Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Acute compartment syndrome
Musculoskeletal medicine and orthopaedics · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Acute compartment syndrome is an immediate surgical emergency
Raised pressure within a closed myofascial space compromises muscle and nerve microcirculation; delay causes necrosis, contracture, rhabdomyolysis, renal failure, infection, amputation and death even while distal pulses remain palpable.
Action: Call a senior orthopaedic decision-maker immediately, release circumferential dressings and expose the limb, correct hypotension, elevate safely and reassess within 30 minutes, perform hourly documented examinations or concurrent pressure monitoring if findings are incomplete, and proceed to NCEPOD-1 decompression as soon as the diagnosis is made.
Overview
Recognise evolving compartment ischaemia from serial clinical change, release external pressure, use concurrent blood-pressure and compartment-pressure data when examination is uncertain, and achieve immediate complete decompression before irreversible injury.
Acute compartment syndrome is dynamic. Record the precise mechanism, time of injury, crush or ischaemia duration, anticoagulants, regional anaesthesia, operations and dressings. Identify high-risk fractures and reperfusion, but remember that compartment syndrome can occur without fracture. Examine the whole limb for wounds, deformity and external constriction. Palpation for tension is subjective, so compare compartments and place greatest weight on change over time, pain behaviour, passive stretch and evolving neurological function.
Examine the muscles and nerves belonging to each compartment rather than writing neurovascularly intact. In the leg, passive toe movement can stress affected muscles, while deep fibular sensation in the first web space and tibial plantar sensation provide named baselines. In the forearm, passive finger or wrist extension may reproduce flexor-compartment pain. Severe injury can damage a nerve independently, so document modalities and trends with the time, examiner and analgesia already given.
Practice
Two practice questions
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Question 1 of 2
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Musculoskeletal medicine and orthopaedicsOriginal SBA
Perfused but painful leg
A patient with a tibial fracture has escalating pain, passive-toe-stretch pain and new first-web-space tingling, but dorsalis pedis and posterior tibial pulses remain palpable. What is the best immediate interpretation?
Sources and review status3 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
BOASt specifies a structured response. Release circumferential dressings completely to skin, correct hypotension, position the limb without compromising perfusion and re-evaluate within thirty minutes. Call a senior surgeon capable of deciding on fasciotomy. Continue hourly documented examination in an at-risk or uncertain patient. Dense nerve block requires a joint anaesthetic-surgical monitoring plan; it is not a reason to abandon surveillance. New symptoms during transfer or after fixation reset the urgency.
Pressure measurement supports, rather than replaces, judgement. Use a validated technique and measure every clinically suspected compartment near the injury, avoiding the fracture haematoma where possible. Record compartment and simultaneous diastolic pressures. A delta pressure below thirty millimetres of mercury indicates increased risk; an absolute pressure above forty millimetres of mercury also prompts urgent decompression consideration. Repeat or continuous measurements are more informative than an isolated value when findings evolve.
A convincing clinical diagnosis proceeds directly to surgery. Decompress the entire length of all involved compartments with incisions that permit inspection, excise clearly non-viable tissue and document each structure and muscle group. In the lower leg, incomplete single-incision release risks leaving deep posterior or anterior tissue pressurised; BOASt recommends a two-incision four-compartment technique. Associated vascular injury, fracture stabilisation and contamination require a coordinated operative sequence without allowing definitive fixation to delay perfusion or release.
Leave fasciotomy wounds open at the index operation. Mark questionable tissue, plan critical-care support and return for re-examination and further debridement as physiology and muscle demarcation require. BOASt asks for plastic-surgical discussion within twenty-four hours and re-exploration within seventy-two hours or sooner. Delayed presentation is difficult: opening a compartment containing established necrosis may release toxic products and infection, so two consultants should weigh operative and non-operative protection with renal assessment.
After release, treat the whole reperfusion syndrome. Monitor ECG, potassium, acid-base state, creatine kinase, renal function and urine output, and manage hyperkalaemia immediately. Reassess pulses and nerves because arterial injury may coexist. Rehabilitation begins after tissue viability and coverage are secure and addresses joint movement, scar, muscle loss, splintage, neuropathic pain and psychological harm. Explain that timely decompression reduces risk but does not guarantee normal function after severe initial ischaemia.
