Compartment Syndrome

• Causes: fractures (especially tibial shaft and forearm), crush injury, tight casts or dressings, reperfusion after vascular injury, burns, and bleeding into a compartment on anticoagulation.
• The cardinal early sign is pain out of proportion to the injury, worsened by passive stretch of the muscles in the compartment. This appears long before the other findings.
• The classic "6 Ps" — pain, pressure, paraesthesia, pallor, paralysis, pulselessness — are misleading if used as a checklist: pulselessness and pallor are late, and normal pulses do not exclude the diagnosis, because compartment pressure rarely exceeds systolic arterial pressure.
• Diagnosis is clinical. Compartment pressure measurement helps in the obtunded or equivocal patient; a delta pressure (diastolic minus compartment pressure) below about 30 mmHg supports the diagnosis.
• Treatment is emergent fasciotomy. Remove casts and circumferential dressings immediately, keep the limb at heart level (elevation reduces perfusion), and do not delay for imaging.
• Complications: Volkmann ischaemic contracture, rhabdomyolysis with hyperkalaemia and acute kidney injury, and limb loss.

Increased compartment content (most common)

• Fracture: ~three-quarters of cases follow fracture; tibial shaft is the single most common site, followed by distal radius and forearm (supracondylar humerus fracture in children). Bleeding from fracture ends plus soft-tissue oedema raises intracompartmental volume within an inelastic fascial envelope.
• Crush and prolonged limb compression: the found-down patient after opioid or alcohol overdose, seizure, or entrapment; direct myocyte injury plus reperfusion oedema.
• Reperfusion injury: after revascularisation of an ischaemic limb, embolectomy, or prolonged tourniquet/cross-clamp time — capillary leak floods the compartment once flow is restored.
• Haemorrhage into a compartment: anticoagulants, antiplatelet agents, haemophilia, or arterial injury.
• Iatrogenic: IV infiltration/extravasation, intraosseous line misplacement, high-pressure injection injury, aggressive fluid resuscitation in burns or sepsis.
• Envenomation and infection: pit-viper bite, necrotising soft-tissue infection.

Decreased compartment volume

• Circumferential constriction: tight casts, splints, bulky dressings, military anti-shock trousers, and circumferential full-thickness burn eschar (which requires escharotomy, not fasciotomy).
• Fascial defect closure or tight fascial repair.

Non-modifiable risk factors

• Young age and male sex: examiners plant a young man with a tibial fracture; larger muscle mass within a tight, non-compliant fascial envelope raises risk relative to older patients with atrophic muscle.
• High-energy mechanism and open fracture: an open fracture does not decompress the compartment and does not exclude the diagnosis.
• Bleeding diatheses.

Modifiable risk factors

• Anticoagulation intensity (supratherapeutic INR, DOACs).
• Constrictive dressings/casts — the most immediately reversible cause.
• Hypotension: lowers perfusion pressure, so a given compartment pressure becomes ischaemic at a lower value; resuscitate rather than tolerate.
• Limb elevation above the heart and ice, which further reduce arterial inflow.
• Dense regional anaesthesia or high-dose opioid PCA, which mask the sentinel pain (a monitoring risk emphasised in the AAOS work on acute compartment syndrome).

The pressure–perfusion cascade

• Fascia is inelastic: a compartment behaves like a closed box with a steep pressure–volume curve. Once the small reserve volume is used, a further small increase in contents (blood, oedema) causes a disproportionate rise in intracompartmental pressure.
• Venous outflow fails first: compartment pressure need only exceed venular pressure — far below systolic arterial pressure — to obstruct outflow. Rising venous pressure lowers the arteriovenous gradient across the capillary bed.
• Perfusion pressure, not absolute pressure, determines ischaemia: tissue perfusion ≈ diastolic blood pressure − compartment pressure. This is the physiologic basis of the delta pressure threshold of about 30 mmHg cited in the Overview, and the reason a hypotensive patient develops ischaemia at a lower measured compartment pressure.
• Vicious cycle: capillary hypoperfusion → endothelial hypoxia → increased permeability → more interstitial oedema → higher compartment pressure → less perfusion. The process is self-amplifying, which is why it progresses over hours and why decompression must be mechanical.
• Arterial inflow is usually preserved: because compartment pressure rarely reaches systolic pressure, distal pulses and capillary refill typically remain intact until very late — the trap behind the 6 Ps.

Why the findings appear in the order they do

• Pain out of proportion reflects ischaemic muscle and stimulation of unmyelinated C-fibre nociceptors by lactate, adenosine, and potassium; passive stretch further raises intracompartmental pressure and elongates ischaemic fibres, reproducing the pain.
• Paraesthesia precedes paralysis: small myelinated sensory fibres (A-delta/A-beta) tolerate ischaemia poorly and fail before larger motor axons and before muscle contractility is lost. In the anterior leg compartment this is first dorsal web space numbness from deep peroneal nerve involvement.
• Muscle infarction begins within hours: skeletal myocytes tolerate roughly 4–6 hours of warm ischaemia; beyond this, necrosis is irreversible and fibrous replacement produces Volkmann ischaemic contracture.
• Reperfusion after decompression releases myoglobin, potassium, phosphate, and creatine kinase into the circulation — the substrate for rhabdomyolysis, hyperkalaemia, and pigment-induced acute kidney injury.

