Download - Compartment Syndrome
Compartment Syndrome
By Ajay Raveendranadh
Guided by: Dr Riju R Menon
• What is Compartment syndrome?
An elevation of the interstitial
pressure in a closed osteofascial compartment
that results in microvascular compromise.
• 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.
Anatomy:Compartment Muscles Vessels Nerves
Anterior Tibialis anterior Anterior tibial Deep peroneal
Ext. halusic longus
Ext digitorumcommunis
Deep Posterior Tibialis posterior Posterior tibial Tibial
Flexor hallusic longus Peroneal
Flexor digitorumlongus
Superficial Gatronemius
Soleus
Plantaris
Lateral Peroneus longus & brevis
• 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.
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
II Increase compartment contents
Fractures : the most common are
• In adults --- closed and open tibial
shaft fracture
• In children --- radial head or neck
fracture.
Increase compartment
contents
• Hemorrhage -- vascular
injury, coagulopathy
• Muscle edema --
severe exercise , crush
injury
• Burn -- increase
capillary permeability
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
• 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
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
5 P’s
1.Pain
2.Paraesthesia
3. Pallor
4.Paralysis
5.Pulselessness
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
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.
• Devices:
Stryker hand-held system Stryker slit catheter
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
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
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
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
Types:
I Single Incision:
II. Double Incision:
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.
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
III. Neurovascular injury
IV. Infection
V. Amputation
VI. Death
Abdominal Compartment Syndrome
ACS is a sustained IAP greater
than 20 mm Hg associated with
new organ dysfunction or failure.
Burch Grading system for intra-abdominal hypertension:
Grade Intra-abdominal pressure (mmHg )
I 12 - 15
II 16 - 20
III 21 - 25
IV ≥25
Abdominal Compartment syndrome:
I. Primary
II. Secondary
III. Tertiary
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.
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
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).
Factors leading to Abdominal
Compartment syndrome:
• Hypothermia
• Massive transfusions
• Sepsis
• Mechanical ventilation
• Pneumonia
• Acidosis
• Excessive fluid resuscitation
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
Cardio Vascular Effects of ACS:• ↑ Intra-thoracic pressure transmitted through
diaphragm
• Compression IVC
• ↑ Central Venous pressure
• ↓ Preload
• ↓ Cardiac Output
• Tachycardia is the common response
to elevated IAP, compensating for the
decrease in stroke volume in order to
maintain cardiac output.
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.
• ↑ Airway pressure
• ↑ End-inspiratory pressure
• Mechanical impairment of diaphragm
• Decreased pulmonary blood flow
All lead to…
• Decreased PaO2
• Intractable hypercarbia
Renal Effects of ACS:
• Renal vein compression
• Renal parenchymal compression
• Shunting blood away from cortex and functioning glomeruli
• ↑ Anti-Diuretic Hormone release
• Oliguria/Anuria
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.
• 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.
Measuring Methods:
Direct:– Direct needle puncture and transducer
Intermittent Indirect:– Bladder pressure transducer
Continuous Indirect:– Continuous bladder irrigation method
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.
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.
Bladder Pressure Treatment
• 10-15 mmHg Monitor
• 16-25 mmHg Monitor
• 26-35 mmHg Decompression
• > 35 mmHg Decompression &
re-exploration
Complication:
The correction of IAH can lead to
ischemia reperfusion injury and send
inflammatory cytokines to other
organs, causing multisystem organ
failure.
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