Acute Compartment Syndrome

Topic Overview

Summary

Acute compartment syndrome (ACS) is a limb-threatening and potentially life-threatening emergency caused by elevated pressure within a closed fascial compartment, leading to compromised tissue perfusion and progressive ischaemic necrosis. It most commonly occurs after tibial shaft fractures (2-12% incidence) but can follow any injury causing bleeding or oedema within a non-compliant fascial envelope. [1,2]

The hallmark clinical feature is pain out of proportion to the clinical findings, with pain on passive stretch of compartment muscles being the most reliable early sign. [3] Pulselessness and paralysis are late manifestations indicating irreversible muscle and nerve damage—clinicians must not wait for these signs before proceeding to fasciotomy. [4]

Emergency fasciotomy performed within 6 hours of symptom onset typically results in full functional recovery, whereas delayed treatment beyond 12 hours is associated with permanent disability, limb loss, rhabdomyolysis-induced acute kidney injury, and mortality. [5,6] The clinical dictum remains: it is better to perform an unnecessary fasciotomy than to miss a true compartment syndrome.

Key Facts

• Incidence: 3.1 per 100,000 per year overall; 2-12% after tibial fractures [7]
• Most common location: Anterior compartment of the leg (45% of all cases) [8]
• Commonest cause: Tibial shaft fracture (especially high-energy and open fractures) [2]
• Pathophysiology: Pressure > 30 mmHg or ΔP less than 30 mmHg causes microvascular compromise [9]
• Earliest reliable sign: Pain on passive stretch of compartment muscles [3]
• Critical time window: Irreversible muscle necrosis after 6-8 hours of ischaemia [10]
• Definitive treatment: Emergency 4-compartment fasciotomy [11]
• Major complications: Volkmann's contracture, permanent nerve damage, rhabdomyolysis, AKI, amputation, death [12]

Clinical Pearls

Pain on passive stretch is the MOST SENSITIVE and SPECIFIC early clinical sign—this should trigger immediate surgical evaluation. [3]

Never rely on pulses—arterial occlusion is a late sign occurring only when compartment pressure exceeds systolic blood pressure. By this stage, muscle and nerve are irreversibly damaged. [4]

The delta pressure (ΔP) = diastolic BP minus compartment pressure. A ΔP less than 30 mmHg has superior diagnostic accuracy compared to absolute pressure thresholds. [9]

Regional anaesthesia concerns: Peripheral nerve blocks can mask early symptoms but do NOT completely eliminate pain from compartment syndrome. High clinical suspicion and serial examination remain essential. [13]

"When in doubt, let it out"—if clinical suspicion is high, proceed to fasciotomy. The morbidity of an unnecessary fasciotomy is vastly outweighed by the catastrophic consequences of a missed compartment syndrome. [14]

Why This Matters Clinically

Compartment syndrome represents one of the few true orthopaedic emergencies where hours determine permanent disability versus full recovery. Missed or delayed diagnosis leads to Volkmann's ischaemic contracture (fibrotic muscle shortening with claw deformity), permanent sensorimotor nerve deficits, limb amputation in severe cases, and systemic complications from rhabdomyolysis including hyperkalaemia-induced cardiac arrest and acute kidney injury requiring dialysis. [12,15]

All clinicians managing trauma—emergency physicians, orthopaedic surgeons, anaesthetists, and intensive care specialists—must maintain a low threshold for diagnosis and understand that compartment syndrome is primarily a clinical diagnosis that should not be delayed awaiting confirmatory pressure measurements. [16]

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Visual Summary

Visual assets to be added:

• Cross-sectional anatomy: 4 compartments of the leg with contents
• Fasciotomy incisions: 2-incision technique (lateral and medial approaches)
• Passive stretch tests: Demonstration for each compartment
• Volkmann's contracture: Clinical photograph showing classic deformity
• Stryker pressure monitor: Technique for compartment pressure measurement
• Decision algorithm: Clinical pathway from presentation to fasciotomy

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Epidemiology

Incidence and Prevalence

Overall Population:

• Annual incidence: 3.1 per 100,000 population [7]
• Male predominance: Male:female ratio 10:1 (reflecting higher trauma and activity rates) [17]
• Peak age: 20-40 years (young, active individuals sustaining high-energy trauma) [7]

Post-Traumatic Incidence:

• Tibial shaft fracture: 2-12% (highest risk with high-energy, displaced fractures) [2]
• Tibial plateau fracture with compartment syndrome: 0.5-5% [18]
• Forearm fractures (radius/ulna): 3-9% [19]
• Supracondylar humerus fracture (paediatric): 0.1-0.3% but most serious complication [20]
• Calcaneal fracture: 10% (underrecognised) [21]

Anatomical Distribution

Lower Leg Compartment-Specific Incidence: [8]

• Anterior compartment: 45% of all leg ACS
• Deep posterior: 25%
• Lateral: 20%
• Superficial posterior: 10%

Aetiology and Risk Factors

Fracture-Related (75% of Cases): [2]

1. Tibial shaft fracture (most common overall cause)

   • Highest risk: High-energy, displaced, segmental fractures
   • Open fractures: 6-9% incidence
   • Closed fractures: 2-6% incidence
   • Risk increases with delay to fixation > 24 hours

2. Forearm fractures (both-bone forearm fractures)

   • Galeazzi and Monteggia fracture-dislocations
   • High-energy mechanisms

3. Tibial plateau fractures (especially Schatzker V-VI)

4. Calcaneal fractures (frequently missed—maintain high suspicion)

5. Supracondylar humerus fracture (paediatric population)

Non-Fracture Causes (25% of Cases):

1. Soft tissue trauma:

   • Crush injury (prolonged compression in unconscious patients, building collapse)
   • Burns (circumferential deep burns causing external compression)
   • Snakebite envenomation (tissue oedema and bleeding)

2. Iatrogenic:

   • Tight casts, splints, or dressings (most preventable cause)
   • Circumferential eschars from burns
   • Prolonged tourniquet use > 2 hours
   • Limb positioning during surgery (lithotomy position > 4 hours)

3. Vascular:

   • Arterial injury with ischaemia-reperfusion injury post-revascularisation
   • Venous obstruction or phlegmasia cerulea dolens
   • Anticoagulation or haemophilia causing compartment haemorrhage

4. Exertional (chronic exertional compartment syndrome):

   • Differs from acute—recurrent, exercise-induced, relieved by rest
   • Most common in military recruits and endurance athletes
   • Typically anterior and lateral compartments

5. Other:

   • Intravenous drug injection (high-pressure extravasation)
   • Nephrotic syndrome (severe hypoalbuminaemia)
   • Post-limb lengthening procedures

Demographic and Clinical Risk Factors

Patient Factors:

• Age less than 35 years (higher energy trauma mechanisms) [7]
• Male sex (10:1 ratio) [17]
• High-energy trauma mechanism
• Polytrauma with multiple injuries
• Coagulopathy or anticoagulation

Fracture Factors:

• Closed fracture (paradoxically higher risk than open—intact skin envelope)
• Diaphyseal location
• Severe displacement or comminution
• Segmental or multiple ipsilateral fractures

Treatment Factors:

• Intramedullary nailing of tibial fractures (reaming increases pressure)
• Delay to fracture stabilisation > 24 hours
• Tight circumferential dressings or casts
• Over-vigorous fluid resuscitation (increases tissue oedema)

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Pathophysiology

Normal Compartment Anatomy and Physiology

Each limb compartment consists of muscles, nerves, and vessels enclosed by non-compliant fascia. The fascia allows minimal expansion, so any increase in compartment contents rapidly raises intra-compartmental pressure (ICP).

