Compartment syndrome

• Acute compartment syndrome is a rise in pressure inside a fixed fascial compartment that eventually exceeds perfusion pressure and kills muscle and nerve.
• Fracture is the commonest trigger, especially of the tibia, but crush injury, tight casts or dressings, burns, prolonged positioning and reperfusion after arterial repair can all cause it.
• The patient has pain far worse than the injury, pain on passive stretch, a tense swollen compartment and early sensory change; pulselessness and pallor are late signs.
• Diagnosis is clinical. When the picture is unclear, measure the pressure: a normal compartment sits under 10 mmHg, danger is 30 mmHg or more, and a diastolic-to-compartment difference under 30 mmHg signals increased risk. ^[1][4]
• Treatment is urgent open fasciotomy of every involved compartment. Waiting for all of the classic signs wastes the opportunity to save the limb.

By the end of this page you should be able to:

1. Define an anatomical compartment and explain why its pressure rises.
2. List the traumatic and non-traumatic causes of acute compartment syndrome.
3. Recognise the condition from pain out of proportion and pain on passive stretch, before late signs appear.
4. Interpret compartment pressure and delta-pressure values and know when to operate.
5. Outline urgent fasciotomy, including which compartments need release.
6. Name the postoperative steps and complications that determine outcome.
7. Adapt the diagnosis and measurement to a patient who cannot report pain or to a low-resource setting.

The human limb is divided into osseofascial compartments by bone and tough fascial membranes. Each compartment contains muscle, nerve and blood vessels, and its volume is essentially fixed. When bleeding or oedema raises the contents, pressure rises inside that fixed space, venous return falls first, then arterial inflow, and tissue dies. The process is self-amplifying: ischaemia produces more oedema, which raises pressure further (reperfusion after arterial repair adds a further rise in pressure through oxygen free radicals and post-ischaemic swelling).

Classification by time course and cause is more useful than an anatomical list:

• Acute traumatic ACS: follows fracture, crush injury, vascular injury or reperfusion. This is the form that threatens the limb and is the subject of this page.
• Acute atraumatic ACS: raised pressure without major trauma. Reported causes include nephrotic syndrome, viral myositis, hypothyroidism, bleeding disorders, malignancy, diabetes mellitus with muscle infarction, ruptured Baker cyst, prolonged lithotomy positioning and, in athletes, sudden unaccustomed exertion. ^[3]
• Acute exertional ACS: a rare presentation after intense exercise in a young adult, distinct from the chronic form. ^[4]
• Chronic (exertional) compartment syndrome: exercise-induced pain and swelling that settle with rest and is not an emergency. British guidance (BOAST, 2025) excludes it from the acute standards. ^[1]
• Abdominal compartment syndrome is a separate, systemic condition of the abdomen and is not covered here. ^[3]

By site, the leg is affected most often, followed by the forearm, arm, thigh, foot, gluteal region and hand. ^[3] Any compartment can be involved, including the small compartments of the hand and foot, each of which has its own pressure threshold (see below).

Acute compartment syndrome is rare but serious. One contemporary review gives an incidence of about 7.3 cases per 100,000 per year in males and 0.7 per 100,000 per year in females. ^[4] Men are affected roughly ten times more often than women. ^[3] Trauma accounts for about three-quarters of cases, with the lower leg and forearm the commonest sites. ^[4]

Younger patients are more vulnerable than older patients with the same injury: their muscle mass is larger relative to compartment volume and their fascia is less compliant. ^[3] Incidence in open and closed fractures is similar, so closing (or not closing) the wound is not protective. ^[3]

The site pattern matters for vigilance:

• The leg is the most common site overall. ^[3]
• Closed tibial shaft fracture is the single most common cause and accounts for roughly one-third of all cases. ^[3]
• Blunt or crushed soft-tissue injury of the limb accounts for about a quarter of cases. ^[3]
• Radius and ulna shaft fractures account for about a fifth. ^[3]
• Foot injury, particularly in motorcycle trauma, accounts for about 6 percent. ^[3]

This is what is worth remembering at the bedside: the syndrome is not a diagnosis of a single disease but a final common pathway of raised intracompartmental pressure.

