Compartment Syndrome

Compartment syndrome is a surgical emergency in which rising pressure within a closed osteofascial space compromises tissue perfusion, leading to ischaemic necrosis of muscle and nerve. It is one of the most heavily tested orthopaedic emergencies in NEET PG—commonly framed around the classic "six Ps", intracompartmental pressure cut-offs, and the timing of fasciotomy. Volkmann's ischaemic contracture is its dreaded late sequela.

Definition & classification

A compartment is a group of muscles, nerves and vessels enclosed by tough, relatively inelastic fascia and bone. When pressure inside such a non-expandable space exceeds a critical threshold, capillary perfusion falls below that needed for tissue viability, producing ischaemia. Persistent ischaemia for more than 4–6 hours produces irreversible muscle and nerve damage.

Classification:

Type	Onset	Typical setting	Reversibility
Acute compartment syndrome (ACS)	Hours	Trauma, fracture, crush, reperfusion, tight casts	Surgical emergency; reversible only if decompressed early
Chronic (exertional) compartment syndrome	Recurrent, exercise-induced	Athletes, runners	Reversible with rest; elective fasciotomy if disabling
Crush syndrome	Hours–days	Prolonged limb compression (earthquake, unconscious patient)	Systemic; rhabdomyolysis + AKI

High-yield: Acute compartment syndrome is the form tested in trauma vignettes. The single most important determinant of outcome is time to fasciotomy—irreversible damage begins by ~6 hours of total ischaemia.

Etiology

Causes are broadly grouped into those that decrease compartment volume and those that increase compartment contents.

Increased contents (most common):

• Fractures — the leading cause. Tibial shaft fracture is the single commonest cause overall; supracondylar fracture of humerus in children is the classic forearm cause.
• Soft-tissue crush injury, contusion.
• Haemorrhage into a compartment (vascular injury, anticoagulants, bleeding diathesis).
• Reperfusion oedema after prolonged ischaemia or vascular repair.
• Burns (circumferential), high-pressure injection injuries, snake bite.
• Intravenous extravasation / infiltration of fluids.

Decreased compartment volume / external constriction:

• Tight plaster casts or circumferential dressings (very common exam answer—first step is to split the cast).
• Tight closure of fascial defects.
• Localised external pressure (lying on a limb while comatose, eschar from burns).

High-yield: Open fractures do not protect against compartment syndrome—the fascial envelope often remains intact. Never assume an open wound has "decompressed" the limb.

Pathophysiology

The core mechanism is the arteriovenous pressure gradient theory:

Rising compartment pressure → venous pressure rises → reduced arteriovenous gradient → fall in capillary perfusion → tissue ischaemia → cell injury & oedema → further rise in compartment pressure (vicious cycle).

Key points:

• The compartment does not need pressure to exceed arterial systolic pressure for ischaemia—perfusion fails well before arterial inflow stops. This is why distal pulses are usually preserved until very late.
• Local capillary perfusion pressure (~25–30 mmHg) is overwhelmed when intracompartmental pressure rises towards diastolic pressure.
• Ischaemia → loss of ATP → cell membrane failure → leak of intracellular contents → myoglobin, potassium, phosphate, urate released → rhabdomyolysis, hyperkalaemia, and myoglobinuric acute kidney injury.
• Reperfusion adds a second hit via oxygen free radicals and reactive oxygen species, worsening oedema.

Muscle tolerates roughly 4 hours of ischaemia with full recovery, irreversible changes by 6 hours, and after 8 hours the damage is essentially complete. Nerve conduction blocks within ~30 minutes and axonotmesis develops by ~12 hours.

Clinical features — the "six Ps"

The cardinal symptom is pain out of proportion to the injury and pain on passive stretch of the muscles within the affected compartment. The classic teaching mnemonic lists six Ps, but note their reliability differs greatly.

