Management of compartment syndromes involving the limbs

1. COMPARTMENT
SYNDROME IN THE
LIMBS
BY
DR. LAWAL GBENGA
REGISTRAR, SURGERY DEPT.
NATIONAL HOSPITAL ABUJA
SUPERVISOR: DR. OPADELE
21/01/16

2. OUTLINE
 INTRODUCTION
 EPIDEMIOLOGY
 RELEVANT ANATOMY
 AETIOLOGY
 PATHOPHYSIOLOGY
 MANAGEMENT
 COMPLICATIONS
 PREVENTION
 PROGNOSIS
 CONCLUSION

3. INTRODUCTION
Definition: Compartment Syndrome is defined as a clinical
condition in which increased pressure within a limited space
(osseofascial compartment) compromises the circulation and
function of the tissues within that space.
Types
depending on the cause of increased intra compartmental
pressure and the duration of symptoms
Classified as :
 Acute compartment syndrome (ACS)
 Chronic compartment syndrome (CCS)

4. Acute compartment syndrome (ACS)
 A surgical emergency which if not recognized and treated
early can lead to devastating disabilities, amputation and even
death in some situations.
 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.
 Commonest sites are the leg and forearm

5. HISTORICAL PERSPECTIVE
Richard Von Volkmann, 1881
“For many years I have noted on occasion, following the use of
bandages too tightly applied, the occurrence of paralysis and
contraction of the limb, NOT … due to the paralysis of the nerve by
pressure, but as a quick and massive disintegration of the contractile
substance and the effect of the ensuing reaction and degeneration.”

6.  1881: Richard von Volkmann documented nerve injury &
subsequent contracture severe limb injuries
 Peterson in 1888 recognized that ischaemic contracture
could occur in the absence of bandaging
 50yrs later, Jepson described ischaemic contractures in
dog hind leg following experimentally induced venous
obstruction.
• 1941: Bywaters & Beall reported on the significance of
crush injury while working with victims of the London
Blitz.

7. • By 2nd world war ,ARTERIAL INJURY THEORY was proposed
(ischaemia is due to injury and spasm)
• Seddon in 1966 challenged it after finding palpable pulses in
up to 50% of cases
• McQuillan & Nolan described a vicious circle of increasing
tension in an enclosed compartment causing venous
obstruction and subsequent arterial
• They concluded that delay fasciotomy is the single most
important cause of treatment failure
• In the 1970s Matson as well as Owen et al, established the
importance of measuring intra compartmental pressure with
the aid of the Wick catheter.

8. EPIDEMIOLOGY
 Commoner in younger patients (M:F ratio is 10:1) under 35
years of age
 Sites: Leg>Forearm>Thigh>Arm>Abd>Buttocks>Feet in DM
patients
• Incidence of ACS in the West =3.1/100,00/yr
• In the US, 2-12% anterior distal LL injuries result in CS
• 30% of Limbs develop CS following vascular injury
• More in closed injuries

9. • Tibial diaphyseal fracture is the most common cause- 36%
• Soft tissue injury-23.2%
• Distal radial fracture=9.8%
• CRUSH syndrome & diaphyseal forearm fractures=7.9% each
• Diaphyseal femoral fractures & tibial plateau fractures = 3.0%
• Hand & tibial pilon fractures 2.5% each
• Foot fracture is 1.8%
• Ankle, pelvis, elbow & humeral diaph. Fractures = 0.6%

10. RELEVANT ANATOMY
Compartments
 Leg 4
 Forearm 4
 Arm 2
 Hand 5
 Thigh 3
 Foot 4

13. 4 Compartments of the Forearm

15. 4 Compartments of the Foot

17. 5 Compartments of the Hand

18. AETIOLOGY
Matson suggested following mechanisms as etiological
Factors:
(a) Factors that cause decrease in compartment
(b) Factors that cause increase in compartmental contents

20. PATHOPHYSIOLOGY
• Trauma (with / without arterial injury) → muscle ischaemia
→ muscle oedema due to histamine release.
This causes:
- increase intra compartmental pressure (impedes venous
returns)
- increase intraluminal venous pressure
- decrease arteriovenous pressure gradient
- Subsequent diminished or absent local perfusion.
• Auto regulatory mechanisms may compensate:
 Decrease in peripheral vascular resistance
 Increased extraction of oxygen

21. • As system becomes overwhelmed:
 Critical closing pressure is reached
 Oxygen perfusion of muscles and nerves decreases

23. Muscle Ischemia
 4 hours - reversible damage
 8 hours - irreversible changes
 4-8 hours – variable
 Myoglobinuria occurs after 4 hours
• Cell death initiates a “vicious cycle”
 increase capillary permeability
 increased muscle swelling