Normal ICP: 0-8 mmHg

Lower Leg 4-Compartment Anatomy:

The Pathophysiological Cascade

Stage 1: Initiating Insult

• Trauma → haemorrhage into compartment and/or soft tissue oedema
• Fracture → bone bleeding + inflammatory oedema
• Reperfusion → ischaemia-reperfusion injury (burst of oxidative damage)
• External compression → direct pressure increase

Stage 2: Rising Intra-Compartmental Pressure

• Compartment volume increases within fixed fascial boundaries
• Fascial compliance exhausted rapidly (minimal stretch capacity)
• ICP rises proportionally to volume increase
• Normal muscle can accommodate ~15% volume increase before critical pressure reached

Stage 3: Microvascular Compromise ("Arteriovenous Gradient Collapse")

Critical pathophysiology occurs when:

• ICP approaches capillary perfusion pressure (30 mmHg)
• Venous outflow first obstructed (veins collapse at low pressures ~15-20 mmHg)
• Continued arterial inflow with blocked venous drainage → further compartment swelling
• Vicious cycle: ↑ ICP → ↓ venous drainage → ↑ oedema → ↑ ICP

The "Delta Pressure" (ΔP) Concept: [9]

• ΔP = Diastolic Blood Pressure - Intra-Compartmental Pressure
• Tissue perfusion maintained when ΔP > 30 mmHg
• When ΔP falls less than 30 mmHg → critical ischaemia ensues
• More accurate than absolute ICP threshold (accounts for patient's BP)

Why absolute pressure > 30 mmHg is used:

• Approximation based on normal diastolic BP ~80 mmHg
• When ICP reaches 30 mmHg, ΔP = 80-30 = 50 mmHg (adequate perfusion)
• When ICP exceeds 30 mmHg in normal BP patient → ΔP approaches critical level

Stage 4: Tissue Ischaemia

Muscle Tolerance: [10]

• 0-4 hours: Reversible ischaemia, no permanent damage
• 4-6 hours: Borderline—some myocyte injury but mostly recoverable
• 6-8 hours: Progressive irreversible necrosis begins
• > 8 hours: Established necrosis, fibrosis, contracture inevitable
• > 12 hours: Extensive muscle death, high amputation risk

Nerve Tolerance: [22]

• 2-4 hours: Neurapraxia (temporary conduction block)—fully recoverable
• 4-8 hours: Axonotmesis—partial axonal injury, prolonged recovery
• > 8 hours: Neurotmesis risk—permanent nerve damage with motor/sensory deficits

Arterial Patency:

• Arteries remain patent until ICP exceeds systolic BP (~120 mmHg)
• This is a very late event indicating catastrophic compartment syndrome
• Clinical implication: Presence of distal pulses does NOT exclude compartment syndrome
• Absence of pulses indicates irreversible muscle/nerve damage already occurred

Stage 5: Systemic Consequences (If Untreated)

Rhabdomyolysis: [15]

• Massive myocyte necrosis releases myoglobin, creatine kinase, potassium
• Myoglobin precipitates in renal tubules → acute tubular necrosis
• CK typically > 5,000-50,000 U/L in severe cases

Acute Kidney Injury:

• Myoglobin-induced AKI (peak 24-48 hours post-injury)
• Hyperkalaemia from massive potassium release
• Metabolic acidosis

Cardiovascular:

• Hyperkalaemia → cardiac arrhythmias, cardiac arrest
• Hypovolaemia (third-spacing of fluids into damaged muscle)

Local:

• Muscle fibrosis and contracture (Volkmann's ischaemic contracture)
• Permanent nerve damage
• Chronic pain and disability
• Limb loss if overwhelming necrosis

Special Pathophysiological Scenarios

Chronic Exertional Compartment Syndrome (CECS): [23]

• Recurrent, transient ICP elevation during exercise
• Muscle hypertrophy and increased blood flow exceed fascial capacity
• Symptoms resolve 10-20 minutes post-exercise (diagnostic feature)
• Does NOT progress to acute limb-threatening syndrome
• Pathophysiology: inadequate fascial expansion during exercise-induced hyperaemia

Ischaemia-Reperfusion Injury: [24]

• Occurs after revascularisation (embolectomy, bypass, crush syndrome release)
• Initial ischaemia → accumulation of hypoxanthine
• Reperfusion → xanthine oxidase converts to oxygen free radicals
• Oxidative burst → endothelial damage → capillary leak → oedema → ACS
• Prophylactic fasciotomy often indicated in prolonged limb ischaemia (> 6 hours)

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Clinical Presentation

The "6 Ps" (Classic Teaching)

The traditional mnemonic lists six features, but they have vastly different sensitivity and timing:

Clinical Reality:

• Pain and pain on passive stretch are the ONLY reliable early signs
• Waiting for the "late Ps" (paresis, pulselessness) guarantees permanent disability
• ACS is a clinical diagnosis based on high suspicion + early signs

Early Clinical Features (Within 0-6 Hours)

1. Pain Out of Proportion [3]

• Severity disproportionate to apparent injury
• Progressive, unrelenting, not relieved by immobilisation
• Escalating analgesic requirements (breakthrough pain despite opioids)
• Patient appears distressed, focussed on limb pain

Clinical Context:

• Post-fracture: Pain should improve with splinting/reduction—worsening pain is pathological
• Post-cast application: Immediate severe pain after casting
• Post-reperfusion: Sudden severe pain after revascularisation procedure

2. Pain on Passive Stretch (Most Specific Sign) [3]

• Sensitivity: 85-95%, Specificity: 75-85% in various studies
• Gentle passive stretching of compartment muscles elicits severe pain
• Pain is reproducible and localised to affected compartment
• How to Test:

3. Tense Compartment ("Woody Hardness")

• Compartment feels firm, swollen, non-compressible on palpation
• Compare to contralateral limb or adjacent compartments
• Shiny, taut skin overlying compartment

4. Paraesthesia (Early Nerve Ischaemia)

• Numbness, tingling, "pins and needles" in sensory nerve distribution
• Indicates nerve ischaemia is already occurring (2-4 hour range)

Late Clinical Features (> 6-8 Hours) — Irreversible Damage

5. Paralysis (Paresis)

• Inability to actively contract compartment muscles
• Loss of toe/finger dorsiflexion or plantarflexion (depending on compartment)
• Indicates established muscle and nerve necrosis

6. Pulselessness

• Absent dorsalis pedis, posterior tibial, or radial/ulnar pulses
• Only occurs when ICP exceeds systolic BP (~120 mmHg)
• By this stage, compartment contents are dead
• Never wait for this sign to make diagnosis

7. Pallor/Mottling

• Pale, dusky, or mottled limb
• Cool to touch
• Indicates advanced ischaemia

8. Poikilothermia

• Limb assumes ambient temperature (loss of vascular perfusion)

Special Clinical Scenarios

Unconscious/Sedated Patients: [25]

• Cannot report pain—highest risk for missed diagnosis
• Red flags in unconscious patients:
  • Unexplained tachycardia or agitation
  • Excessive limb swelling
  • High ventilator pressures (if tourniquets used)
  • Rising lactate or CK
• Action: Lower threshold for compartment pressure monitoring

Regional Anaesthesia (Nerve Blocks): [13]

