAL TREATMENT

58.  Unequivocal clinical findings
 Pressure within 15-20 mm hg of DBP
 Rising tissue pressure
 Significant tissue injury or high risk pt
 > 6 hours of total limb ischemia
 Injury at high risk of compartment syndrome
FASCIOTOMY INDICATIONS

59.  Make early diagnosis
 Full and adequate decompression
 Long extensile incisions
 Release all fascial compartments
 Any muscle necrosis must be thoroughly
debrided to avoid infection
 Preserve neurovascular structures
 Coverage within 7-10 days
 No scope for limited or subcutaneous
fasciotomy
FASCIOTOMY PRINCIPLES

60. Within 6 hours - Almost complete recovery
Within 12 hours ~ 60-70% normal limb function
More than 12 hours ~ 8% normal limb function
TIMING OF FASCIOTOMY

61. LEG

63. APPROACHES
1. Single incision fasciotomy with or without fibulectomy
2. Double incision fasciotomy

65. SINGLE INCISION FASCIOTOMY

67. DOUBLE INCISION FASCIOTOMY
Mubarak and Hargens

68. FOREARM

70. Both volar and dorsal fasciotomies may be performed. In most cases the volar compartment is
approached first through an incision extending from the biceps tendon at the elbow to the palm
of the hand to allow carpal tunnel decompression that is usually necessary .
Fascial incision then allows direct access to the compartment . The deep flexors must be carefully
inspected after fascial incision. Separate exposure and decompression of pronator quadratus may
be necessary.
Usually volar fasciotomy is suff icient to decompress the forearm but if ICP remains elevated in
the dorsal compartment perioperatively, then dorsal compression is easily performed through a
straight dorsal incision .

71. FOREARM FASCIOTOMY

74. ARMS

75. ARM COMPARTMENT

76. Is performed through
anterior and posterior
incisions when the
compartments are easily
visualized.
On rare occasions the
deltoid muscle should also
be decompressed
FASCIOTOMY

77. HAND

79. HAND FASCIOTOMY
 Two Dorsal incisions along 2nd and
4th MC
 Can reach the adductor
compartment via 2nd MC incision

81.  Both thigh compartments
can be approached
through a single lateral
skin incision
 Medial incision can be
used over the adductors if
considered necessary
THIGH

84. FOOT

86.  Traditionally five compartments (lateral, medial, central, interosseous,
and calcaneal)
 Dorsal incisions overlying the second and fourth metacarpals allow
sufficient access to the interosseous compartments and the central
compartment that lies deep to the interosseous compartments .
 The medial and lateral compartments can be accessed around the deep
surfaces of the first and fifth metatarsal, respectively
FOOT FASCIOTOMY

93. Fasciotomy incisions must never be closed primarily because this
may result in persistent elevation of ICP.
 The wounds should be left open and dressed, and approximately 48
hours after fasciotomy a “second look” procedure should be
undertaken to ensure viability of all muscle groups.
Skin closure or cover should not be attempted unless all muscle
groups are viable.
WOUND MANAGEMENT

94. FIRST STEP :
1. VAC - reduces swelling , promotes tissue granulation and increased perfusion
2.. Wet to dry dressings - will remove wound drainage and dead tissues
SECOND STEP : ( wound closure techniques) 2 days after surgery
1. Delayed primary closure
2. Split thickness skin grafting- High long term morbidity
3. Continous traction
4. Acell- creates new layer of skin in fasciotomy wound

96. • Altered sensation within the margins of the wound (77%)
• Dry, scaly skin (40%)
• Pruritus (33%)
• Discolored wounds (30%)
• Swollen limbs (25%)
• Tethered scars (26%)
• Recurrent ulceration (13%)
• Muscle herniation (13%)
• Pain related to the wound (10%)
• Tethered tendons (7%)
FASCIOTOMY- COMPLICATIONS

97. Delay to fasciotomy of more than 6 hours is likely to cause significant
sequelae
 Volkmann’s contracture
 Weak dorsiflexors
 Claw toes
 Sensory loss
 Chronic pain
 Amputation
LATE SEQUELE