24. Nerve Ischemia
 1 hour - normal conduction
 1- 4 hours – neuropraxic damage; reversible damage
 8 hours – axonotmesis; irreversible change

25. MANAGEMENT
ATLS protocol :
 Primary survey and Resuscitation
 Secondary survey; Definitive Care
 Tertiary survey
i. History and examination
ii. Investigations
iii. Treatment

26. Diagnosis
 ACS is a surgical emergency
 Clinical diagnosis
 High index of suspicion
 Syndrome
 History
 Physical Exam

27.  Difficult Diagnosis
 Classic signs of the 6 P’s - ARE NOT RELIABLE:
 pain
 pallor
 paralysis
 pulselessness
 paresthesias
 Pressure (tension)
 These are signs of an ESTABLISHED compartment syndrome
where ischemic injury has already taken place
 These signs may be present in the absence of compartment
syndrome.
 Palpable pulses are usually present in acute compartment
syndromes unless an arterial injury occurs

28. Diagnosis (contd)
 Clinical Features
The most important symptom of an impending
compartment syndrome is PAIN DISPROPORTIONATE
TO THAT EXPECTED FOR THE INJURY/STIMULUS
 Compartment pressure

29. CLINICAL FEATURES
Pain
 Passive muscle stretching
 Out of proportion
 Progressive
 Not relieved by immobilization
 May be worse with elevation
 Patient will not initiate motion on own
Be careful with coexisting nerve injury

30. Parasthesia / Hypoesthesia
 Secondary to nerve ischemia
 Must be differentiated from nerve injury
Paralysis / Paresis
 Ischemic muscles lose function
 Tense compartment on palpation

31. INVESTIGATIONS
 LAB STUDIES
Often normal - not helpful in diagnosing or excluding CS
FBC, Creatine phosphokinase , Urine myoglobin, Serum myoglobin, Urinalysis, PT
& APTT, Urine toxicology screen, Complete metabolic Profile, X-RAY of affected
extremity
- Definitive diagnosis is compartment pressure measurement
using a tonometer if available.

32. Compartment pressure measurement
Objective method of diagnosing ACS
 Involves dynamic measurement of ICP which was introduced in 1970
following Matson unified concept of identifying increase ICP irrespective of
aetiology.
 Normal tissue pressure
 0-4 mm Hg
 8-10 with exertion
 Absolute pressure theory
 30 mm Hg - Mubarak
 45 mm Hg – Matsen
 Pressure gradient theory (∆P)
 < 20 mm Hg of diastolic pressure – Whitesides (1975)
 < 30 mm Hg of diastolic pressure McQueen, et al

33. Tissue-Pressure: Principles
 Heckman et al demonstrated
that pressure within a given
compartment is not uniform
 They found tissue pressures
to be highest at the site or
within 5cm of the injury
 3 of their 5 patients requiring
fasciotomies had sub-critical
pressure values 5cm from the
site of highest pressure

34. High risk patients
High energy fractures
 Severe communition
 Joint extension
 Segmental #
 Bilateral #s
 Floating knee
 Open fractures
Impaired Sensorium
 Alcohol
 Drug
 Decreased GCS
 Unconscious
 Chemically unconscious
 Neurologic deficit
 Cognitively challenged

35. Measurement Methods
 Infusion
 manometer
 saline
 3-way stopcock
(Whitesides, 1975)
 Catheter
 wick
 slit catheter
 Arterial line
 16 - 18 ga. Needle
(5-19 mm Hg higher)
 transducer
 monitor
 Stryker device
 Side port needle

36. Infusion method

37. Most Common Locations
 Leg: deep posterior and the anterior
compartments
 Forearm: volar compartment, especially in the
deep flexor area

38. TREATMENT
 Remove restricting bandages if any
 Stabilize the patient
 Additional O2 should be given - Ischemic injury is basis for CS
 IV hydration is essential - Hypovolemia worsens ischemia.
 Do not elevate the affected limb-decreases arterial pressure
 Sympathetic blockage – stellate ganglion, paravertebral plexus
 Fasciotomy
 Arterial exploration

40. Sheridam and Matsen, Rorabeck and Macinat and other
authors concluded that catastrophic clinical results were
inevitable if fasciotomy were delayed for over 12hrs but
full recovery was achieved if decompression was
performed within six hours of making diagnosis.