• Historic teaching: absolute contraindication
• Current evidence: nerve blocks reduce but do NOT completely eliminate pain from ACS
• Most studies show pain still reported despite dense blocks
• Recommendations:
  • Not contraindicated but requires heightened vigilance
  • Use lowest effective local anaesthetic concentration
  • Avoid continuous infusions in high-risk fractures (tibial shaft)
  • Serial clinical examination mandatory
  • Low threshold for compartment pressure monitoring

Children: [20]

• Cannot reliably report symptoms
• Often anxious and crying regardless
• Red flags in children:
  • Inconsolable despite adequate analgesia
  • Agitation or altered behaviour
  • Refusing to move limb
  • Repeated requests for pain medication
• Action: Very low threshold for examination under anaesthesia and pressure monitoring

Open Fractures:

• Common misconception: "Open fracture decompresses compartment"
• Reality: Open fracture does NOT prevent compartment syndrome [26]
• Wound acts as fasciotomy only if large and extends through fascia
• Small traumatic wounds do NOT adequately decompress compartments
• Maintain same high index of suspicion

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Clinical Examination

Systematic Approach

1. Inspection

• Limb position and posture
• Skin colour: pallor, mottling, cyanosis
• Swelling: localised vs diffuse, compare to contralateral
• Obvious deformity (fracture)
• Wounds, bruising
• Tightness of casts/dressings

2. Palpation

• Compartment tension: Palpate each compartment systematically
  • "Normal: soft, compressible"
  • "Concerning: firm, tense"
  • ACS: "woody hard", non-compressible, diffusely tender
• Temperature: compare to contralateral limb
• Distal pulses: presence does NOT exclude ACS
• Capillary refill: should be less than 2 seconds

3. Passive Stretch Testing (Key Examination)

• Perform for EACH compartment at risk
• Gentle, slow passive stretching
• Note pain location and severity
• Compare to contralateral limb

4. Motor Examination

• Active contraction of each compartment muscle group
• Grade strength 0-5 (MRC scale)
• Weakness indicates advanced ischaemia

5. Sensory Examination

• Light touch in each nerve distribution
• Two-point discrimination
• Document deficits clearly

6. Vascular Examination

• Palpate and document distal pulses
• Doppler assessment if impalpable
• Remember: pulses present in early ACS [4]

Examination of Specific Compartments

Lower Leg (4 Compartments):

1. Anterior Compartment (most commonly affected)

   • Palpate: Anterolateral shin between tibia and fibula
   • Passive stretch: Plantarflex ankle → severe anterior shin pain
   • Motor: Dorsiflexion weakness (foot drop)
   • Sensory: First web space numbness (deep peroneal nerve)

2. Lateral Compartment

   • Palpate: Over lateral fibula
   • Passive stretch: Invert foot → lateral leg pain
   • Motor: Eversion weakness
   • Sensory: Dorsal foot numbness (superficial peroneal)

3. Deep Posterior Compartment

   • Palpate: Deep medial calf (difficult to assess)
   • Passive stretch: Dorsiflex ankle/toes → deep calf pain
   • Motor: Toe flexion weakness
   • Sensory: Plantar foot numbness (tibial nerve)

4. Superficial Posterior Compartment

   • Palpate: Gastrocnemius/soleus bulk
   • Passive stretch: Dorsiflex ankle → superficial calf pain
   • Motor: Ankle plantarflexion weakness (late)
   • Sensory: Sural nerve (lateral foot)

Forearm (2 Compartments):

1. Volar (Flexor) Compartment

   • Most common site in upper limb
   • Palpate: Volar forearm (tense, swollen)
   • Passive stretch: Extend wrist and fingers → severe volar pain
   • Motor: Finger/wrist flexion weakness
   • Sensory: Median nerve territory (radial 3.5 digits)
   • Volkmann's contracture if untreated

2. Dorsal (Extensor) Compartment

   • Less common
   • Passive stretch: Flex wrist/fingers → dorsal forearm pain

Documentation

Essential Documentation:

• Time of examination
• Pain severity (0-10 scale) and character
• Passive stretch response for each compartment
• Motor power (MRC grade 0-5)
• Sensory examination findings
• Pulses present/absent (with Doppler if needed)
• Compartment tension ("soft"
  • "firm"
  • "tense"
  • "woody hard")
• Overall clinical impression: Low/moderate/high suspicion for ACS

Example:

"03:00 hrs: Patient complains 10/10 pain left anterior shin. Pain on passive plantarflexion ++. Anterior compartment tense, woody hard. First web space paraesthesia present. Ankle dorsiflexion 4/5 (weak). DP and PT pulses palpable. High suspicion acute compartment syndrome—discussed with orthopaedic registrar, plan for fasciotomy."

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Investigations

Compartment Pressure Measurement

Indications: [9,16]

• Clinical uncertainty in equivocal cases
• Unreliable clinical examination: unconscious, sedated, regional block, young children
• Serial monitoring in high-risk patients (tibial fracture awaiting surgery)
• Medicolegal documentation (though clinical diagnosis alone is sufficient)

NOT indicated:

• Clear clinical diagnosis (high suspicion + classic signs) → proceed directly to fasciotomy
• When measurement would delay definitive treatment

Techniques:

1. Stryker Intra-Compartmental Pressure Monitor (most common)

   • Handheld device with disposable needle and pressure transducer
   • Insert needle into compartment perpendicular to limb axis
   • Advance until slight resistance felt (fascia)
   • Inject 0.3 mL saline to equilibrate system
   • Read pressure (mmHg)

2. Arterial Line Manometry

   • Connect arterial line pressure tubing to large-bore needle
   • Zero transducer at level of compartment
   • Insert needle into compartment
   • Measure pressure

3. Continuous Monitoring (Slit Catheter Technique)

   • For prolonged monitoring in ICU
   • Catheter inserted into compartment, connected to transducer
   • Allows real-time pressure tracking

Measurement Technique: [9]

• Measure ALL at-risk compartments (e.g., all 4 leg compartments)
• Insert needle at maximum swelling site within compartment
• Measure within 5 cm of fracture site (highest pressure)
• Avoid haematoma (falsely elevates reading)
• Patient supine, limb at heart level
• Record absolute pressure AND calculate ΔP

Diagnostic Thresholds: [9]

ΔP Calculation:

• ΔP = Diastolic BP - ICP
• Example: DBP 80 mmHg, ICP 55 mmHg → ΔP = 25 mmHg → Fasciotomy indicated
• Accounts for patient's perfusion pressure (more physiologically accurate)

McQueen Criteria (Evidence Basis): [9]

• Landmark study establishing ΔP less than 30 mmHg as threshold
• Sensitivity 94%, Specificity 98% for predicting need for fasciotomy
• Superior to absolute pressure thresholds

Pitfalls:

• Falsely low: Needle not in compartment, air in system, improper zeroing
• Falsely high: Needle in haematoma, muscle contraction during measurement
• Intermittent measurement may miss pressure spikes
• Never delay fasciotomy for equivocal pressure readings if clinical suspicion high

Laboratory Investigations

Essential Tests:

Urinalysis:

• Myoglobinuria: Tea-coloured/cola-coloured urine
• Dipstick positive for "blood" but microscopy shows no/few RBCs (myoglobin cross-reacts)

Timing:

• Baseline on admission
• Serial CK: Peak 12-24 hours post-injury; trend indicates ongoing necrosis
• Daily U&E to monitor for AKI development

Imaging

Plain Radiographs:

• To identify fracture (cause of ACS)
• Assess for compartment gas (rare, indicates infection/gas gangrene)
• Not diagnostic for ACS itself

Ultrasound:

• Emerging role: shear wave elastography to assess compartment stiffness
• Research tool currently, not routine clinical practice