Causes (cross-check these each time you see a limb at risk):

• Fracture, especially tibia, and especially when displaced or comminuted.
• Crush injury, including entrapment and direct blow. Crush lowers the time to irreversible damage (see Prognosis).
• Tight casts, splints or dressings, including postoperative bandaging around a swollen limb.
• Reperfusion after arterial injury or obstruction: surgical repair, thrombolysis or sudden restoration of flow can precipitate swelling.
• Direct arterial injury with haemorrhage into the compartment.
• Burns, especially high-voltage electrical burns and circumferential eschar.
• Prolonged positioning, particularly lithotomy.
• Bleeding disorders, anticoagulation and non-accidental medical conditions (see Definition above).
• Exertion in unconditioned muscle.

The Emergency Medicine coverage of open fractures (the library's fracture principles topic) reinforces that any open fracture assessment must document vascular and neurological status, repeat it systematically after splinting, and manage suspected compartment syndrome by British guidance. ^[2]

Risk factors fall into two groups. Injury-related factors (high energy, displaced fracture, arterial injury, significant soft-tissue swelling, burn, prolonged extrication) and patient-related factors (young age, male sex, bleeding tendency, anticoagulation, impaired consciousness, regional anaesthesia that masks pain). The last two are dangerous precisely because the early diagnostic symptom is pain, and these patients cannot report it. ^[3][1]

The mechanism is the reason the treatment works.

1. A trigger (bleed or oedema) raises the volume inside a compartment whose walls cannot stretch.
2. Pressure rises above venous pressure, so drainage fails and venous pooling adds to the volume.
3. Capillary and then arteriolar perfusion fall; tissue becomes hypoxic and cells switch to anaerobic metabolism.
4. Ischaemia worsens capillary leak, adding oedema; the cycle drives pressure higher.
5. Reperfusion later in the course (or after surgical revascularisation) floods the damaged microcirculation with oxygen free radicals, producing more capillary injury. ^[4]

Tissue tolerance is time-limited and temperature-dependent. Experimental work shows that pressures of 40 to 80 mmHg sustained for four hours do not necessarily cause permanent nerve dysfunction, but pressures sustained for twelve hours or more do. ^[3] Muscle dies before nerve, and sensation changes before motor loss: paraesthesia is the first sign of nerve ischaemia, followed by hypoaesthesia, then anaesthesia, then weakness, then paralysis. ^[3]

The guideline editions named here agree on the central message: once perfusion falls, the amount of necrosis tracks duration, so every hour of delay worsens outcome. The clinical literature summarised in the references puts the landmarks at about four hours for potentially irreversible muscle damage and about eight hours for nearly complete myonecrosis, with crush injury shortening even those intervals. ^[4]

The hallmark is pain out of proportion to the injury, often described by the patient as deep, burning or relentless. It worsens with passive movement of the muscles in the involved compartments (passive stretch) and may not respond to analgesia that would normally control the injury pain. It is typically present at rest and out of proportion even before swelling is obvious. Sensory change starts distally and moves proximally in relation to the area of compression. ^[3][4]

Symptoms the patient volunteers include:

• severe pain in the limb, especially on movement or stretch
• early pins and needles or numbness in the territory of a nerve running through the compartment
• weakness or an inability to use the limb because of pain
• a feeling of tightness or swelling

Diagnosis lives in the examination. Examine serially, preferably by one clinician, comparing both limbs. ^[3]

The classic list is the five Ps: pain, pallor, paraesthesia, paralysis and pulselessness. ^[3][4] They are a memory aid, not a checklist to wait for. Pain is the early, reliable finding; pallor, paralysis and pulselessness are late or unreliable, and pulselessness usually reflects arterial injury or systemic hypotension rather than compartment syndrome itself. ^[3]

Key findings in an awake patient:

• pain out of proportion to the injury and pain on passive stretch of the muscles in the involved compartments (the most specific early sign)
• a tense, swollen, "wooden" compartment
• sensory change on pinprick, light touch or two-point discrimination, starting distally
• motor weakness that may be limited by pain; complete paralysis is late
• capillary refill usually preserved even in well-established disease
• pulses usually present