41. INDICATIONS FOR FASCIOTOMY
1. Clinical features highly suggestive of ACS
2. Absolute compartment pressure >30-40 mmHg
3. Mean arterial pressure – ICP >40mmHg
4. Diastolic BP – ICP (delta p) <30mmHg

42. Fasciotomy of the Leg
 One incision - with or without Fibulectomy
 Two incisions

43. Perifibular Fasciotomy
 One incision
 Head of fibula to proximal tip of lateral malleolus
 Incise fascia between soleus and FHL distally and extended proximally to origin
of soleus from fibula
 Deep posterior compartment released off the interosseous membrane,
approached from the interval between the lateral and superficial posterior
compartments

44.  Lateral compartment
 Anterior compartment

45. Two incisions:
2 vertical incisions separated by
skin bridge of at least 8 cm
 Lateral
 Medial

46. Fasciotomy of the thigh
 Rare
 Crush injury with femur fracture
 Over distraction
 Treatment based upon
compartment involvement
 Usually Quadriceps and Hamstrings
 Usually, a single lateral incision will
suffice

47. Fasciotomy of the Forearm
Henry Approach
 Incision begins proximal to antecubital
fossa and extends across carpal tunnel
 Begins lateral to biceps tendon, crosses
elbow crease and extends radially, then it
is extended distally along medial aspect
of brachioradialis and extends across the
palm along the thenar crease
 Alternatively, a straight incision from
lateral biceps to radial styloid can be
used.

48. Fasciotomy of the Hand

49. Fasciotomy of the Foot

50. POST FASCIOTOMY
 Must get bone stability
 Intramedullary level
 External fixation
 ~48hrs after procedure, patient should be brought
back to OR for further debridement
 Delayed skin closure, vacuum dressings or skin-grafting
3-7 days after.

51. Skin graft was necessary to close the fasciotomy wound which is seen 8
months post op with near-normal recovery due to the early recognition and
prompt tx of the condition

52. CHRONIC (EXERTIONAL) COMPARTMENT
SYNDROME
 Transient rise in compartmental pressure following
activity
 Symptoms
 Pain
 Weakness
 Neurologic deficits

53.  Stress Test
 Serial Compartment
Pressure
 Resting >15mm Hg
 5 min post-ex.
>25mm Hg

54. Treatment
- NSAIDs
- electro stimulation
- massage
- muscle relaxants
- Sympathetic blockage
- modification of activity
- Splinting
- Elective Fasciotomy

55. COMPLICATIONS
 Muscle necrosis (Rhabdomyonecrosis)
 Ischaemic contracture (Volkmann’s)
 Infection
 Delayed healing of fracture
 Crush syndrome/Renal failure
 Ischaemic - Reperfusion syndrome
 Amputation
 Cosmetic deformity from fasciotomy
 Death

56. DIFFERENTIAL DIAGNOSIS of ACS
 Cellulitis
 DVT and Thrombophlebitis
 Gas Gangrene
 Necrotizing Fasciitis
 Peripheral Vascular injuries
 Rhabdomyolysis

58. PREVENTION
 High index of suspicion on complaint of extremity
pain especially post high velocity injury and patient
on cast
 Health education of patient on cast on recognition
of symptoms and early re-presentation in the
hospital
 Waiting for swellings to resolve b4 application of
cast
 Timely splitting of cast
 Routine measurement of ICP
 Prompt treatment on diagnosis

59. FUTURE TREND
• Near infrared spectroscopy (NIRS)- measure skin
temperature difference
• Scintigraphy
• Laser doppler flowmetry
• Ultra sound – measure sub-micrometer displacement of
fascia
• MRI

60. PROGNOSIS
• Excellent to poor - depending on how quickly ACS is
diagnosed and treated, and whether or not
complications develop
• Nerve dysfunction maybe reversible with time but
infarcted muscle is damaged permanently.
• Early surgery gives good functional outcome but delay
results in muscle ischaemia & necrosis

61. CONCLUSION
 Very important to make diagnosis
 There is still no conclusive answer to the critical
threshold of intra compartmental pressure at which
fasciotomy should be performed.
 Prevention and early decompression are emphasized
in the management of ACS as treatment of
complicated cases is unrewarding.
 Missed compartment syndrome is devastating
 Re-examine patient!

62. REFERENCES
 Apley’s System of Orthopaedics and Fractures, 9th ed.
 Campbell’s Operative Orthopaedics 12th ed.
 Schwartz principles of surgery, 10th ed.
 www.emedicine.medscape.com
 April 2007 By Kumar V Saeed, A Panagopoulos, PJ Parker
 Wheeless’ Textbook of Orthopaedics- Compartment syndrome of the Foot.
 Acute Compartment Syndrome Update on Diagnosis and treatment by TE
Whitesides and MM Heckman Academy of Orthopaedic Surgery July 1996