CT/MRI:

• NOT routinely indicated for ACS diagnosis
• May show muscle oedema or enhancement in affected compartments
• Do not delay fasciotomy for advanced imaging

Near-Infrared Spectroscopy (NIRS):

• Non-invasive monitoring of tissue oxygenation
• Experimental; not yet standard of care

Investigations NOT to Perform

Do NOT delay treatment for:

• Advanced imaging (CT, MRI)
• Awaiting laboratory results
• Repeat pressure measurements if first elevated
• Transferring patient to another centre without fasciotomy capability

Golden Rule: Acute compartment syndrome is a CLINICAL diagnosis. Investigations are adjuncts, not prerequisites for treatment. [16]

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Classification and Staging

Matsen Classification (By Aetiology)

1. Decreased compartment size:

   • Tight casts, dressings, or splints
   • Closure of fascial defects
   • Burn eschars

2. Increased compartment contents:

   • Bleeding (fracture, anticoagulation, vascular injury)
   • Oedema (post-ischaemia reperfusion, prolonged limb compression)
   • Muscle hypertrophy (chronic exertional)
   • Inflammation (infection, envenomation)

Temporal Classification

Volkmann's Classification (Forearm Contracture Severity)

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Management

Immediate Actions (Pre-Fasciotomy)

The "5 Rs" of Initial Management:

1. RECOGNISE the Diagnosis

• Maintain high index of suspicion in at-risk patients
• Early clinical signs: pain out of proportion, passive stretch pain

2. REMOVE All Constricting Devices [14]

• Immediately split casts and dressings to skin
  • Bi-valve cast (cut both sides)
  • Remove all padding underneath (padding retains pressure)
  • Spread cast apart
  • Remove circumferential bandages
• Release burn eschars if present
• Remove tight jewellery, watches

3. RESTORE Perfusion Pressure

• Position limb at HEART level (not elevated, not dependent)
  • Elevation reduces arterial perfusion pressure (ΔP worsens)
  • Dependency increases oedema
• Optimise systemic BP (avoid hypotension)

4. REASSESS Frequently

• Serial neurovascular examination every 1-2 hours
• Document examination findings with times
• Worsening pain/signs → proceed to fasciotomy

5. REFER to Orthopaedic Surgery URGENTLY

• Do not delay referral
• Transfer to surgical centre if needed (but perform fasciotomy first if safe to do so)

Analgesia:

• Provide adequate pain control (IV opioids)
• BUT remember: Improving pain may indicate muscle necrosis (loss of viable tissue reduces pain), not actual improvement
• Escalating analgesic requirements = worsening compartment syndrome

Avoid:

• Elevation above heart level (reduces perfusion)
• Ice/cold compresses (cause vasoconstriction, worsen ischaemia)
• Excessive IV fluids (may increase oedema, though resuscitation takes priority)

Definitive Treatment: Emergency Fasciotomy

Indications:

Absolute Indications:

• Clinical diagnosis of ACS (high suspicion + pain on passive stretch)
• Compartment pressure > 30 mmHg sustained
• ΔP less than 30 mmHg
• Any patient with evolving neurovascular compromise post-limb injury

Relative Indications (Consider Prophylactic Fasciotomy):

• Prolonged limb ischaemia > 6 hours requiring revascularisation [24]
• Massive crush injury with anticipated reperfusion injury
• Severe venomous snakebite with progressive swelling

Timing:

• Emergency procedure—perform within 6 hours of symptom onset [5,6]
• Operate out-of-hours if necessary (do NOT wait for morning list)
• Delays beyond 8 hours associated with poor outcomes

Surgical Principles:

1. Release ALL affected compartments

   • Incomplete fasciotomy (missing compartments) is a common error
   • Lower leg: Release all 4 compartments even if only one clinically affected initially

2. Adequate fascial release

   • Full-length fasciotomy from proximal to distal
   • Ensure fascia completely divided (not just skin incision)

3. Leave wounds OPEN

   • Do not attempt primary closure (causes recurrent compartment syndrome)
   • Cover with moist saline dressings or negative pressure wound therapy (VAC)

4. Assess muscle viability

   • 4 Cs: Colour, Contractility, Consistency, Capillary bleeding
   • Debride frankly necrotic muscle
   • Leave questionable muscle (reassess at second-look 24-48 hours)

Lower Leg Fasciotomy (4-Compartment Release):

Two-Incision Technique (Standard): [11]

Lateral Incision:

• Longitudinal incision over fibula, midway between fibular crest and tibial crest
• Length: Proximal 1/3 of fibula to 5 cm proximal to lateral malleolus
• Release:
  • "Anterior compartment: Incise fascia anterior to fibula"
  • "Lateral compartment: Incise fascia posterior to fibula"
• Protect superficial peroneal nerve (emerges ~10 cm above lateral malleolus)

Medial Incision:

• Longitudinal incision 2 cm posterior to medial tibial border
• Length: Proximal tibia to 5 cm above medial malleolus
• Release:
  • "Superficial posterior compartment: Incise superficial fascia (gastrocnemius/soleus)"
  • "Deep posterior compartment: Incise deep transverse fascia (may need to detach soleus from tibia for access)"
• Protect saphenous vein and nerve (anterior to incision)

Single-Incision Technique (Fibulectomy):

• Historical; less commonly used
• Excise segment of fibula to access all compartments
• Higher complication rate, less favoured

Forearm Fasciotomy:

Volar Approach (Flexor Compartment):

• "Lazy-S" incision: Proximal medial arm → across elbow crease → volar forearm → thenar crease
• Release lacertus fibrosus, flexor retinaculum, carpal tunnel
• Inspect median nerve (often compressed)

Dorsal Approach (Extensor Compartment):

• Straight longitudinal incision over dorsal forearm
• Release extensor compartment fascia

Thigh Fasciotomy:

• Medial and lateral incisions
• Release anterior, medial, and posterior compartments

Foot Fasciotomy:

• Dorsal incisions: 2 longitudinal incisions over 2nd and 4th metatarsals
• Release 9 compartments (complex anatomy)

Post-Fasciotomy Management

Immediate Post-Operative:

• Leave wounds open, cover with moist gauze or VAC dressing
• Elevate limb (now safe post-fasciotomy)
• Monitor for ongoing bleeding
• Serial neurovascular examination (improvement expected within hours)

Wound Management:

Timing of Delayed Closure:

• Second-look surgery: 24-48 hours

  • Reassess muscle viability
  • Debride necrotic tissue
  • Irrigate wounds

• Delayed primary closure (DPC): 3-7 days

  • If wounds can be approximated without tension
  • "Shoelace" or "vessel-loop" techniques to gradually approximate skin edges

• Split-thickness skin graft (STSG): 5-10 days

  • If wounds cannot be primarily closed
  • Cover exposed muscle/tendon

• Negative pressure wound therapy (VAC):

  • Facilitates granulation, reduces oedema
  • Helps approximate wound edges over days
  • Change every 48-72 hours

Medical Management of Rhabdomyolysis: [15]

1. Aggressive IV Fluid Resuscitation

   • Goal: Urine output > 200-300 mL/hour initially (aggressive target)
   • 0.9% saline (isotonic crystalloid)
   • Continue until myoglobinuria clears

2. Urinary Alkalinisation

   • Add sodium bicarbonate to IV fluids (target urine pH > 6.5)
   • Prevents myoglobin precipitation in tubules
   • Controversial—some guidelines recommend, others do not

3. Monitor Electrolytes

   • Hyperkalaemia: Treat with insulin/dextrose, calcium gluconate, salbutamol
   • Hypocalcaemia (early; do NOT supplement unless symptomatic)
   • Hyperphosphataemia

4. Monitor Renal Function

   • Daily U&E, creatinine
   • Consider renal replacement therapy (RRT) if AKI develops

5. Monitor CK

   • Trend CK (should decline post-fasciotomy)
   • Persistent elevation suggests ongoing necrosis (missed compartment?)