Examination of the unconscious, sedated, multiply injured or regionally anaesthetised patient is the difficult case. Most clinical signs cannot be elicited, and regional blocks or strong analgesia can mask the early symptom. British guidance requires shared decision-making about regional anaesthesia, written consent, an agreed monitoring policy with named responsibility, and either invasive monitoring or review by staff trained in regional anaesthesia and compartment assessment. ^[1] Suspected compartment syndrome should be screened for at least hourly in these patients, with findings (present or absent) recorded along with time, mechanism of injury, level of consciousness, neurological and vascular status, pain score and response to analgesia. ^[1]

Other examination steps worth recording (BOAST 2025): hourly assessment of at-risk patients; analgesic doses; when pressure is measured, concurrent blood pressure and the site of measurement; the decision-maker's interpretation. ^[1]

The diagnosis is clinical. Objective measurement is an adjunct, not a replacement, and is most useful when the patient cannot describe pain or when the examination is equivocal. ^[1][3]

General approach when considering a measurement (BOAST 2025): release all circumferential dressings to skin, elevate the limb to heart level, maintain blood pressure, re-evaluate within thirty minutes, document repeated examinations hourly, and involve a senior decision-maker. ^[1]

Measure in all suspected compartments within about 5 cm of the injury; pressure can vary with distance from the fracture site. ^[3] Post-mortem and clinical data support continuous monitoring rather than a single reading, because a one-off measurement can have a high false-positive rate. ^[3]

Immediate (first hour)

• Remove the cause of external compression: split or cut all casts and dressings to skin, elevate the limb to heart level, remove rings and jewellery.
• Record neurovascular status and pain before and after; reassess at short intervals.
• Maintain blood pressure; normal perfusion pressure is required for any pressure-based criterion to make sense.
• Keep the patient nil by mouth, start analgesia and arrange senior surgical review; suspected acute compartment syndrome is a surgical, not medical, problem.
• Do not apply ice or a further tight wrap around the limb.

Definitive treatment is surgical fasciotomy, and it should follow the diagnosis without waiting for all of the classic signs. ^[1][3]

• Open decompression of all involved compartments, not the one most obvious. The appearance, viability and debridement of each structure in each compartment must be recorded. ^[1]
• Lower leg: a two-incision, four-compartment decompression (medial and lateral), using the same incisions recommended for open-fracture debridement. ^[1][2]
• Forearm: release of the volar compartment (volar incision extending across the carpal tunnel), checking dorsal and mobile-wad pressures afterwards; a lazy S-shaped incision that includes the proximal palm is used. ^[3]
• Hand, foot and thigh: site-specific incisions, with attention to the ten compartments of the hand and the neurovascular structures at each site. ^[3][4]
• Debridement of all non-viable muscle at operation; viable muscle is pink or red and contracts when stimulated. ^[3]

Postoperative care and timing

• Discuss every patient with a plastic surgeon within 24 hours of fasciotomy and re-explore within 72 hours (or sooner if indicated), with a documented plan for definitive soft-tissue management. ^[1]
• Delayed presentation carries a high risk of complications with surgery; non-operative management with renal protection becomes an option, and decision-making should involve two consultants. ^[1]
• Wound management after decompression: loose primary closure if swelling allows; otherwise negative pressure therapy or assisted dynamic (shoelace) closure; skin grafting if delayed. ^[3][4]
• Document vascular status, muscle viability and wound plans at each stage.

Regional anaesthesia and analgesia follow a written policy: shared decision-making with the patient, documented consent, named responsibility for postoperative monitoring, and either invasive pressure measurement or review by staff trained in compartment assessment when a block is used. ^[1]

• Muscle and nerve death, producing Volkmann ischaemic contracture, neuropathy and permanent weakness if decompression is delayed. ^[3][4]
• Rhabdomyolysis with myoglobinuric acute kidney injury; crush injury shortens the safe interval to irreversible damage. ^[3][4]
• Limb loss and sepsis in the most severe neglected cases. ^[3]
• Fracture healing problems: about half of tibial shaft fractures complicated by compartment syndrome go on to delayed union or non-union, compared with under a fifth without it. ^[3]
• Fasciotomy morbidity: chronic altered sensation and pain in the scar (reported in about 77 percent of one surgical series), a high rate of skin grafting, long-term calf muscle pump dysfunction and chronic venous insufficiency. ^[3][4]
• Medicolegal risk: in published series, more than half of claims relating to compartment syndrome are decided against the treating clinicians. ^[3]
• Abdominal compartment syndrome is not a sequela of limb disease; the term is used here only so readers do not confuse the two.

