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.

THANK YOU