compartment syndrome

COMPARTMENT SYNDROMECOMPARTMENT SYNDROME

Dr.Chowdhury Iqbal Mahmud

MBBS,FRCS(UK),MCh(MS, Ortho,Uk)

PG Cert. in Plaster Technology (UK)

Fellow in Orthopaedics ( Singapore)

Registrar (Orthopaedics)

BIRDEM & IMC

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ACUTE COMPARTMENT ACUTE COMPARTMENT SYNDROMESYNDROME

Compartment Syndrome is a true orthopaedic emergency andits outcome depends on the timeliness of the Intervention.

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Why it is important to treat urgently

Volkmann’s Ischaemic contracture

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History:

Volkmann 1881 (described) Petersen 1888 (treatment) Hildenbrand 1906 (ischaemic contracture) Rowlands 1910 (reperfusion) Murphy 1914 (fasciotomy) WW2 (arterial spasm) Kelly & Whitesides (1967) 4 Compartment Leg McQueen & Court-Brown (1990’s)

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INTRODUCTIONINTRODUCTION

What is CS?

Definition:

Compartment syndrome is a condition characterised by raised pressure within a closed space with a potential to cause irreversible damage to the contents of the closed compartment.

Acute compartment syndrome is a potentially devastating condition in which the pressure within an osseofascial compartment rises to a level that decreases the perfusion gradient across tissue capillary beds, leading to cellular anoxia, muscle ischemia, and death.

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Where does it occur?Compartment syndrome (CS) is a condition in which the perfusion pressure

falls below the tissue pressure in a closed anatomic space ( compartment), with

subsequent compromise of tissue circulation and function.

Each muscle or muscle group is enclosed in a compartment bound by relatively

rigid walls of bone and fascia. The compartments of the lower leg and the volar

forearm are particularly prone to developing elevated compartment pressures.

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Where does it occur?

Lower Extremity Gluteal Thigh Lower Leg Foot

Upper Extremity Deltoid Arm Forearm Hand

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ETIOLOGYETIOLOGY

Why does it occur?Any condition that reduces the volume of a compartment or increasesthe content of a compartment can lead to an acute compartment syndrome.

Reduce the Volume Cast or Splint Circumferential constricting dressing Closure of fascia Military antishock trousers (MAST) 3rd degree Burns (circumferential) Lithotomy position Malfunctioning sequential compression devices (SCDs) Tight ski boots

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ETIOLOGYETIOLOGY

Gunshot wound to thigh Drug/alcohol abuse and coma Compartment fluid injection Crush injuries Gastronomies or peroneus muscle

tear Androgen abuse/muscle

hypertrophy Knee arthroscopy Ruptured Baker cyst

Increase the Content

Fractures, direct tissue trauma Hemorrhage: vascular injury,

coagulopathy, anti-coagulation Increased capillary permeability

after burns Infusion or injection (infiltrated

line) Extravasation of arthroscopic fluid Reperfusion after period of

ischemia Basement membrane damage

transudate after arterial inflow is reestablished

Why does it occur?

As many as 45% of all cases of CS are caused by tibial fractures

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ETIOLOGYETIOLOGY

Both close and open fracture can cause compartment syndrome

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ETIOLOGYETIOLOGY

Don’t ForgetCS can occur withopen fracture

198 open fracture

9.1% CS

Blic et al JBJS 1986

Why does it occur?

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PATHOPHYSIOLOGYPATHOPHYSIOLOGY

Compartment Pressures Rise

Venous obstruction occurs, causing further pressure escalation

Low intramuscular arteriolar pressure is exceeded

MUSCLE AND NERVE ISCHEMIA

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Muscle – reversible damage after 4 hours; irreversible after 8 hours

Nerve damage irreversible after 8 hours Tissue perfusion is directly related to the perfusion

gradient in the compartment. Episodes of HYPOTENSION will therefore increase the

extent of irreversible muscle damage In tissue damaged by injury, resistance to ischemia is

decreased. A pressure of 20mm Hg below diastolic shown to cause ischemia

Decreased tissue perfusion

tissue death

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Ischaemic fibrotic contracture

Areas of muscle infarction

•Rabdomyolysis•Hypovolumia•Hyperkalamia•Increase uric acid•Metabolic acidosis

Hypovolumia + myoglobulinaemia

Acute renal failure

Hyperkalamia Cardiac arrest

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Tissueswelling

IschaemiaIschaemia

Muscle

Pain & spasm

Nerve

Paraesthesia

Compartment

pressure

Arteriolar

stasis

Venous

stasis

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MANAGEMENTMANAGEMENT

Pre-hospital/at site management

Oxygen; high flow

Do NOT ice; ice increase vasoconstriction

Do NOT elevate; keep in position where found or position of comfort

Splint for comfort and protection only when necessary ( i. e. long transport)

Transport to appropriate medical facility (trauma?);heads up to receiving medical facility

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The initial evaluation of a patient with an injury should always follow the principles and guidelines of the Advanced Trauma Life Support System.