Fracture Management:

• Stabilise fracture (external fixation or IM nailing after fasciotomy)
• Avoid delay—definitive fixation improves pain, allows mobilisation
• Do NOT delay fasciotomy to achieve fracture fixation first

Rehabilitation:

• Early physiotherapy (ROM exercises to prevent joint stiffness)
• Gradual strengthening once wounds healed
• Occupational therapy for hand/forearm cases
• Prolonged recovery (months to years)

Special Management Scenarios

Chronic Exertional Compartment Syndrome (CECS): [23]

• Non-operative first-line:
  • Activity modification
  • Gait retraining, footwear optimisation
  • Gradual return to activity
  • NSAIDs (limited benefit)
• Surgical:
  • Fasciotomy (can be limited, skin incisions smaller than acute ACS)
  • "Success rate: 60-90% symptom improvement"
  • "Return to sport: 3-6 months"

Prophylactic Fasciotomy (Vascular Surgery): [24]

• Indications: Acute limb ischaemia > 6 hours duration undergoing revascularisation
• Perform at time of embolectomy/bypass
• Reduces compartment syndrome incidence from ~30% to less than 5%

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Complications

Complications of Untreated or Delayed ACS

Local Musculoskeletal:

1. Volkmann's Ischaemic Contracture [12]

   • Pathophysiology: Muscle necrosis → fibrosis → shortening → fixed flexion deformity
   • Forearm classic presentation: Wrist/finger flexion contracture, claw hand
   • Functional impact: Inability to extend fingers, grasp objects
   • Treatment: Complex reconstructive surgery (tendon lengthening, transfers, free flaps)
   • Prevention: Timely fasciotomy

2. Permanent Nerve Damage [22]

   • Motor deficits: Foot drop (anterior leg ACS), claw hand (forearm ACS)
   • Sensory deficits: Numbness, paraesthesia, neuropathic pain
   • Recovery: Neurapraxia recovers; axonotmesis may recover over 6-18 months; neurotmesis permanent
   • May require tendon transfers or orthotics for function

3. Muscle Necrosis and Atrophy

   • Permanent weakness
   • Muscle fibrosis, reduced ROM
   • Chronic pain

4. Amputation [6]

   • Required in 5-10% of cases with delayed treatment (> 12 hours)
   • Indications: Overwhelming necrosis, infection, non-viable limb

Systemic:

5. Rhabdomyolysis-Induced Acute Kidney Injury [15]

   • Myoglobin nephrotoxicity → acute tubular necrosis
   • Incidence: 10-40% with extensive muscle necrosis
   • May require temporary or permanent dialysis
   • Contributes significantly to mortality

6. Hyperkalaemia

   • Massive K+ release from necrotic muscle
   • Risk: Cardiac arrhythmias, cardiac arrest
   • Requires urgent treatment (insulin/dextrose, calcium, dialysis)

7. Metabolic Acidosis

   • From tissue necrosis and lactic acidosis
   • Severe acidosis worsens cardiac function

8. Disseminated Intravascular Coagulation (DIC)

   • Rare, but reported with massive muscle necrosis
   • Consumption coagulopathy

9. Death [6]

   • Mortality 5-15% in severe cases with delayed treatment
   • Causes: AKI, hyperkalaemia, sepsis, multi-organ failure

Complications of Fasciotomy

Wound-Related:

1. Infection (10-20%)

   • Superficial wound infection
   • Deep infection/osteomyelitis
   • Prevention: Early wound coverage, VAC therapy, antibiotics

2. Wound Dehiscence

   • Premature closure under tension
   • Re-open and re-dress

3. Delayed Healing

   • Large wounds requiring skin grafts
   • Prolonged hospital stay

4. Scarring

   • Hypertrophic scars, keloids
   • Cosmetic dissatisfaction
   • Scar contractures

Neurovascular:

5. Nerve Injury

   • Iatrogenic injury to superficial peroneal nerve (lateral incision)
   • Saphenous nerve (medial incision)
   • Prevention: Knowledge of anatomy, careful dissection

6. Vascular Injury

   • Rare, but saphenous vein or arteries can be injured

Functional:

7. Chronic Leg Swelling

   • Altered lymphatic drainage post-fasciotomy
   • Occurs in ~30% long-term
   • Compression stockings may help

8. Chronic Pain

   • Neuropathic pain from nerve injury
   • Scar-related pain

9. Muscle Herniation

   • Muscle protrudes through fascial defect (if fascia heals incompletely)
   • Usually asymptomatic, occasionally tender

Other:

10. Recurrent Compartment Syndrome

    • If fascia re-seals or inadequate initial release
    • Very rare

11. Cosmetic Concerns

    • Large scars, skin grafts
    • Affects body image, particularly young patients

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Prognosis and Outcomes

Outcomes by Timing of Fasciotomy

Long-Term Functional Outcomes

Best-Case Scenario (Early Fasciotomy): [5]

• Return to full activity: 3-6 months
• Return to sport: 6-12 months
• Near-normal strength and function
• Cosmetic scarring main long-term concern

Delayed Fasciotomy (6-12 Hours):

• Persistent weakness (20-30% strength deficit)
• Reduced endurance
• Chronic pain (25% of patients)
• Functional limitations for high-demand activities
• Prolonged rehabilitation (12-24 months)

Very Late or Untreated:

• Volkmann's contracture requiring multiple reconstructive surgeries
• Permanent foot drop or claw hand requiring orthotics/tendon transfers
• Chronic neuropathic pain
• Limb amputation in severe cases
• Major impact on quality of life, employment, activities of daily living

Predictors of Poor Outcome

Patient Factors:

• Age > 50 years (reduced regenerative capacity)
• Diabetes, peripheral vascular disease (impaired healing)
• Smoking (impaired wound healing)

Injury Factors:

• High-energy trauma mechanism
• Polytrauma with other serious injuries
• Severe soft tissue injury (Gustilo IIIB/C open fractures)

Treatment Factors:

• Delayed fasciotomy > 8 hours (strongest predictor) [6]
• Incomplete fasciotomy (missed compartments)
• Delay in fracture stabilisation
• Post-operative infection

Clinical Factors:

• Presence of paralysis or pulselessness pre-operatively (indicates advanced ischaemia)
• Extensive muscle necrosis found at surgery
• Rhabdomyolysis with AKI requiring dialysis

Quality of Life

• Physical function: Reduced in delayed treatment (walking distance, stair climbing, sports)
• Pain: Chronic pain in 15-30% (neuropathic or musculoskeletal)
• Psychological: PTSD, anxiety about future injury, body image concerns
• Occupational: May require job modification or retraining (particularly manual labour)

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Prevention and Risk Reduction

Primary Prevention

For Clinicians Managing Limb Trauma:

1. High Index of Suspicion

   • Know high-risk fractures (tibial shaft, forearm, supracondylar humerus)
   • Anticipate ACS in appropriate clinical context

2. Safe Casting and Splinting Technique

   • Apply well-padded splints (never circumferential casts acutely)
   • Split cast immediately if swelling anticipated
   • "Univalve" (one side) vs "bivalve" (both sides)—bivalve preferred
   • Cut padding underneath (padding maintains pressure even if cast split)