98. TIME LAPSE BETWEEN INJURY & INTERVENTION –
FASCIOTOMY WITHIN 6HRS : ≈100% FULL RECOVERY
WITHIN 12HRS : 68%
BEYOND 12HRS : 8%
PROGNOSIS

99. Minimize the external application of pressure
Not closing Fascial defects
Minimizing tissue Ischemia
Performing prophylactic fasciotomy protecting soft tissue
Avoiding excessive limb elevation above the level of the heart
PREVENTION

100. VIC

101. Definition
History
Casuses
Pathogenesis
Classification
Clinical features
Measurement of ICP
Deformities
Investigations
Treatment
VOLKMANNS ISCHEMIC CONTRACTURE

102.  COMMON ETIOLOGY:
1. Neglected compartment syndrome
2.Fractures
3.Crush syndrome
4. Bleeding disorder

103.  VIC is the end result of prolonged ischemia of muscles and nerves in an extremity.
Primary target – Muscle
Secondary target- Nerve
Muscle undergoes necrosis, fibrosis and contracture
Nerve injury causes further muscle dysfunction, sensory deficit or chronic pain.
PATHOGENESIS

106.  Elbow flexion
Forearm pronation
 Wrist flexion
MCPJ extension
 IPJ flexion
 Thumb flexion & adduction
 Median & ulnar nerve neuropathy
DEFORMITY IN UPPER EXTREMITY

107. INTRINSIC MUSCLE CONTRACTURES
 Intrinsic plus deformity
Flexion (MCPJ) + Extension (PIPJ)
VOLKMANN'S CONTRACTURE
 Intrinsic minus deformity
Hyperextension (MCPJ) + Flexion (PIPJ)
◼ Although the two entities resultant clawmay occur simultaneously, the hand
deformity is determined by the more powerful extrinsic finger contracture flexors

108. 1. SEDDONS CLASSIFICATION
Grade I: Ischaemia
 Grade II: Ischaemic contracture
 Grade III: Ischaemic contracture with nerve involvement
2. ZANCOLLI ( upon the structures involved) :
Type I: Contracture involving forearm muscles with normal intrinsic muscles
Type II: Contracture involving forearm muscles with paralysis of intrinsic muscles
Type III: Contracture involving forearm muscles with contracture of the intrinsic
muscles
Type IV: Combined type
CLASSIFICATION

109. 3. HOLDENS CLASSIFICATION ( Based on etiology) ;
 Type 1- proximal arterial injury as in supracondylar fracture more extensive
Ischemia
Type 2 - Direct injury as in crush injury of the forearm
4. TSUGES (presentation );
mild( involving FDP)
moderate( FDP, FDS, FPL,FACT,FCU)
 severe ( both flexors and extensors)

110. 1. MILD (LOCALIZED)
 Limited to extrinsic finger flexors
 Usually 2 or 3 fingers
Hand sensibility & strength are normal
Intrinsic muscles not involved
 Fixed joint contracture not present
 Usually occur in young adults
 Most are caused by fractures or crush injury
No paralysis of the extrinsic or intrinsic muscles and no fixed joint contractures.

111. MODERATE
 Classic type
 Primarily affects FDP & FPL
Occasionally FDS, FCR & FCU
Wrist & thumb are flexed
Wrist is held in a flexed position and the fingers show an intrinsic minus deformity
Claw hand deformity
 Secondary nerve compression
 median > ulnar nerve
The muscle degeneration is moderate , leaving enough intact contractile elements for active
flexion even in the deep flexer compartment , a muscle slide technique is performed with release

112. SEVERE
Affect forearm extensors & flexors
Commonly due to brachial artery damage
Median nerve is always involved with the ulnar nerve also severely involved
Forearm muscle mass has a firm"Woody consistency"
Often encountered:
 Loss of nerve function
 Malunion or nonunion
 Cutaneous scarring
 Contractures