Outcome is dominated by time. Potentially irreversible muscle damage can begin within about four hours and nearly complete myonecrosis within about eight hours, with crush injury producing damage even sooner. ^[4] The experimental literature on pressor thresholds puts permanent nerve change at twelve hours or more under elevation. ^[3]

With prompt fasciotomy, function can be preserved even after major soft-tissue injury. Late presentation carries a high risk of complications and forces difficult decisions about non-operative management with renal protection. ^[1] A significant minority of patients retain altered sensation or pain years after the wound has healed, so rehabilitation and informed consent about expectations matter as much as the operation. ^[4]

Prevention is really early recognition:

• Compartment syndrome should be part of the routine, documented evaluation of anyone presenting with a limb injury, after extremity surgery or after any prolonged procedure that may produce hypoperfusion. ^[1]
• Avoid circumferential casting in the acute phase; split or bivalve instead and reassess as swelling rises.
• Maintain a low threshold after high-energy injury, arterial injury, significant swelling, tight casts, burns and in any patient who cannot report pain. ^[1][2]
• Screen at-risk patients hourly, and whenever analgesia, splints or dressings change, writing down the time and mechanism of injury, level of consciousness, neurovascular status, pain and analgesic response. ^[1]
• In open fractures, follow British guidance for wound debridement (immediately for high contamination or vascular compromise; within twelve hours for high-energy injuries; within twenty-four hours otherwise) using fasciotomy lines wherever possible, and remember that the management of suspected compartment syndrome follows the compartment syndrome guideline itself. ^[1][2]
• Teach patients and families the warning signs before discharge after tibial fracture or fixation, because many patients go home still at risk. ^[3]

Children. Acute compartment syndrome is well described in children with long-bone fractures, and the leg is often involved. Thresholds of greater than 30 mmHg are still used in this age group, and normal pressures are about double adult values, so absolute numbers must be interpreted against age. ^[3][4] Forearm compartment syndrome is the pattern most often reported in neonates, and early skin changes (ecchymosis, bullae, distal gangrene) should trigger surgery within hours. ^[4] Fasciotomy scars can impair function as the child grows. ^{[4] [1]}

Older adults. They are less likely to develop ACS from the same trauma than younger patients, but when they do present it may be delayed and confused with chronic vascular or neuropathic pain. ^[3] Fractures are often fragility fractures, and comorbidity and skin quality influence both diagnosis and treatment.

Pregnancy. Pregnancy itself is not a recognised risk factor for limb compartment syndrome; risk comes with trauma, crush injury and prolonged positioning in labour or surgery. ^[3] Management follows the same principles, with shared decision-making between orthopaedic, obstetric and anaesthetic teams.

• Prompt physical examination, attention to mechanism and time, and knowledge of the classic five Ps are often the best diagnostic tools available. ^[4]
• A hand-held or home-made pressure measurement using a needle, arterial line tubing, a three-way stopcock, syringe and mercury manometer (Whitesides method) converts a basic kit into a quantitative test; an 18-gauge needle, intravenous tubing and normal saline are usually sufficient. ^[3][4]
• Whitesides method is less precise than commercial side-ported devices, so use the same numbers with caution and a wide safety margin. ^[3][4]
• The consequences of delayed diagnosis are worse where transfer is slow: gangrene, Volkmann contracture and chronic disability occur more readily, so a low threshold for fasciotomy and a high index of suspicion are paramount. ^[4]

Emergency Medicine topic on fracture principles and open fractures; hand injuries (injuries to the hand and forearm compartments); trauma resuscitation and massive transfusion; peripheral arterial injury and limb ischaemia; rhabdomyolysis and acute kidney injury; peripheral nerve injury; osteomyelitis and fracture-related infection; rehabilitation after major trauma.