Sign (the 6 Ps)	Reliability	Comment
Pain (severe, out of proportion, increasing)	Earliest & most reliable	Worse on passive stretch
Paraesthesia	Early	First sign of nerve ischaemia
Pallor	Late / unreliable	Skin may look normal
Paralysis	Late	Indicates established damage
Pulselessness	Very late	Often present—do NOT wait for it
Poikilothermia (cold limb)	Late

High-yield: Pulselessness, pallor and paralysis are late, ominous signs—by the time they appear, irreversible necrosis is likely. The two earliest and most important clinical findings are pain out of proportion and pain on passive stretch.

High-yield: A palpable distal pulse does NOT rule out compartment syndrome. Capillary refill can also be normal early. Never reassure based on a present pulse.

Diagnostic approach in the conscious patient: the diagnosis is largely clinical. Watch for a tensely swollen, "wood-hard" compartment, escalating analgesic requirements, and pain on passive stretching. In an obtunded, anaesthetised or unreliable patient (or a child), clinical signs are unreliable—here intracompartmental pressure measurement becomes essential.

Diagnosis & investigation of choice

Stepwise approach:

1. Clinical suspicion in any swollen, painful limb after trauma/cast → high index of suspicion is the most important step.
2. Measure intracompartmental pressure (ICP) — the investigation of choice when the diagnosis is in doubt or the patient is unconscious. Done with a Stryker needle / slit catheter / wick catheter inserted into the compartment, measured within ~5 cm of the fracture.
3. Calculate ΔP (delta pressure) = diastolic BP − measured compartment pressure.
4. Supportive bloods: CK (markedly raised in rhabdomyolysis), serum potassium, renal function, urine myoglobin.

Pressure thresholds (must memorise):

Parameter	Threshold for fasciotomy
Absolute intracompartmental pressure	> 30 mmHg (some use 30–45)
Within 30 mmHg of diastolic pressure	Indication to decompress
ΔP (diastolic − compartment pressure)	< 30 mmHg → fasciotomy

High-yield: Normal resting compartment pressure is 0–10 mmHg. Capillary blood flow is compromised at ~20 mmHg. The most modern and reliable criterion is ΔP < 30 mmHg (delta pressure = diastolic minus compartment pressure), as it accounts for the patient's blood pressure—a hypotensive patient is at risk at lower absolute pressures.

Note: angiography, Doppler and imaging have no routine role—they delay treatment. Diagnosis must not be deferred for investigations when clinical signs are unequivocal.

Management — fasciotomy is the only definitive treatment

Immediate (pre-decompression) measures:

Remove all external constriction → split & spread the cast and all dressings down to skin → keep the limb at the level of the heart (NOT elevated) → correct hypotension/hypovolaemia → high-flow oxygen → adequate analgesia.

• Do not elevate the limb above heart level: elevation reduces arterial inflow and lowers the arteriovenous gradient, worsening ischaemia. Keep it at heart level.
• Do not apply ice (vasoconstriction worsens perfusion).
• Splitting a tight cast can reduce pressure by ~30–50%; if inadequate, proceed to surgery.

Definitive treatment — emergency fasciotomy:

• Indicated when ICP > 30 mmHg, ΔP < 30 mmHg, or strong clinical signs.
• All involved compartments must be completely decompressed with long skin and fascial incisions (skin is itself a limiting envelope—a small incision is inadequate).
• Wounds are left open and dressed; delayed primary closure, split-skin grafting, or shoelace/vacuum-assisted closure at 48–72 h once swelling subsides.
• Debride frankly necrotic (non-contractile, non-bleeding) muscle.

High-yield: The leg has four compartments (anterior, lateral, superficial posterior, deep posterior) decompressed by a two-incision (medial + lateral) fasciotomy, or a single lateral parafibular (Kocher–McReynolds) approach. The deep posterior compartment is the one most often missed.