113. Plain radiograph
Angiography
MRI
Direct nerve stimulation
INVESTIGATIONS

114. ROBERT JONES METHOD :
Wooden tongue depressors were
used to correct established
deformities gradually from distal to
proximal
BANJO SPLINT:
Permits the fingers to be exercised
at all times and is most efficient
CONSERVATIVE MANAGEMENT

115. MILD (EARLY)
 Normal hand sensibility & strength: conservative
 Dynamic splintage
At night - extension splints
Satisfactory outcome with early treatment
MILD (LATE)
Excision of infarcted muscle
Lengthening the tendon
Principles of management

116. MODERATE
Max pages muscle sliding operation : This consists of releasing the common
flexor origin from the medial epiconyle and passively stretching the fingers . This
slides the origin of the muscle down and releases the contractures
Other muscle sliding operation –
1. Inglis and Cooper
2. Williams and haddad
Neurolysis : It consists of freeing the peripheral nerves from the surrounding
fibrous tissue
Tendon transfers

117. RELEASE OF SECONDARY NERVE COMPRESSION
 Signs of gradual recovery: 12month period
MEDIAN NERVE CAN BE CONSTRICTED IN
Lacertus fibrosus
 2 heads of Pronator teres
Proximal arch of FDS
Carpal tunnel

118. ULNAR NERVE COMPRESSION
 Incidence much lower
 Btw ulnar & humeral heads of FCU
RADIAL NERVE COMPRESSION
Rarely involved
Under tendinous origin of supinator
(arcade of Frohse)

119. Treatment of Contractures be performed at the time of, or subsequent to, nerve
decompression
1. INFARCT EXCISION
6 months of splinting before surgery (Seddon)
Resection of all muscles reduced to solid scar
Postop immobilization (supination & extension)
2. FLEXOR TENDON LENGTHENING OR EXCISION
Z lengthening of FDP, FDS, FPL, PT ( Goldner)
Disadvantage: weakness

120. 3) TENDON TRANSFERS
Usually delayed till after nerve recovery
 After maximal contracture correction
A. PHALEN & MILLER (1947)
Digital flexion & thumb opposition
ECRL → FDP, ECU → thumb opposition, EPB → ECUs

121. SEVERE TYPE
•Excision of the scar
•Proximal or distal row carpectomy
•Arthrodesis of the wrist in functional position
•Amputation for very severe cases of VIC with gangrene

122. • COMPARTMENT SYNDROME HAS DISASTROUS CONSEQUENCES IF PERMITTED TO
RUN ITS COURSE.
• TRUE ORTHOPEDIC EMERGENCY
• Early FASCIOTOMY has better outcome
• Reliable, safe, and effective
• The only treatment for compartment syndrome, when performed in time
SUMMARY

123.  Cambells orthopedics
 Rockwood and Green's Fractures in Adults
 Compartment syndrome by Jorma Styf
 Wheeless textbook of orthopedics
 McRaes orthopedics and trauma
 Fasciotomy in the treatment of the acute compartment syndrome. J Bone Joint Surg
Am. 1976 Jan;58(1):112-5
REFERENCES

124. 1. Compartment pressure and it's relevance in the management of Compartment syndrome (MAY
'07)
2. Describe the anatomy of Compartments of the leg. Describe the methods of measuring the
Compartment pressure .Add a note on treatment of compartment syndrome (NOV '12)
3. Describe the anatomy of compartments of the leg .How will you diagnose and manage a case of
compartment syndrome of the leg (MAY '09)
4. Compartment syndrome (NOV '12) , (APRIL' 08)
5. Discuss the management of a patient with communited fracture of tibia plateau with
Compartment syndrome (MAY ' 14)
6. Discuss the pathophysiology of volkmans ischemic contracture. Discuss the clinical features and
principles of management of impending volkmans ischemia involving forearm ( SEP '07)
7. Volkamns ischemic contracture (MAY '07)
QUESTIONS ASKED

125. THANK YOU