Earliest and most reliable findings

• Pain out of proportion to the injury: escalating opioid requirement or pain that returns despite adequate analgesia; caused by ischaemic nociceptor stimulation. A rising analgesic demand in a casted patient is itself a red flag.
• Pain on passive stretch of the involved muscles: the most sensitive physical sign. Passive toe/ankle dorsiflexion provokes pain in the deep posterior compartment; passive plantarflexion provokes anterior compartment pain; passive finger extension provokes volar forearm pain.
• Tense, "woody" compartment on palpation: firmness disproportionate to the contralateral limb. Palpation is insensitive and cannot exclude the diagnosis.

Later findings (each implies established nerve or muscle ischaemia)

• Paraesthesia and hypoaesthesia: small sensory fibres fail first. First dorsal web space numbness = deep peroneal nerve = anterior leg compartment; volar fingertip numbness = median nerve = volar forearm.
• Paresis/paralysis: weak ankle dorsiflexion (foot drop) or weak finger flexion; indicates motor axon failure and impending infarction.
• Pallor, pulselessness, poikilothermia: very late or absent. Normal pulses and normal capillary refill do not exclude compartment syndrome — their absence should prompt evaluation for arterial injury or occlusion instead.

Special populations where the exam is unreliable

• Obtunded, intubated, intoxicated, or head-injured patients and young children cannot report pain; suspect the diagnosis from a tense compartment, unexplained tachycardia, or agitation, and measure pressures. In children the 3 As — agitation, anxiety, and increasing analgesic requirement — replace the classic pain description.
• Patients with a dense peripheral nerve block or epidural: analgesia can obscure the sentinel symptom; serial pressure monitoring is preferred.

Step 1 — serial clinical assessment

• Repeated examination at short intervals documenting pain, pain on passive stretch, compartment tenderness/tension, sensation in each nerve distribution, and motor function. A single normal exam is not reassuring; trajectory is the diagnostic information.
• Remove all circumferential casts, splints, and dressings down to skin before reassessing — constriction alone can produce the syndrome.

Step 2 — intracompartmental pressure measurement (when the exam is unreliable)

• Indications: obtunded, intubated, intoxicated, or head-injured patients; young children; dense regional anaesthesia; polytrauma; equivocal findings.
• Technique: needle manometry (e.g., a *Stryker*-type handheld intracompartmental pressure monitor) or slit/side-port catheter, measured within 5 cm of the fracture, where pressures are highest, and in every compartment of the segment (all four in the leg — anterior, lateral, superficial posterior, deep posterior; the deep posterior is the one most often missed).
• Thresholds: delta pressure = diastolic BP − compartment pressure; < 30 mmHg supports the diagnosis and is preferred over an absolute value because it accounts for systemic perfusion. An absolute pressure above roughly 30 mmHg is also used but is less specific and over-diagnoses in hypertensive patients. Continuous monitoring is more informative than a single reading.

Step 3 — supporting labs (never diagnostic, but guide resuscitation)

• Creatine kinase: markedly elevated with muscle necrosis; trend it.
• Potassium, creatinine, phosphate, calcium, bicarbonate/lactate: screen for hyperkalaemia, AKI, and metabolic acidosis.
• Urinalysis: dipstick positive for blood with few or no red cells on microscopy = myoglobinuria.
• ECG if hyperkalaemia is suspected.
• Coagulation studies in anticoagulated patients.

Immediate bedside measures (minutes, before surgery)

• Release all constriction: bivalve and spread the cast, cut through cast padding, and remove circumferential dressings down to skin. This alone can substantially lower compartment pressure.
• Position the limb at the level of the heart — not elevated. Elevation lowers arterial inflow and narrows the perfusion gradient; ice causes vasoconstriction and is avoided.
• Optimise perfusion pressure: treat hypotension with isotonic crystalloid and correct hypoxaemia. Because perfusion ≈ diastolic pressure − compartment pressure, restoring blood pressure buys tissue time.
• Analgesia: opioids (e.g., IV morphine) titrated; avoid dense regional/epidural blockade that abolishes the sentinel sign in an undecompressed limb.
• Reverse anticoagulation if bleeding is the cause — vitamin K plus four-factor prothrombin complex concentrate for warfarin, idarucizumab for dabigatran, and factor replacement in haemophilia, per ACC/ACCP anticoagulant-reversal guidance.
• Urgent surgical consultation; keep NPO.