Key points
Suspect acute compartment syndrome from the trajectory: worsening pain, passive-stretch pain, swelling, sensory change and analgesic escalation matter more than any single normal earlier examination.
Do not use palpable pulses to exclude it. Pulselessness is late or indicates a separate arterial emergency and should prompt simultaneous vascular and orthopaedic action.
BOASt requires hourly assessment of an at-risk patient, documenting time, mechanism, consciousness, neurology, circulation, pain, analgesic dose and response, interpretation and management rationale.
For symptoms or signs, split or remove circumferential dressings, expose and safely elevate the limb, correct systemic hypotension and re-evaluate within 30 minutes with senior review.
If clinical assessment is incomplete or inconclusive, measure every suspected compartment with concurrent blood pressure; a diastolic-minus-compartment pressure below 30 mmHg indicates increased risk.
An absolute compartment pressure above 40 mmHg supports considering urgent decompression, but a reassuring single reading does not overrule progressive clinical findings or exclude another compartment.
Once diagnosed, perform immediate open decompression of every involved compartment and excise non-viable muscle; lower-leg treatment generally uses a two-incision four-compartment fasciotomy.
Aetiology
01
Fracture and soft-tissue trauma
Tibial-shaft, forearm and high-energy peri-articular fractures cause bleeding and oedema within closed compartments, with risk driven by energy rather than radiographic displacement alone.
02
Reperfusion and crush
Restored arterial inflow after ischaemia and release after prolonged compression generate capillary leak and muscle swelling that can raise pressures rapidly.
03
External restriction
Circumferential casts, tight bandages, pneumatic devices, burn eschar or limb positioning can add extrinsic pressure to an already swollen compartment.
04
Bleeding and iatrogenic causes
Anticoagulation, coagulopathy, vascular puncture, infusion extravasation and prolonged surgery can fill a compartment without an associated fracture.
Pathophysiology
1
Falling perfusion gradient
As intracompartmental pressure approaches diastolic pressure, capillary flow falls and tissue oxygen delivery becomes inadequate despite continued flow in larger distal arteries.
2
Oedema amplification
Ischaemic endothelium leaks fluid, increasing compartment volume and pressure in a positive feedback loop that further reduces microvascular perfusion.
3
Nerve and muscle injury
Peripheral nerves develop conduction failure and muscle fibres undergo irreversible necrosis with prolonged ischaemia, producing weakness, contracture and chronic neuropathic pain.
4
Systemic toxin release
Necrotic muscle releases potassium, phosphate, myoglobin and acids, causing arrhythmia, metabolic acidosis and pigment-associated acute kidney injury.
5
Pulse preservation
Compartment pressure usually compromises capillary flow before arterial inflow, so palpable pulses and normal capillary refill cannot exclude dangerous muscle ischaemia.
Clinical features and red flags
Early evolving syndrome
Increasing pain, passive-stretch pain and analgesic escalation in a swollen at-risk limb precede many objective sensory or motor abnormalities.
Progressive nerve ischaemia
New tingling, reduced two-point or light-touch sensation and weakness across a compartment nerve distribution indicate deterioration and shorten the safe decision window.
Unreliable examination
Intubation, intoxication, cognitive impairment, childhood or dense regional block removes pain reporting and increases the value of objective repeated examination and pressure monitoring.
Reperfusion-associated syndrome
A limb that swells and becomes tense after arterial repair or crush release can develop compartment pressure despite restored distal pulses.
Late destructive syndrome
Anaesthesia, paralysis, fixed contracture, pallor and systemic hyperkalaemia imply advanced muscle and nerve injury rather than a reassuring absence of pain.
Concurrent arterial injury
Pulse inequality, coolness, delayed refill or persistent dysvascularity after realignment requires immediate vascular input alongside compartment assessment.
Red flags requiring action
Increasing pain out of proportion to the injury, pain on passive stretch of muscles crossing the compartment, a tense swollen segment or rapidly rising opioid requirement requires immediate reassessment and escalation.