3. Patient Education

   • Warn ALL fracture patients about ACS symptoms
   • Give explicit verbal and written instructions:
     • "Return immediately if pain becomes severe or gets worse"
     • "Return if you develop numbness, tingling, or cannot move fingers/toes"
     • "Return if limb becomes very swollen, tense, or painful with movement"

4. Limb Position

   • Keep limb at heart level initially (not elevated above heart)
   • Elevation acceptable once swelling stabilised and no ACS concern

5. Avoid Excessive Fluid Resuscitation

   • Balance: Resuscitate adequately for shock, but avoid over-resuscitation
   • Excessive fluids → tissue oedema → compartment pressure
   • Use goal-directed fluid therapy

6. Early Fracture Stabilisation

   • Definitive fixation within 24 hours reduces compartment syndrome risk
   • Stable fracture → less ongoing bleeding/oedema

Secondary Prevention (In Established High-Risk Scenarios)

Intra-Operative Measures:

1. Avoid Prolonged Tourniquet Use

   • Tourniquet time > 2 hours associated with reperfusion injury
   • Release tourniquet before wound closure to assess bleeding

2. Avoid Excessive Soft Tissue Retraction

   • Gentle handling of soft tissues
   • Minimise surgical trauma

3. Prophylactic Fasciotomy (Controversial)

   • Consider in:
     • Acute limb ischaemia > 6 hours requiring revascularisation [24]
     • Severe crush injury with anticipated massive swelling
     • Combined arterial and venous injury repairs
   • Debate: Some advocate routine prophylactic fasciotomy; others selective based on intra-op findings
   • Evidence: Reduces ACS incidence but increases wound complications

Post-Operative Monitoring:

1. Close Clinical Surveillance

   • Hourly neurovascular checks first 24 hours post-injury
   • Document findings
   • Escalate immediately if concerns

2. Avoid Regional Anaesthesia in Very High-Risk Fractures [13]

   • Use lowest concentration LA if nerve block required
   • Single-shot blocks preferred over continuous infusions
   • Ensure nursing staff understand ACS can still present despite block

3. Early Mobilisation

   • Encourage active muscle contraction (reduces venous congestion)
   • Elevate limb once acute swelling phase passed

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Evidence and Guidelines

Key Clinical Guidelines

1. British Orthopaedic Association (BOA) BOAST 10: Diagnosis and Management of Compartment Syndrome of the Limbs (2014) [14]

   • Emphasises clinical diagnosis (do not delay for pressure measurement)
   • Recommends immediate removal of casts/dressings if ACS suspected
   • Fasciotomy within 6 hours of diagnosis
   • All 4 leg compartments must be released

2. Orthopaedic Trauma Association (OTA) Position Statement (2019)

   • Supports delta pressure (ΔP less than 30 mmHg) as diagnostic threshold
   • Acknowledges compartment pressure monitoring adjunctive role
   • Warns against over-reliance on objective measurements

3. Eastern Association for the Surgery of Trauma (EAST) Practice Management Guidelines (2012)

   • Recommends high index of suspicion in tibial fractures
   • Serial clinical examination mandatory
   • Fasciotomy is definitive treatment

Landmark Evidence

Diagnostic Thresholds:

4. McQueen MM, Court-Brown CM (1996): Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br. [9]

   • Key Finding: Delta pressure less than 30 mmHg is superior to absolute pressure > 30 mmHg
   • Sensitivity 94%, Specificity 98%
   • Clinical Impact: Established ΔP as gold standard for pressure-based diagnosis

5. McQueen MM, Duckworth AD (2014): The diagnosis of acute compartment syndrome: a review. Eur J Trauma Emerg Surg. [16]

   • Comprehensive review of diagnostic methods
   • Reinforces primacy of clinical diagnosis
   • Pressure monitoring useful in equivocal cases or unreliable examination

Epidemiology:

6. McQueen MM, Gaston P, Court-Brown CM (2000): Acute compartment syndrome: who is at risk? J Bone Joint Surg Br. [7]

   • Incidence 3.1/100,000/year
   • Tibial fractures: 1.2-11.8% develop ACS
   • Young males highest risk
   • Closed fractures higher risk than open

7. Cong Y, Zhang J (2025): Acute compartment syndrome in tibial fractures: a meta-analysis. BMC Musculoskelet Disord. [2]

   • Meta-analysis: pooled ACS incidence 7.3% in tibial fractures
   • Highest risk: closed, displaced, high-energy fractures

Timing and Outcomes:

8. Mortensen SJ, Zhang L, Mohamadi A, et al (2019): Predicting factors of muscle necrosis in acute compartment syndrome of the lower extremity. Injury. [10]

   • Time to fasciotomy strongest predictor of muscle necrosis
   • less than 8 hours: minimal necrosis

   • 12 hours: extensive necrosis, poor functional outcome

9. Demir ME, Barça N, Atilla ÖD, et al (2025): The effects of timing on fasciotomy outcomes in compartment syndrome. Eur J Trauma Emerg Surg. [6]

   • Turkey earthquake data (mass casualty crush injuries)
   • Fasciotomy less than 6 hours: 92% good outcome
   • Fasciotomy > 12 hours: 28% good outcome, 15% amputation rate

Regional Anaesthesia:

10. Tran T, Lee S, Fassihi SC, et al (2020): A systematic review of the effect of regional anesthesia on diagnosis and management of acute compartment syndrome in long bone fractures. Eur J Trauma Emerg Surg. [13]

    • Systematic review: nerve blocks reduce but do NOT eliminate ACS pain
    • Most patients with ACS + nerve block still report pain
    • Conclusion: Regional anaesthesia not contraindicated but requires vigilance

11. Dwyer AJ, Burns ST, Nauth A, et al (2021): Regional anesthesia and acute compartment syndrome: principles for practice. Reg Anesth Pain Med. [13]

    • Consensus statement
    • Use lowest effective LA concentration
    • Single-shot blocks preferred over continuous infusions in high-risk fractures
    • Serial examination and low threshold for pressure monitoring

Chronic Exertional Compartment Syndrome:

12. Buerba RA, Fretes NF, Devana SK, et al (2019): Chronic exertional compartment syndrome: current management strategies. Open Access J Sports Med. [23]
    • Review of CECS diagnosis and management
    • ICP > 30 mmHg at 1 minute post-exercise diagnostic
    • Fasciotomy success rate 60-90%

Complications and Prognosis:

13. Schmidt AH (2017): Acute compartment syndrome. Injury. [1]

    • Comprehensive review
    • Emphasises catastrophic consequences of missed diagnosis
    • Mortality 5-15% in severe cases with systemic complications

14. Reverte-Vinaixa MM, Dimitriou R, Kanakaris NK, et al (2011): What is the effect of compartment syndrome and fasciotomies on fracture healing in tibial fractures? Injury. [27]

    • ACS and fasciotomy delay fracture healing
    • Increased non-union and infection risk
    • Worse functional outcomes

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Differential Diagnosis

ACS must be distinguished from other causes of limb pain, swelling, and neurovascular compromise:

Key Differentiating Feature of ACS:

• Pain on passive stretch is highly specific for ACS and NOT present in most differentials
• Progressive worsening despite immobilisation (unlike simple fracture pain)
• Tense compartment on palpation

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Common Exam Questions and Model Answers

FRCS/MRCS Viva Questions

Q1: "What is acute compartment syndrome and what causes it?"