Definitive management

• Emergent fasciotomy is the only definitive treatment, recommended by the AAOS and standard trauma practice, ideally performed as soon as the diagnosis is made — outcomes deteriorate sharply beyond roughly 6 hours of ischaemia.
• Leg: standard two-incision, four-compartment fasciotomy (lateral incision for anterior and lateral compartments; medial incision for superficial and deep posterior compartments). Every compartment must be released; incomplete release of the deep posterior compartment is a classic failure.
• Forearm: volar (extended carpal tunnel release) ± dorsal fasciotomy. Circumferential burn eschar requires escharotomy, which may be combined with fasciotomy.
• Wounds are left open, with delayed primary closure or split-thickness skin grafting once swelling resolves; serial debridement of necrotic muscle as needed.

Adjuncts and contraindications

• Aggressive isotonic IV fluid for rhabdomyolysis to maintain urine output, with treatment of hyperkalaemia (calcium gluconate for membrane stabilisation, insulin with dextrose, and potassium removal); KDIGO frames prevention of pigment-induced AKI around early volume expansion. Routine bicarbonate and mannitol are not established.
• Contraindicated/avoid: limb elevation, ice, tight closure, delay for imaging, and vasopressor-dependent hypotension without volume repletion. Fasciotomy in a late-presenting limb with established necrosis is controversial — reperfusing dead muscle risks lethal rhabdomyolysis and infection.

Of untreated or late-treated compartment syndrome

• Volkmann ischaemic contracture: infarcted muscle is replaced by fibrous tissue that shortens across joints. Classically the volar forearm after a paediatric supracondylar humerus fracture, producing a fixed claw hand with flexed wrist and fingers; in the leg it produces equinus/claw toes. Irreversible — prevention is the only treatment.
• Permanent nerve injury: foot drop from deep peroneal ischaemia, sensory loss, or chronic neuropathic pain.
• Rhabdomyolysis — an emergency. Signalled by markedly elevated creatine kinase, tea-coloured urine with a dipstick positive for blood but no red cells on microscopy, hyperkalaemia, hyperphosphataemia, hypocalcaemia, and metabolic acidosis.
• Hyperkalaemia is the immediately lethal element: peaked T waves progressing to widened QRS, sine wave, and cardiac arrest. Obtain an ECG and treat before waiting for a repeat potassium.
• Pigment-induced acute kidney injury from myoglobin cast obstruction, tubular toxicity, and renal vasoconstriction; KDIGO frames prevention around early isotonic volume expansion. Severe cases require renal replacement therapy.
• Limb loss: amputation for non-salvageable necrotic muscle or overwhelming infection.
• Reperfusion syndrome after decompression: a transient washout surge of potassium and acid with hypotension and arrhythmia — anticipate it at the moment of fasciotomy.

Of fasciotomy itself

• Wound infection, osteomyelitis, and necrotising infection of the open wound — an emergency if there is crepitus, systemic toxicity, or grey "dishwater" drainage.
• Iatrogenic nerve injury: the superficial peroneal nerve is at risk in the lateral leg incision; the saphenous nerve and vein in the medial incision.
• Incomplete release, most often of the deep posterior compartment, with persistent pain and rising pressures after surgery — mandates return to the operating room.
• Chronic wound morbidity: need for split-thickness grafting, tethered scars, chronic oedema/venous insufficiency, and muscle herniation through the fascial defect.
• Delayed fracture union and prolonged hospitalisation.

• Pain out of proportion to injury, worsened by passive stretch, is the earliest and most reliable finding, and is the phrase the stem will use. A patient whose opioid requirement keeps climbing after a tibial shaft fracture in a cast has compartment syndrome until proven otherwise.
• Palpable pulses do not exclude the diagnosis. Compartment pressure obstructs venous outflow long before it approaches systolic pressure, so pallor and pulselessness are late or never present. Treating the 6 Ps as a checklist is the classic distractor; if the limb truly is pulseless and cold, think arterial injury or acute limb ischaemia as well.
• Single best next step in the awake patient with a suspected compartment syndrome in a cast: remove the cast and all circumferential dressings down to skin, then reassess. Next step if the diagnosis is clinically evident: emergent fasciotomy — not imaging, not pressure measurement.
• Delta pressure = diastolic BP − compartment pressure; < 30 mmHg supports the diagnosis. Measure pressures only when the exam is unreliable (obtunded, intubated, intoxicated, young child, dense regional block).
• Do not elevate the limb and do not ice it — keep it at heart level. Elevation drops arterial inflow and worsens ischaemia; this is a favourite wrong answer.
• The one association examiners test: **supracondylar humerus fracture in a child → volar forearm compartment syndrome → *Volkmann ischaemic contracture* (fixed claw hand). In children, watch for agitation, anxiety, and escalating analgesic requirement**.
• After fasciotomy, anticipate reperfusion: check potassium, creatine kinase, creatinine, and an ECG; give isotonic IV fluids for rhabdomyolysis and treat hyperkalaemia immediately (calcium for membrane stabilisation first).
• Leg fasciotomy releases all four compartments through two incisions; the deep posterior compartment is the one most commonly missed, and persistent pain after fasciotomy means incomplete release until proven otherwise. An open fracture does not decompress the compartment.