Investigations
01First-line serial clinical examinationFirst stepFirst line
Why
Detect change early enough for limb-saving decompression.
Interpretation and limitations
Perform and document at least hourly in at-risk patients, increasing frequency with symptoms; include pain trajectory, passive stretch, tension, nerves and circulation.
02Concurrent compartment and diastolic pressures
Why
Support diagnosis when examination is incomplete or equivocal.
Interpretation and limitations
A delta pressure below 30 mmHg indicates increased risk; measure every suspected compartment and interpret trends with the clinical picture and senior judgement.
03Absolute compartment pressure
Why
Provide an additional objective danger signal.
Interpretation and limitations
A pressure above 40 mmHg supports urgent decompression consideration, but systemic pressure and measurement site affect meaning and no single value safely clears a deteriorating limb.
04Arterial assessment and CT angiography
Why
Detect coexisting macrovascular injury rather than misattributing ischaemia.
Interpretation and limitations
Realign a pulseless deformity and repeat examination; use urgent CT angiography for persistent suspected arterial injury when it will not delay emergency revascularisation.
Differential diagnosis
01
Arterial occlusion
A cold pale pulseless limb with abrupt neurological deficit suggests macrovascular ischaemia, although arterial injury and compartment syndrome can coexist after trauma or repair.
02
Expected fracture pain
Severe early pain may respond predictably to alignment and analgesia, whereas compartment pain escalates, becomes disproportionate and recurs despite treatment.
03
Peripheral nerve injury
A focal deficit matching one nerve at the injury site differs from progressive dysfunction across nerves traversing a tense compartment.
04
Deep-vein thrombosis
Calf swelling and tenderness usually evolve less acutely and do not cause passive-stretch pain or a tense post-traumatic compartment, but still need assessment.
05
Necrotising infection
Toxic illness, rapidly spreading tenderness, skin discolouration and fascial infection can create compartment-like pain and may require both radical debridement and decompression.
Management
01SuspectedRelease pressure and reassessFirst stepEscalationAn at-risk limb develops disproportionate pain, passive-stretch pain, tension, analgesic escalation or neurological change.+
1Contact senior orthopaedics immediately and record examination, time, analgesia, blood pressure and the change that triggered concern.
2Remove circumferential dressings to skin, correct hypotension, expose and position the limb safely and re-evaluate within 30 minutes.
3Continue hourly structured examination and obtain concurrent pressure monitoring when pain reporting or the clinical picture is incomplete.
4Maintain arterial surveillance and activate vascular care if perfusion remains abnormal after realignment or external pressure release.
02ConfirmedDecompress every involved compartmentClinical findings establish the diagnosis or senior interpretation of pressure and examination data indicates dangerous perfusion.+
Complications
01
Volkmann contracture
Muscle necrosis heals with fibrosis and shortening, creating fixed deformity, weakness and loss of hand or foot function that may require complex reconstruction.
02
Rhabdomyolysis and renal injury
Myoglobin, hyperkalaemia and acid load after necrosis or reperfusion cause arrhythmia, acute kidney injury, dialysis requirement and systemic deterioration.
03
Infection and amputation
Dead muscle and open fasciotomy wounds invite deep infection; extensive necrosis or uncontrolled sepsis may make limb salvage impossible.
04
Chronic neurological deficit
Delayed decompression can leave permanent numbness, motor loss, neuropathic pain and impaired gait or dexterity despite fracture union.
05
Wound morbidity
Fasciotomy requires planned re-exploration, debridement and delayed coverage and can cause scarring, graft morbidity, hernia and prolonged rehabilitation.
Monitoring and follow-up
Use an hourly compartment chart for every at-risk patient, recording negative as well as positive findings, interpretation and the named clinician responsible for action.
Record all opioid doses, infusion rates, regional blocks and pain response so increasing treatment requirement is visible rather than dismissed as expected fracture pain.
Repeat named nerve, pulse, Doppler, temperature and capillary-refill findings after dressing release, realignment, fasciotomy, vascular repair and each handover.