Primary Survey (ABCDE) & Resuscitation Adjuncts to Primary Survey & Resuscitation Consider need for Patient Transfer Secondary Survey (with AMPLE History) Continued Post-Resuscitation Monitoring & re-evaluation Transfer to Definitive Care

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NEVER FORGET TO DO

PRIMARY SURVEY

A - Airway & Cervical Spine Control

B - Breathing & Oxygenation

C - Circulation & Haemorrhage Control

D - Dysfunction & Disability of the CNS

E - Exposure & Environmental Control

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History

Type of trauma Mechanism of trauma Time since trauma Risk factors Co- morbidities

Physical Examination

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Risk FactorsSpecific injuries

Tibia fractures Distal humerus fractures Forearm fractures Arterial Injury Venous Injury Crush injury Entrapment

Systemic Shock/ Hypotension Overdose/

Unconsciousness

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Diagnosis

Compartment syndrome is a clinical diagnosis Frequently confusing Many classic signs may be absent High index of suspicion is critical

◦ Recognize the risk factors

◦ Inform and educate patient, family, caregivers

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DiagnosisClassic FeaturesThe 5 P’s PainParesthesias Paralysis Pallor Pulselessness

Never have more than two “P”sPulse may be palpable in CS

These are not always reliable clinical feature

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Diagnosis

Pain out of proportion to injury. The pain is also deep and aching in nature and is worsened by passive stretching of the involved muscles. The patient may describe a tense feeling in the extremity. Pain, however, should not be a sine qua non of CS. Paresthesia, or numbness, is an unreliable early symptom.

First complaint of a conscious patient High analgesia requirement Not improved with repositioning or immobilization Transient, minimal relief after release of dressings

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DiagnosisPhysical Exam

Firm, tense, tender and swollen compartments.

Pain on passive stretch most sensitive sign before onset of ischemic nerve and muscle dysfunction.

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Late Diagnostic sign

Hypesthesia or paresthesia Motor deficits Pulselessness should not develop in the absence of arterial

injury Capillary refill is usually unaffected Loss of distal pulses and capillary refill rarely occur in

compartment syndrome without arterial injury or pressures approaching the patient’s SYSTOLIC BP

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DiagnosisSequence of findings: Pain out of proportion, not

relieved by repositioning or removal of dressings

Firm compartments Pain on passive toe motion Mild EHL weakness Florid EDL weakness 1st web space

hypoesthesia

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Diagnosis

Key point: Pain will diminish after pressure-induced ischemia

affects the conductivity of the nerves in the compartment.

A painless state will ensue.

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DiagnosisConfounding Factors Pain and swelling are expected sequelae of trauma and

surgery Neurologic deficits may result from initial injury and not

compartment syndrome Patient may not be able to cooperate with exam Regional anesthesia may mask pain

If compartment syndrome is possible, this is a relative

contraindication to: Long-acting nerve blocks Continuous epidural anesthesia

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Diagnosis

TISSUE PRESSURE MEASUREMENT Compartment syndrome is a clinical diagnosis Don’t need to measure to prove it May need to measure to exclude it Reference point for pain level

INDICATIONS Polytrauma Patients History and symptoms unobtainable Low diastolic pressures Recommend regular checks or continuous monitoring Chemically overdosed or head injury Inconclusive clinical diagnosis Coexisting nerve injury and swelling

Portable Stryker pressure monitor

Manometer

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Diagnosis

Tissue pressure measurement

What tissue pressure is abnormal?

Absolute 45 mm Hg if diastolic 70mm Hg or higher

Relative < 20-30 mm Hg below diastolic pressure (Whitesides et al., Journal of American Academy of Orthopaedic

Surgeons, 1996 )

[Normal compartment pressures < 10 mm HG]

Diastolic pressure - compartment pressure less than 30 mm Hg

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Differential diagnosis Cellulitis Deep Venous Thrombosis and Thrombophlebitis Gas Gangrene Necrotizing Fasciitis Peripheral Vascular Injuries Rhabdomyolysis

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MANAGEMENT MANAGEMENT (INVESTIGATION)(INVESTIGATION)

Lab Studies Hematology/chemistry laboratory studies – Serum myoglobin and CK

measurements should be obtained to determine the degree of muscle necrosis. ◦ Serial CK levels may show increases indicative of a developing CS. ◦ High CK levels should alert the physician to possible rhabdomyolysis.