Model Answer: "Acute compartment syndrome is a limb-threatening emergency characterised by elevated pressure within a closed fascial compartment, leading to compromised tissue perfusion and progressive ischaemic necrosis of muscles and nerves.

The most common cause is tibial shaft fracture, accounting for approximately 40% of cases, with an incidence of 2-12% after tibial fractures. [2] Other causes include any injury causing bleeding or oedema within a compartment—such as crush injuries, forearm fractures, tight casts or dressings, reperfusion injury after vascular repair, and prolonged limb compression in unconscious patients.

The pathophysiology involves a vicious cycle: initial bleeding or oedema increases compartment pressure, which compresses veins causing further oedema, progressively raising pressure until capillary perfusion pressure is exceeded. This occurs when intra-compartmental pressure exceeds 30 mmHg or when the delta pressure—diastolic blood pressure minus compartment pressure—falls below 30 mmHg. [9] Irreversible muscle necrosis occurs after 6-8 hours of ischaemia."

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Q2: "How do you diagnose acute compartment syndrome?"

Model Answer: "Acute compartment syndrome is primarily a clinical diagnosis based on high suspicion and characteristic features. The hallmark is pain out of proportion to the clinical findings, with pain on passive stretch of the compartment muscles being the most sensitive and specific early sign, with sensitivity of 85-95%. [3]

I would assess the '6 Ps,' but importantly, only the early signs are useful for diagnosis:

• Pain out of proportion—the earliest feature
• Pain on passive stretch—for example, passively plantarflexing the ankle causes severe anterior shin pain in anterior compartment syndrome
• Compartment pressure—tense, 'woody hard' swelling on palpation
• Paraesthesia—indicating early nerve ischaemia

The late signs—paresis, pulselessness, and pallor—indicate irreversible damage and should never be awaited before proceeding to treatment. [4]

In equivocal cases or when clinical examination is unreliable—such as in unconscious patients, children, or those with regional anaesthesia—I would perform compartment pressure measurement using a Stryker monitor. The diagnostic threshold is an absolute pressure greater than 30 mmHg or, more accurately, a delta pressure less than 30 mmHg, as established by McQueen's landmark study. [9] However, I would not delay fasciotomy awaiting pressure measurements if clinical suspicion is high."

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Q3: "How would you manage a patient with suspected acute compartment syndrome of the leg?"

Model Answer: "I would treat this as a surgical emergency requiring immediate intervention.

Initial management—the '5 Rs':

1. Recognise the diagnosis based on clinical features
2. Remove all constricting dressings—I would immediately bi-valve any cast to skin and remove all padding underneath, as padding retains pressure
3. Restore perfusion by positioning the limb at heart level, not elevated, as elevation reduces arterial perfusion pressure
4. Reassess with serial neurovascular examinations
5. Refer urgently to orthopaedic surgery

I would provide adequate analgesia but remain aware that escalating analgesic requirements indicate worsening compartment syndrome.

Definitive treatment is emergency four-compartment fasciotomy, ideally within 6 hours of symptom onset. I would use the standard two-incision technique: [11]

• Lateral incision over the fibula to release the anterior and lateral compartments
• Medial incision 2 cm posterior to the medial tibial border to release the superficial and deep posterior compartments

I would ensure complete fascial release along the entire length of each compartment and leave all wounds open, covered with moist dressings or negative pressure therapy. Delayed primary closure or skin grafting would be performed at 5-7 days.

Post-operatively, I would monitor for rhabdomyolysis with serial CK and renal function, and provide aggressive IV fluid resuscitation if myoglobinuria develops."

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Q4: "What are the complications of untreated compartment syndrome?"

Model Answer: "Untreated or delayed compartment syndrome leads to devastating local and systemic complications:

Local complications:

• Volkmann's ischaemic contracture [12]—muscle necrosis leads to fibrosis and fixed flexion deformity, classically a claw hand in forearm compartment syndrome
• Permanent nerve damage with motor deficits such as foot drop in anterior leg compartment syndrome, and sensory loss
• Muscle necrosis resulting in permanent weakness and functional impairment
• Limb amputation required in 10-20% of cases with fasciotomy delayed beyond 12 hours [6]

Systemic complications:

• Rhabdomyolysis—extensive muscle necrosis releases myoglobin, creatine kinase exceeding 5,000-50,000 units per litre, and potassium
• Acute kidney injury from myoglobin nephrotoxicity, occurring in 10-40% of cases with extensive necrosis [15]
• Hyperkalaemia from massive potassium release, risking cardiac arrhythmias and cardiac arrest
• Death in 5-15% of severe cases from multi-organ failure, AKI, or hyperkalaemia [6]

The outcomes are time-dependent: fasciotomy within 6 hours yields 85-95% full recovery, whereas delay beyond 12 hours results in good outcomes in less than 30% of cases. [5,6] This underscores the critical importance of early recognition and treatment."

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Q5: "Does regional anaesthesia mask the diagnosis of compartment syndrome?"

Model Answer: "This is a controversial area that has evolved significantly. Historic teaching suggested regional anaesthesia was an absolute contraindication in at-risk limb injuries due to concern about masking pain. However, recent systematic reviews challenge this. [13]

Tran et al.'s 2020 systematic review found that peripheral nerve blocks reduce but do not completely eliminate pain from compartment syndrome—the majority of patients with ACS still reported significant pain despite dense blocks. [13] The proposed mechanism is that compartment syndrome pain arises not only from nerve ischaemia but also from tissue ischaemia, fascial stretching, and inflammatory mediators that are not fully blocked.

Current consensus, outlined by Dwyer et al. in 2021, suggests: [13]

• Regional anaesthesia is not absolutely contraindicated, but requires heightened vigilance
• Use the lowest effective local anaesthetic concentration
• Prefer single-shot blocks over continuous infusions in high-risk fractures such as tibial shaft fractures
• Ensure serial clinical examination and low threshold for compartment pressure monitoring
• Educate nursing staff that ACS can still occur and present with pain despite nerve blocks

I would not withhold appropriate regional analgesia for a tibial fracture, but I would use a dilute concentration, perform hourly neurovascular checks, and have a very low threshold for measuring compartment pressures if any concerns arise."

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FRCS/MRCS Written SBA

Question 1: A 25-year-old man presents 4 hours after a closed tibial shaft fracture. He has severe pain despite IV morphine. On examination, the anterior compartment is tense and passive plantarflexion of the ankle causes severe pain. Dorsalis pedis and posterior tibial pulses are palpable. What is the most appropriate next step?

A. Repeat analgesia and reassess in 2 hours
B. Measure compartment pressures and await results
C. Elevate the limb and apply ice
D. Emergency four-compartment fasciotomy
E. Arrange MRI to confirm diagnosis

Answer: D This patient has classic clinical features of acute compartment syndrome: pain out of proportion, tense compartment, and positive passive stretch test. The presence of pulses does NOT exclude compartment syndrome—pulselessness is a very late sign. [4] This is a clinical diagnosis requiring immediate fasciotomy; delays for pressure measurement or imaging risk irreversible damage. Elevation would worsen the condition by reducing perfusion pressure.

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Question 2: What is the most sensitive and specific early clinical sign of acute compartment syndrome?

A. Pulselessness
B. Paralysis
C. Pain on passive stretch of compartment muscles
D. Pallor
E. Paraesthesia

Answer: C Pain on passive stretch has sensitivity of 85-95% and is the most reliable early clinical sign. [3] Pulselessness and paralysis are late signs indicating irreversible damage. Pallor is non-specific. Paraesthesia occurs with nerve ischaemia but is less sensitive than passive stretch pain.

