Compartment syndrome occurs when increased pressure within a muscle compartment reduces blood supply, potentially leading to permanent muscle and nerve damage if untreated for over 6 hours. It can be acute, often due to severe injuries, or chronic, typically linked to athletic exertion, with symptoms including severe pain, swelling, and loss of function. Management involves timely diagnosis and intervention, including fasciotomy in severe cases, and both non-operative and operative strategies depending on the severity of the condition.

1. Compartment
Syndrome
By Ajay Raveendranadh
Guided by: Dr Riju R Menon

2. • What is Compartment syndrome?
An elevation of the interstitial
pressure in a closed osteofascial compartment
that results in microvascular compromise.

3. • Compartments are groups of
muscles surrounded by
inelastic fascia.
• Increased pressure within a
muscle compartment
causes decreased blood
supply to affected muscles.
• Any swelling of muscles
leaves no room for
expansion and blood supply
is progressively shut off.
• If affected muscles are
deprived of blood supply for
> 6 hours, nerve and muscle
tissue can be permanently
damaged.

4. Anatomy:
Compartment Muscles Vessels Nerves
Anterior Tibialis anterior Anterior tibial Deep peroneal
Ext. halusic longus
Ext digitorum
communis
Deep Posterior Tibialis posterior Posterior tibial Tibial
Flexor hallusic longus Peroneal
Flexor digitorum
longus
Superficial Gatronemius
Soleus
Plantaris
Lateral Peroneus longus &
brevis

6. • Types of Compartment syndrome:
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.

7. Etiology:
I. Decrease compartment size
-Tight dressings/closure of fascial defect
-External pressures : casts, splints , burn eschar,
lying on limb for long period, lithotomy position

8. II Increase compartment contents
 Fractures : the most common are
• In adults --- closed and open tibial
shaft fracture
• In children --- radial head or neck
fracture.

9. Increase compartment
contents
• Hemorrhage -- vascular
injury, coagulopathy
• Muscle edema --
severe exercise , crush
injury
• Burn -- increase
capillary permeability

10. Pathophysiology
 Increased intra compartmental
Pressure
 increases local venous P
 narrowed AV perfusion
gradient
 compartment tamponade
 decrease capillary blood flow
 O2 deprivation
 local tissue necrosis
 nerve injury and muscle
ischemia

11. • Whiteside’s Theory:
The development of a compartment syndrome also
depends on
• MPP = DBP(Diastolic BP) – CP(Intracompartment P)
• Muscle perfusion pressure(MPP) < 30 mmHg
 Tissue hypoxia

12. Clinical Presentation:
• Swelling/ Tightness of compartment
• Inappropiate and uncontrolled pain
• Severe pain at rest or passive stretching
• Pallor/Cyanosis
• Hyperesthesia/Paresthesia
• Paralysis : full recovery is rare

13. 5 P’s
1.Pain
2.Paraesthesia
3. Pallor
4.Paralysis
5.Pulselessness

14. Evaluation:
• Physical examination :
• Pain at compartment on passive stretching :
• test each compartment separately
• Thigh : - anterior compartment - passive knee flexion
- posterior compartment - passive knee extension
- medial compartment - passive hip abduction
• Hyperesthesia/Paresthesia
• Peripheral pulses absent - amputation usually inevitable

15. Measuring the pressure:
• Indications : High risk injuries in
• polytrauma patients
• patient not alert/unreliable
• inconclusive physical exam findings
• Technique : performed each compartments at
close to the fracture site as possible (highest
pressure) or maximal swelling area.

16. • Devices:
Stryker hand-held system Stryker slit catheter

19. Management:
• Early Management:
- Remove cast/bandage
- Positioning of the limb at the level of the heart
Do not elevate the affected limb  decreases arterial
pressure
- IV hydration
- Oxygen supplement

20. Management:
I Non-operative
Observation
ΔPressure >30 mmHg, no clinical
presentation of compartment syndrome
II Operative
Emergency fasciotomy
Positive clinical presentation
CP = 30-45 mm Hg
Δ Pressure <30 mmHg

21. FASCIOTOMY
• Surgical incision to the fascia to relieve tension or pressure.
• Complete opening of all fascial envelopes.
• The wound should be left open and inspected 2 days
later.
• If there is muscle necrosis  debridement.
• If the tissues are healthy, the wound can be
- sutured (without tension)
OR
- skin-grafted
OR
- allowed to heal by secondary intention

22. If ∆P < 30mmHg
FASCIOTOMY
If no facilities for
compartmental
pressure
measurement, the
decision to operate
will make on clinical
grounds
Examine the limb at 15
minutes intervals. If no
improvement within 2
hours of removing the
dressings
Muscle will be
dead after >4
hours of total
ischemia

23. Types:
I Single Incision:

25. II. Double Incision:

27. Complications:
I. Myonecrosis : after an ischemic insult of > 4 hrs.
Treatment:
fasciotomy + debridement of the muscles + neurolysis
• May lead to myoglobinuria and eventually renal
failure.
• Diuresis ( by mannitol,diuretics or IV fluids ) should
be prompted to increase the tubular flushing and
eliminate the proteinaceous material.