Renal function/chemistry panel ◦ Blood urea nitrogen (BUN) and creatinine are measured. ◦ Potassium level is needed in cases of rhabdomyolysis. ◦ Severe hyperkalemia may result in a wide complex and possibly fatal

arrhythmia. Complete blood cell count (CBC) and coagulation studies

◦ Anemia worsens muscle ischemia. ◦ Look for disseminated intravascular coagulation (DIC), which is rare.

Preoperative laboratory studies Urinalysis to determine myoglobin and CK (if available)

◦ A urine dip may show blood but no red blood cells (RBCs), which indicates the presence of myoglobin.

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MANAGEMENT MANAGEMENT (INVESTIGATION)(INVESTIGATION)

Imaging Studies Plain radiographs of the affected extremity are used to

determine fracture pattern, soft-tissue injury, and radiographic clues that may indicate occult fractures.

MRIs may show increased signal intensity in an entire compartment on T2-weighted, spin-echo sequences.

Computed tomography (CT) scanning is especially useful if pelvic or thigh CS is in the differential diagnosis.

Lower extremity venous Doppler or arterial ultrasonography (US) is performed as needed to address possible DVT or arterial occlusion.

US alone is not useful in making the diagnosis of CS.

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MANAGEMENT (TREATMENT)MANAGEMENT (TREATMENT)

Medical therapy Place the affected limb(s) at the level of the heart. Elevation

is contraindicated because it decreases arterial blood flow and narrows the arteriovenous pressure gradient and thus worsens the ischemia.

Remove cast, bandages and any dressing. Reduce compartment pressure by releasing one side of a plaster cast, which can reduce the pressure by 30%; bivalving can produce an additional 35% reduction and cutting bandages decrease the compartmental pressure by 10-20%.

Correct hypo perfusion with crystalloid solution and blood products.

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Medical therapy

Mannitol may reduce compartment pressures and lessen reperfusion injury.

Vasodilator drugs or sympathetic blocking drugs appear to be ineffective in the treatment of CS, probably because, in this condition, maximal local vasodilatation is already present.

Administer antivenin in cases of snake bite; this may reverse a developing CS.

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Surgical Therapy

The definitive surgical therapyfor compartment syndrome isemergent fasciotomy(compartment release) with subsequent orthopedicreduction or fracturestabilization and vascularrepair, if needed.The goal of decompression isrestoration of muscle perfusionwithin 6 hours.

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Surgical TherapyFasciotomy in different parts

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MANAGEMENT (TREATMENT)MANAGEMENT (TREATMENT) Surgical treatment( Fasciotomy )in Lower Leg:Surgical treatment( Fasciotomy )in Lower Leg:

Anterior compartment ◦ Dorsiflexion muscles of the ankle and foot

Tibialis anterior Extensor digitorum longus Extensor hallucis longus Peroneus tertius

◦ Anterior tibial artery – Commonly injured in lateral tibial plateau fractures

◦ Deep peroneal nerve – Provides sensation to the first dorsal web space

Lateral compartment ◦ Peroneus brevis and peroneus longus –

Plantar flexor and evertor muscles of the foot

◦ Superficial peroneal nerve – Provides sensation to the dorsum of the foot

Deep posterior compartment ◦ Plantar flexor and phalangeal flexor

muscles Tibialis posterior Flexor digitorum longus (FDL) Flexor hallucis longus

◦ Posterior tibial and peroneal arteries ◦ Posterior tibial nerve – Provides

sensation to the sole of the foot

Superficial posterior compartment ◦ Plantar flexor muscles of the foot

Gastrocnemius Plantaris Soleus

◦ Sural nerve – Provides sensation to the lateral aspect of the foot and distal calf

Relevant anatomy of lower leg compartment39


Surgical Treatment

( Fasciotomy ) in Lower Leg:

Single- and double-incision techniques have been described. The double-incision technique is safer and more effective and should be used in general.

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Surgical Treatment( Fasciotomy )in Lower Leg:

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Surgical Treatment( Fasciotomy )in Lower Leg:

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The anterior and lateral compartments are approached through 1 incision.

