Forearm Compartment Syndrome

Forearm compartment syndrome is a surgical emergency. Pressure rises inside the closed osteofascial compartments of the forearm, which have little compliance, until tissue perfusion is compromised and the muscles and nerves within suffer progressive ischaemic injury. Normal compartment pressure is 0-8 mmHg.

What the pressure does. Tissue perfusion depends on the pressure gradient between arterioles and venules. As compartment pressure rises, venous outflow is compromised first, venous pressure climbs and the arteriovenous gradient narrows, so capillary perfusion falls even though arterial inflow is still present. This is the arteriovenous gradient theory, and it is why the pulse is preserved until late.

What follows. Muscle ischaemia progresses to necrosis, and nerve ischaemia produces a sensory and then a motor deficit. Left untreated, the necrotic flexor muscle is replaced by fibrous tissue, and the hand is left with Volkmann's ischaemic contracture.

Causes. Anything that adds volume to a compartment or compresses it from outside will do: a fracture bleeding into the muscle, a crush, a tight cast, or reperfusion after an arterial repair.

High-risk fractures. These are the injuries after which serial neurovascular examination is not optional.

1. Supracondylar fractures in children - highest risk, especially displaced type III
2. Both-bone forearm fractures - significant soft tissue injury
3. Floating elbow - combined supracondylar and forearm fracture
4. Monteggia and Galeazzi fractures - high-energy injury pattern
5. Distal radius fractures with severe swelling or displacement

Patient factors. The typical patient is a young man after high-energy trauma.

The compartments. The forearm has three to four compartments depending on the classification: two volar, one dorsal, and the mobile wad, which some consider part of the dorsal compartment and which is released through the dorsal approach. A fasciotomy is only complete if the surgeon knows what lies in each of them.

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The cascade. Bleeding, oedema or external compression raises the pressure; venous outflow is obstructed first; the arteriovenous gradient falls and capillary perfusion with it. Muscle is more sensitive than nerve initially. Ischaemic cells swell, which raises the pressure further, a positive feedback loop that only decompression breaks.

Pain on passive stretch is the most reliable early sign. Volar involvement hurts on passive finger extension; dorsal involvement hurts on passive finger flexion. The pain is disproportionate to the injury itself, and the analgesic requirement keeps climbing despite adequate initial dosing.

The five Ps are the classic list, and the last two are late:

• Pain - out of proportion to the injury, the earliest sign
• Pressure - a tense, wood-like compartment on palpation
• Paraesthesia - numbness as nerve ischaemia begins
• Pallor - late, indicating advanced ischaemia
• Pulselessness - very late, and irreversible damage is likely

Nerve findings. Numbness in the first web space (AIN, median nerve) is the sensory sign; ulnar-distribution numbness is less common, and the PIN is motor only, with no sensory territory. Motor weakness follows the same nerves: an AIN palsy with a weak FPL (thumb IP) and weak FDP to the index, then weak finger flexion (FDS, FDP) and weak wrist flexion.

When to measure. The diagnosis is clinical, and high clinical suspicion alone is sufficient: do not delay fasciotomy for pressure measurement, imaging or laboratory results, because time to fasciotomy is the critical factor. Pressure measurement is most valuable exactly where the examination fails you - the obtunded, intubated, blocked or very young patient who cannot report pain:

• Equivocal clinical examination
• Obtunded or uncooperative patient
• Unreliable examination (intoxication, head injury)
• Serial monitoring when clinical suspicion is moderate

Technique. The method matters:

1. Use a calibrated device (Stryker STIC, arterial line transducer)
2. Measure in the zone of maximum injury or swelling
3. Measure all compartments if there is any suspicion
4. Position the limb at the level of the heart
5. Infiltrate 0.3ml of saline to confirm placement

The threshold. Delta P is the diastolic blood pressure minus the compartment pressure. It represents the perfusion pressure gradient and so accounts for the patient's haemodynamic status: a patient with a diastolic pressure of 70 mmHg and a compartment pressure of 45 mmHg has a ΔP of 25 mmHg, and fasciotomy is indicated. The threshold to quote is ΔP under 30 mmHg sustained over 2 hours; the older absolute reading of over 30 mmHg is superseded, because it is common and transient after injury, and on its own it is a prompt to reassess urgently rather than an indication to operate.

Why the differential is the one to quote. Perfusion of a compartment depends on the gradient between the patient's diastolic pressure and the pressure inside the compartment, so a hypotensive trauma patient can infarct muscle at an absolute pressure that would be harmless in someone normotensive. That is the whole argument, and it is why the threshold is expressed as diastolic minus compartment pressure rather than as a fixed number. It is also the threshold with validated diagnostic performance.