28. II. Reperfusion syndrome : influx of myoglobin, potassium, and
phosphorus into the circulation
 characterized by hypovolemic shock and hyperkalemia
• Evaluation :
• Fluid loss, Shock
• Acidosis
• Hyperkalemia
• Myoglobinuria, Renal failure
• Management :
• Preoperative hydration
• Mannitol
• Bicarbonate

29. III. Neurovascular injury
IV. Infection
V. Amputation
VI. Death

31. Abdominal Compartment
Syndrome

32. ACS is a sustained IAP greater
than 20 mm Hg associated with
new organ dysfunction or failure.

33. Burch Grading system for intra-abdominal hypertension:
Grade Intra-abdominal pressure (mmHg )
I 12 - 15
II 16 - 20
III 21 - 25
IV ≥25

34. Abdominal Compartment syndrome:
I. Primary
II. Secondary
III. Tertiary

35. Primary:
• Sustained acute elevation of 10-20 mm Hg
• Physiologic effects are generally well compensated
and thus usually clinically non-significant.
• Non-operative therapy may be required.

36. Secondary:
• Sustained acute elevation of 21-35 mm Hg.
• Therapy is generally necessary.
Caused by Non-abdominal conditions:
–Major burns
–Sepsis
–Conditions requiring massive fluid resuscitation

37. Tertiary:
• Sustained acute elevation >35 mm Hg.
• Also known as recurrent ACS, develops after
treatment of primary and secondary ACS.
• Operative abdominal decompression is always
indicated (ACS).

38. Factors leading to Abdominal
Compartment syndrome:
• Hypothermia
• Massive transfusions
• Sepsis
• Mechanical ventilation
• Pneumonia
• Acidosis
• Excessive fluid resuscitation

39. Clinical Presentation:
I. Abdominal pain
II. Increased abdominal girth
III. Difficulty in breathing
IV. Decreased urine output
V. Syncope
VI. Malaena
VII.Nausea & vomiting
VIII.H/O Pancreatitis
IX. Cyanosis

40. Cardio Vascular Effects of
ACS:
• ↑ Intra-thoracic pressure transmitted through
diaphragm
• Compression IVC
• ↑ Central Venous pressure
• ↓ Preload
• ↓ Cardiac Output

41. • Tachycardia is the common response
to elevated IAP, compensating for the
decrease in stroke volume in order to
maintain cardiac output.

42. Pulmonary Effects of
ACS:
• Both diaphragms are pushed upwards decreasing
the thoracic volume.
• Decreased volume predisposes to atelectasis and
decreases alveolar clearance.
• Pulmonary infections may result.
• Pneumonia is a typical early complication in
abdominal hypertension from diffuse peritonitis.

43. • ↑ Airway pressure
• ↑ End-inspiratory pressure
• Mechanical impairment of diaphragm
• Decreased pulmonary blood flow
All lead to…
• Decreased PaO2
• Intractable hypercarbia

44. Renal Effects of ACS:
• Renal vein compression
• Renal parenchymal compression
• Shunting blood away from cortex and
functioning glomeruli
• ↑ Anti-Diuretic Hormone release
• Oliguria/Anuria

45. GI Effects
• As IAP increases ,abdominal vascular pressure increases.
• causing diminished arterial blood flow to the organs and
resistance to drainage into the veins.
• The diminished oxygenation to the gut leads to
intramucosal acidosis.
• The ischemic intestine loses its protective mucosal barrier
and becomes more permeable to the intestinal
contents.
• Edema develops in the intestinal wall and further
increases the IAP.

46. • blood flow decreases in both the hepatic artery
and the portal vein.
• This change in blood flow leads to:
decreased glucose metabolism,
mitochondrial malfunction
decreased lactate clearance
• Diminished lactate clearance leads to lactic
acidosis.

47. Measuring Methods:
Direct:
– Direct needle puncture and transducer
Intermittent Indirect:
– Bladder pressure transducer
Continuous Indirect:
– Continuous bladder irrigation method

51. Methods to lower the IAP:
I. Drainage of intra-abdominal fluid
collection
II. Muscle relaxation
III. Avoiding primary closure of the
incision by applying mesh or Vacuum
assisted closure.

52. Treatment:
I. Treatment should not be based only upon IAH but
also associated organ dysfunction.
II. Move the patient to emergency immediately
III. Remove any constricting garments
IV. Avoid overly aggressive fluid resuscitation.

53. Bladder Pressure Treatment
• 10-15 mmHg Monitor
• 16-25 mmHg Monitor
• 26-35 mmHg Decompression
• > 35 mmHg Decompression &
re-exploration

54. Complication:
The correction of IAH can lead to
ischemia reperfusion injury and send
inflammatory cytokines to other
organs, causing multisystem organ
failure.

55. THANK YOU