Make an approximately 15-cm incision over the anterior intermuscular septum, centered halfway between the fibular shaft and the crest of the tibia( 2 cm lat. To the ant. Tibial border). The incision must be large enough to provide adequate visualization. In an elective decompression, a 4- to 5-cm incision may be adequate.

Use subcutaneous dissection for wide exposure of the fascial compartments.

Make a transverse incision to expose the lateral intermuscular septum and to identify the superficial peroneal nerve just deep to the septum.

Make a small nick in the anterior intermuscular septum midway between the septum and tibial crest.

Using Metzenbaum scissors or a fasciotome, release the anterior compartment proximally (aim for the patella) and distally (aim for the center of the ankle) in line with the tibialis anterior.

Then, perform a longitudinal fasciotomy of the lateral compartment in line with the fibular shaft. Direct the scissors toward the lateral malleolus to stay posterior to the superficial peroneal nerve.

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Make a second longitudinal incision 1-2 cm posterior to the posterior medial margin of the tibia.

Use wide subcutaneous dissection to allow identification of the fascial planes.

Retract the saphenous vein and nerve anteriorly. Make a transverse incision to identify the septum between the deep and superficial posterior compartments. Release the fascia over the superficial posterior compartment. Release the fascia over the gastrocsoleus complex along the length of the compartment.

Make another fascial incision over the FDL muscle and release the entire deep posterior compartment.

As the surgical dissection is carried proximally, note the origin of the soleus from the proximal third of the tibia. Detach the soleal bridge, and retract to expose the FDL and tibialis posterior.

After release of the posterior compartment, identify the tibialis posterior muscle compartment. If increased tension is evident in this compartment, release it over the extent of the muscle body.

Pack the wound open and apply a posterior plaster splint with the ankle held at 90°. Return the patient to the operating room for debridement in 1-3 days if necessary or for skin closure.

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Fracture Fixation

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Post-operative wound closure

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Contraindication to Fasciotomy If CS is diagnosed late, fasciotomy is of little

benefit. In fact, fasciotomy is probably contraindicated after the third or fourth day following the onset of CS, and when performed late, severe infection usually develops in the necrotic muscle.

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OUTCOMEOUTCOME

Depends upon the timeliness of diagnosis and treatment

Dependent upon etiology and age of patient

If recognized and treated before my necrosis, >90% recover function

May have some loss of muscle power due to the fasciotomy

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Chronic exertional compartment Chronic exertional compartment syndromesyndrome

Chronic exertional compartment syndrome is an exercise-induced neuromuscular condition that causes pain, swelling and sometimes even disability in affected muscles of the legs or arms. The condition can occur in both beginning and seasoned athletes in sports that involve repetitive movements, such as running, fast walking, biking and swimming. Chronic exertional compartment syndrome is sometimes called chronic compartment syndrome or exercise-induced compartment syndrome.

In chronic exertional compartment syndrome, the repetitive activity causes tissue in the affected muscle area, or compartment, to swell. That, in turn, increases pressure within the compartment, leading to a decreased blood supply to the muscles. This can cause injury to the muscle and nerves, sometimes resulting in permanent damage.

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SUMMARYSUMMARY

Acute compartment syndrome is a potentially devastating condition in which the pressure within an osseofascial compartment rises to a level that decreases the perfusion gradient across tissue capillary beds, leading to cellular anoxia, muscle Ischemia, and death.

A variety of injuries and medical conditions may initiate acute compartment syndrome, including fractures, contusions, bleeding disorders, burns, trauma, post-ischemic swelling, and gunshot wounds.

Diagnosis is primarily clinical, supplemented by compartment pressure measurements.

Certain anesthetic techniques, such as nerve blocks and other forms of regional and epidural anesthesia, reportedly contribute to a delay in diagnosis.

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SUMMARYSUMMARY

Basic science data suggest that the ischemic threshold of normal muscle is reached when pressure within the compartment is elevated to 20 mm Hg below the diastolic pressure or 30 mm Hg below the mean arterial blood pressure.

On diagnosis of impending or true compartment syndrome, immediate measures must be taken.

Complete fasciotomy of all compartments involved is required to reliably normalize compartment pressures and restore perfusion to the affected tissues.

Recognizing compartment syndromes requires having and maintaining a high index of suspicion, performing serial examinations in patients at risk, and carefully documenting changes over time.

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MY WEB SITE WWW.ORTHODOC.AAOS.ORG/MAHMUDFRCS

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