After decompression, trend ECG, potassium, bicarbonate, calcium, phosphate, CK, creatinine and urine output for reperfusion and rhabdomyolysis.
Inspect muscle and wounds at planned re-exploration, documenting further necrosis, infection, swelling and suitability for closure or coverage.
Follow joint range, power, sensation, contracture, neuropathic pain, scar tolerance and patient-defined hand, walking, work or self-care goals.
Special situations
The diagnosis is a trend
A normal examination at admission cannot clear a limb exposed to continuing bleeding, swelling or reperfusion over subsequent hours.
Delta pressure includes physiology
The same measured compartment pressure is more dangerous when diastolic blood pressure falls, explaining why shock correction is part of limb care.
Measure the right place
Pressure varies between compartments and along a limb, so sampling a single convenient site can miss focal dangerous pressure.
Analgesia is still required
Withholding humane pain relief is not a diagnostic test; structured dose and response documentation reveals escalation while preventing unnecessary suffering.
Fasciotomy is not a small incision
A limited skin opening without complete fascial release along every involved compartment leaves the causal pressure uncorrected.
Late release needs senior judgement
Established necrosis changes the balance because decompression can add reperfusion toxicity and infection without restoring dead muscle.
Common pitfalls
01
Using present pulses, normal capillary refill or a single pressure measurement to exclude compartment syndrome.
02
Writing neurovascularly intact without named nerve modalities, time, analgesic exposure and comparison with the previous examination.
03
Leaving the inner cast padding or circumferential bandage intact after splitting only the hard outer shell.
04
Waiting for paralysis, pallor, pulselessness, CK elevation or MRI before surgical decision-making.
05
Releasing only the most obvious compartment or using an incision too short for complete fascial decompression.
06
Closing fasciotomy wounds under tension at the index operation or omitting planned re-exploration and plastic-surgical input.
Discuss the patient with plastic surgery within 24 hours and re-explore within 72 hours or earlier when indicated, leaving a documented plan for definitive soft-tissue management.
New paraesthesia, sensory loss or weakness indicates progressive nerve ischaemia; paralysis, pallor and absent pulses are late findings or suggest concurrent arterial injury and must never be awaited.
An obtunded, intubated, very young or cognitively impaired patient and a limb under dense regional blockade cannot report pain reliably, so objective surveillance and pressure measurement thresholds become particularly important.
Revascularisation, crush, high-energy tibial or forearm fracture, tight casts, bleeding disorders and prolonged limb compression create high-risk settings even when the initial examination was reassuring.
05
Rhabdomyolysis and renal panel
Why
Identify systemic consequences of muscle necrosis and reperfusion.
Interpretation and limitations
Trend potassium, creatinine, bicarbonate, calcium, phosphate, creatine kinase and urine output; treat ECG or biochemical hyperkalaemia without awaiting CK.
06Operative muscle assessment
Why
Define viability and completeness of release directly.
Interpretation and limitations
Document colour, bleeding, consistency and contractility of every muscle group and plan repeat inspection when viability remains uncertain.
1
Proceed to NCEPOD-1 surgery without waiting for MRI, further laboratory results or development of late pulse or motor changes.
2Open all involved compartments completely, inspect and document each muscle and neurovascular structure and remove clearly non-viable tissue.
3Coordinate fracture stabilisation and vascular repair while preserving rapid release and consider fasciotomy routinely after revascularisation.
4Leave wounds open, label uncertain tissue and set the planned time, team and physiological targets for repeat exploration.
03AftercareControl reperfusion and reconstruct functionFasciotomy is complete or delayed presentation contains established muscle necrosis.+
1Monitor ECG, potassium, acid-base state, CK, renal function and urine output and treat hyperkalaemia and shock through critical care.
2Discuss with plastic surgery within 24 hours and re-explore within 72 hours or earlier for deterioration or uncertain viability.
3DefinitivePlan delayed closure, graft or flap only after swelling, contamination and tissue viability permit safe definitive coverage.
4Provide nerve, muscle, joint, scar, pain and psychological rehabilitation and explain realistic functional and amputation risks.