The performance figures belong to continuous monitoring, not to a one-off stab. In 850 patients with tibial diaphyseal fractures monitored continuously and analysed against the operative findings at fasciotomy and against the absence of contracture or neurological deficit at a mean of 59 weeks, sensitivity was 94%, specificity 98% and positive predictive value 93% (DOI). Of 152 fasciotomies, 141 were true positives and only 6 were false positives. Those numbers describe a monitored trend, and they do not transfer to a single needle reading taken once, which is far more vulnerable to catheter position, depth and technique.

Both errors are real, and missing it is the graver one. A missed forearm compartment syndrome produces a Volkmann's contracture and a permanently useless hand, so if the clinical picture says compartment syndrome you decompress regardless of what the needle says; a normal pressure never overrides convincing clinical signs. But the opposite error is not harmless: an unnecessary forearm fasciotomy means two long wounds, a likely skin graft, infection risk and lasting cosmetic and functional cost. That is why an isolated absolute reading over 30 in an awake, comfortable patient with a soft compartment and no pain on passive stretch is a reason to measure again and keep watching, not to operate on the spot. Practice genuinely varies between units, so know your own institution's written protocol.

Continuous monitoring has its own indications:

• Multiple trauma patient requiring sedation or ventilation
• Post-operative monitoring after high-risk surgery
• Burns with circumferential involvement
• Serial measurements impractical

Other tests. CK rises with muscle necrosis, myoglobin is the marker of rhabdomyolysis, lactate marks tissue ischaemia, renal function is monitored for myoglobinuric AKI, and coagulation studies are sent if a bleeding diathesis is suspected. Radiographs identify the underlying fracture and guide its management; CT and MRI are not routine and may delay treatment; Doppler ultrasound assesses arterial flow, but the presence of a pulse is not the same as adequate perfusion.

Remove every constrictor. Bivalve all casts, release all circumferential dressings and cut down to skin. Keep the limb at heart level and do not elevate it, because elevation reduces arterial perfusion. Removal of every constrictive element comes before definitive fasciotomy.

Optimise perfusion. Maintain the blood pressure and avoid hypotension, correct hypovolaemia and coagulopathy, give supplemental oxygen and keep the patient normothermic.

Book theatre. Contact theatre immediately and consent for fasciotomy. Plan for both volar and dorsal release, warn the patient that the wounds will be left open, and plan the return to theatre at 48-72 hours.

The decision. Time to fasciotomy is the most critical determinant of outcome, and the pathway depends on how sure you are:

1. High clinical suspicion (pain out of proportion, pain on passive stretch): proceed directly to fasciotomy
2. Uncertain diagnosis (equivocal examination, obtunded patient): measure pressures in all compartments, apply the Delta P threshold, and monitor serially if the values are borderline
3. Established diagnosis: urgent fasciotomy within 6 hours of symptom onset, releasing volar and dorsal if the mechanism was high-energy or there is any doubt, and always including carpal tunnel decompression

Fasciotomy within 6 hours of symptom onset has significantly better outcomes than delayed decompression; after 8 hours, irreversible damage is highly likely.

Set-up. Supine, arm on a radiolucent hand table. A tourniquet is applied but used judiciously, inflated only if bleeding obscures the view, and there is a case for avoiding it altogether so that tissue perfusion can be assessed.

Consent. The patient should hear these before the anaesthetic:

• The wounds will be left open
• Risk of incomplete decompression
• Nerve and vessel injury
• Return to theatre at 48-72 hours
• A skin graft may be required
• Ongoing muscle or nerve damage despite surgery

Missed or delayed diagnosis. The first of the sequelae is permanent.

Volkmann's ischaemic contracture is the irreversible fibrotic contracture of the forearm flexors that follows untreated compartment syndrome. Severity is graded by Tsuge, in the classification section above, and the shortened flexors set the hand in a classic posture:

• Wrist flexion
• MCP hyperextension
• IP joint flexion
• Thumb adduction

The cascade sign is its signature: passive wrist extension makes the fingers flex further, because the muscle is shortened.

Complications of the fasciotomy itself. Early: wound infection, bleeding, iatrogenic nerve or vessel injury, skin edge necrosis and incomplete release. Late: unsightly scars, skin graft contracture, chronic wound healing, tethering of tendons, altered sensation and the need for secondary reconstruction.

The wounds. Leave them completely open and never close primarily. Apply a loose non-adherent dressing (Jelonet, Adaptic), and consider negative pressure wound therapy if significant oedema persists, the wound is large with exposed structures, or a dressing is difficult to maintain.