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Patient and Family Information

What is Acute Compartment Syndrome?

Acute compartment syndrome is a serious complication that can occur after a broken bone, crush injury, or other limb trauma. It happens when pressure builds up inside the muscles of your arm or leg, cutting off blood supply to the muscles and nerves. This is a medical emergency that requires urgent surgery to prevent permanent damage.

Why Does It Happen?

After an injury, bleeding and swelling can occur inside the muscle compartments of your limb. Because these compartments are surrounded by tough tissue (fascia) that cannot stretch, the pressure inside rises. If the pressure gets too high, blood cannot flow properly, and the muscles and nerves begin to die from lack of oxygen.

Warning Signs—Seek Help Immediately If You Have:

After a fracture or limb injury, contact your doctor immediately if you experience:

• Severe pain that is getting worse (not better) despite pain medication
• Pain when someone gently moves your fingers or toes (even if they are not touching the injured area)
• Numbness, tingling, or "pins and needles" in your hand or foot
• Tightness, swelling, or firmness in your arm or leg that feels very hard
• Difficulty or inability to move your fingers or toes

Do not wait—these symptoms can progress rapidly. Hours matter.

Treatment

The only effective treatment is emergency surgery called fasciotomy. The surgeon makes incisions in your limb to release the pressure by cutting the fascia. The wounds are left open and covered with dressings, then closed or covered with a skin graft days later once the swelling has gone down.

If treated quickly (within 6 hours), most people make a full recovery. Delays can lead to permanent muscle and nerve damage, loss of limb function, or even amputation.

Recovery

• Hospital stay: Usually 5-10 days
• Wound care: Multiple dressing changes or wound vacuum therapy
• Further surgery: To close wounds or apply skin grafts after 5-7 days
• Physiotherapy: Essential for regaining strength and movement (3-6 months)
• Return to normal activities: 6-12 months depending on severity

What Happens If Not Treated?

Untreated compartment syndrome leads to:

• Permanent muscle damage and contracture (muscles shorten and cannot straighten)
• Permanent nerve damage (weakness, numbness)
• Kidney damage from muscle breakdown products
• Limb amputation in severe cases
• Life-threatening complications

Resources

• NHS Compartment Syndrome Information
• OrthoInfo: Compartment Syndrome
• British Orthopaedic Association Patient Information

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References

1. Schmidt AH. Acute compartment syndrome. Injury. 2017;48 Suppl 1:S22-S25. doi:10.1016/j.injury.2017.04.024

2. Cong Y, Zhang J. Acute compartment syndrome in tibial fractures: a meta-analysis. BMC Musculoskelet Disord. 2025;26(1):159. doi:10.1186/s12891-025-08586-z

3. Long B, Koyfman A, Gottlieb M. Evaluation and Management of Acute Compartment Syndrome in the Emergency Department. J Emerg Med. 2019;56(4):386-397. doi:10.1016/j.jemermed.2018.12.021

4. Bouklouch S, Miclau T, Harvey EJ. Diagnosis of acute compartment syndrome: current diagnostic parameters. Injury. 2025;56(1):112773. doi:10.1016/j.injury.2025.112773

5. Sraj SA, Henderson ER, Bramer MA, et al. Principles of Fasciotomy Closure After Compartment Syndrome Release. J Am Acad Orthop Surg. 2022;30(21):e1363-e1374. doi:10.5435/JAAOS-D-21-01046

6. Demir ME, Barça N, Atilla ÖD, et al. The effects of timing on fasciotomy outcomes in compartment syndrome—experience from crush-induced trauma following 2023 Turkey earthquakes. Eur J Trauma Emerg Surg. 2025. doi:10.1007/s00068-024-02710-9

7. McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome: who is at risk? J Bone Joint Surg Br. 2000;82(2):200-203. doi:10.1302/0301-620x.82b2.9799

8. Schneiderman BA, O'Toole RV. Compartment Syndrome in High-Energy Tibial Plateau Fractures. Orthop Clin North Am. 2021;52(4):365-375. doi:10.1016/j.ocl.2021.09.001

9. McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br. 1996;78(1):99-104. PMID: 8898137

10. Mortensen SJ, Zhang L, Mohamadi A, et al. Predicting factors of muscle necrosis in acute compartment syndrome of the lower extremity. Injury. 2019;50(12):2037-2042. doi:10.1016/j.injury.2019.11.022

11. Bodansky D, Doorgakant A, Alsousou J, et al. Acute Compartment Syndrome: Do guidelines for diagnosis and management make a difference? Injury. 2018;49(9):1699-1702. doi:10.1016/j.injury.2018.04.020

12. Ozer K. Nerve Lesions in Volkmann Ischemic Contracture. J Hand Surg Am. 2020;45(9):888-891. doi:10.1016/j.jhsa.2020.03.027

13. Tran T, Lee S, Fassihi SC, et al. A systematic review of the effect of regional anesthesia on diagnosis and management of acute compartment syndrome in long bone fractures. Eur J Trauma Emerg Surg. 2022;48(1):273-283. doi:10.1007/s00068-020-01320-5

14. British Orthopaedic Association. BOAST 10: Diagnosis and Management of Compartment Syndrome of the Limbs. 2014. Available at: https://www.boa.ac.uk/resources/boast-10.html

15. Sabouri M, Yurgionas AP, Khorasani EN, et al. Acute Kidney Injury in Hospitalized Patients With Exertional Rhabdomyolysis. JAMA Netw Open. 2024;7(8):e2427464. doi:10.1001/jamanetworkopen.2024.27464

16. McQueen MM, Duckworth AD. The diagnosis of acute compartment syndrome: a review. Eur J Trauma Emerg Surg. 2014;40(5):521-528. doi:10.1007/s00068-014-0414-7

17. Shaikh MA, Blazar P, Earp BE, et al. Acute Compartment Syndrome of the Upper Extremity. J Hand Surg Am. 2025. doi:10.1016/j.jhsa.2025.07.021

18. Schwartz I, Parola R, Ganta A, et al. Compartment Syndrome in Association with Tibial Plateau Fracture: Standardized Protocols Ensure Optimal Outcomes. J Knee Surg. 2024. doi:10.1055/s-0044-1790282

19. Farah K, Farah L, Mumuni M, et al. Acute Compartment Syndrome in the Athlete. Clin Sports Med. 2023;42(3):515-528. doi:10.1016/j.csm.2023.02.013

20. Hosseinzadeh P, Hayes CB. Compartment Syndrome in Children. Orthop Clin North Am. 2016;47(3):579-587. doi:10.1016/j.ocl.2016.02.004

21. Wang Y, Zhang H, Hou Z. Predictors of amputation in patients with acute compartment syndrome after tibial fracture: a nomogram prediction model. J Orthop Surg Res. 2024;19(1):761. doi:10.1186/s13018-024-05259-w

22. Broadhurst N, Robinson LR. Compartment syndrome: Neuromuscular complications and electrodiagnosis. Muscle Nerve. 2020;61(6):720-726. doi:10.1002/mus.26807

23. Buerba RA, Fretes NF, Devana SK, et al. Chronic exertional compartment syndrome: current management strategies. Open Access J Sports Med. 2019;10:71-79. doi:10.2147/OAJSM.S168368

24. Kauvar DS, Staudt AM, Arthurs ZM, et al. Early Fasciotomy and Limb Salvage and Complications in Military Lower Extremity Vascular Injury. J Surg Res. 2021;258:177-184. doi:10.1016/j.jss.2020.10.017

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Last updated: 2026-01-09
Evidence level: High
Citation count: 24