The splint holds the position of function to prevent contracture, and it must not itself compress the compartments, so avoid tight circumferential dressings:

• Wrist: 20-30° extension
• MCP joints: 70-90° flexion
• IP joints: full extension
• Thumb: abduction and opposition

Monitoring. Neurovascular observations every 2 hours for the first 24 hours, watching for persistent pain (inadequate decompression), a worsening motor or sensory deficit, signs of bleeding, and the systemic complication, rhabdomyolysis.

Rhabdomyolysis. Check CK daily initially, serum and urine myoglobin, creatinine and eGFR, and lactate as a marker of tissue ischaemia, and maintain a urine output over 1ml/kg/h. Treatment is aggressive IV hydration to that urine output target, urinary alkalinisation with IV sodium bicarbonate, potassium monitoring for hyperkalaemia, dialysis if AKI develops, and treatment of the underlying cause.

Return to theatre at 48-72 hours. The wound is reassessed and closed by whichever method the tissues allow.

Rehabilitation follows the wound, and the hand therapist is involved from the start.

Watch for the late complication. A progressive finger flexion posture, a positive cascade sign and grip weakness are the signs of a developing Volkmann's contracture, and a contracture needs prompt referral to hand surgery.

Timing. Time to fasciotomy is the dominant determinant of outcome. In the series that defined the early-versus-late divide (Sheridan and Matsen, in the evidence section), fasciotomy performed early, under 12 hours after onset, gave normal function in 68% of extremities, and only 8% of late fasciotomies did, with complication rates of 4.5% early against 54% late. Outcome worsens continuously with delay, which is why contemporary practice aims for decompression as soon as the diagnosis is made, ideally within 6 hours.

Other prognostic factors are the severity of the initial injury, the associated fractures and soft tissue trauma, the patient's age (younger patients have better recovery potential), rehabilitation compliance, and complications such as infection and rhabdomyolysis.

Recovery runs over months to years.

Volkmann's contracture. An established contracture is irreversible, and the only treatment is reconstruction, so prevention by early fasciotomy is the whole strategy. When reconstruction is needed, the result tracks the Tsuge grade.

Medicolegal. Missed or delayed compartment syndrome is one of the most common and costly sources of orthopaedic litigation internationally, and claims are frequent and high-value in multiple jurisdictions (analyses of UK NHS Resolution and US closed-claims data), driven by the catastrophic and irreversible nature of the sequelae. The common allegations are delayed diagnosis, failure to monitor or document neurovascular status, and an inadequate, incomplete fasciotomy. Prevention is meticulous time-stamped documentation, a low threshold for fasciotomy, and early senior or specialist involvement; the record should contain:

1. Time-stamped neurovascular examinations
2. Compartment pressure measurements (if performed)
3. Clinical decision-making rationale
4. Patient and family discussions about risks
5. Informed consent including the risk of Volkmann's contracture
6. Time from symptom onset to surgical decompression

Differential Diagnosis

Compartment syndrome must be distinguished from other causes of a painful, swollen or neurologically compromised forearm. The two most dangerous mimics to exclude are arterial injury and an evolving compartment syndrome masked by a nerve block.

Global Epidemiology

The largest population series (McQueen et al, J Bone Joint Surg Br 2000, PMID 10755426) of 164 consecutive acute compartment syndromes found an associated fracture in 69%, with forearm cases linked to distal radius fractures and occurring predominantly in young men under 35 years. The Lancet Emergency Surgery Series review (von Keudell et al 2015, PMID 26460664) confirms acute compartment syndrome affects upper and lower limbs in both adults and children and that there remains no internationally agreed diagnostic gold standard. Forearm compartment syndrome in children is most often associated with displaced supracondylar humeral fractures (Mubarak & Carroll, PMID 479251).

Guideline & Registry Comparison

There is no orthopaedic registry that systematically captures forearm compartment syndrome in the way arthroplasty registries (AOANJRR, NJR, AJRR) capture joint replacement; incidence and outcome data derive from single-centre and national trauma series rather than registry datasets.

Practice Variation & Regional Considerations

The principal area of international practice variation is the diagnostic pathway: continuous intracompartmental pressure monitoring is favoured in some UK and European units for high-risk or obtunded patients, whereas a clinically-driven "decompress if suspected" approach predominates in many trauma centres internationally (von Keudell 2015, PMID 26460664). The ΔP less than 30 mmHg threshold (McQueen, PMID 8898137) is the most widely adopted pressure criterion worldwide.

In trauma centres internationally, standardised serial neurovascular observation is applied after high-risk fractures, and first-generation cephalosporin prophylaxis (e.g. cefazolin) is the standard at fasciotomy. In rural and remote settings where transfer time may exceed 4-6 hours, local surgeons should have a low threshold to perform fasciotomy before transfer rather than risk irreversible ischaemia in transit. VTE prophylaxis follows standard trauma protocols, with mechanical methods preferred initially given the bleeding risk into freshly decompressed compartments.