Leg compartments — quick reference:

Compartment	Key muscles	Nerve	Earliest sign
Anterior (most commonly affected)	Tibialis anterior, EHL, EDL	Deep peroneal	Pain on passive toe flexion; numb 1st web space; foot drop
Lateral	Peronei	Superficial peroneal	Numb dorsum of foot
Superficial posterior	Gastrocnemius, soleus	Sural	Pain on dorsiflexion
Deep posterior	Tib. posterior, FDL, FHL	Tibial	Pain on toe extension; sensory loss sole

Forearm — Volar (3) + Dorsal (1) + mobile wad: the volar (flexor) compartment is most affected; median nerve most vulnerable. Forearm fasciotomy releases volar and dorsal compartments and the carpal tunnel.

Crush syndrome / rhabdomyolysis management:

• Aggressive IV fluids (crystalloids) to maintain urine output.
• Treat hyperkalaemia (calcium gluconate, insulin-dextrose, etc.).
• Urinary alkalinisation (sodium bicarbonate) ± mannitol is traditionally used to prevent myoglobinuric AKI (evidence debated).
• Monitor for AKI; dialysis if needed.

Complications

Early:

• Myonecrosis, infection, sepsis.
• Rhabdomyolysis → hyperkalaemia (cardiac arrest) → myoglobinuric acute kidney injury.
• Amputation if presentation is too late and the limb is non-viable.

Late:

• Volkmann's ischaemic contracture (VIC) — the classic late sequela in the forearm, especially after a supracondylar fracture of the humerus in children. Ischaemic necrosis of the flexor muscles is followed by fibrosis and contracture, producing a claw hand with flexion at wrist and fingers; passive finger extension is possible only when the wrist is flexed ("Volkmann's sign").

Volkmann's contracture — Tsuge classification (severity):

Grade	Severity	Muscle involvement
Mild	Localised	FDP of 2–3 fingers; little/no sensory loss
Moderate	Classic	FDP + FPL; median (± ulnar) sensory loss; clawing
Severe	Extensive	All flexors + often extensors; severe disability

High-yield: The classic exam triad linking the topics: supracondylar fracture of humerus → injury to brachial artery / compartment ischaemia → Volkmann's ischaemic contracture. The muscles first and worst affected are flexor digitorum profundus and flexor pollicis longus (deep flexors, watershed zone of perfusion).

Key differentials

Condition	Distinguishing feature
Arterial injury / occlusion	Absent pulses early, cold pale limb from the outset, hard distal ischaemia signs; angiography helps. Compartment syndrome keeps pulses till late
Deep vein thrombosis	Swelling + tenderness but no pain on passive stretch out of proportion; Doppler positive
Cellulitis	Erythema, warmth, fever, raised inflammatory markers; no compartment tensing
Crush syndrome	Systemic (renal, metabolic) emphasis; compartment may or may not be tense
Stress fracture / shin splints	Chronic exertional; pain relieved by rest (vs ACS which progresses)
Gas gangrene	Crepitus, foul discharge, systemic toxicity, gas on X-ray

Recently asked / exam angle

• Earliest and most reliable clinical sign of acute compartment syndrome → pain on passive stretch / pain out of proportion (NOT pulselessness).
• Investigation of choice when diagnosis uncertain → intracompartmental pressure measurement (Stryker needle / slit catheter).
• Pressure cut-off for fasciotomy → absolute > 30 mmHg, or ΔP < 30 mmHg (within 30 mmHg of diastolic).
• Commonest fracture causing leg compartment syndrome → tibial shaft fracture.
• Most commonly involved leg compartment → anterior compartment; nerve at risk = deep peroneal, leading to foot drop and numbness of the first web space.
• Position of the limb in suspected compartment syndrome → at the level of the heart (not elevated, not iced).
• First step with a tight POP cast and rising pain → split the cast down to skin (bivalve).
• Late sequela of forearm ischaemia after supracondylar fracture → Volkmann's ischaemic contracture; deep flexors (FDP, FPL) affected first.
• Number of leg compartments released in fasciotomy → four; most commonly missed = deep posterior.
• A palpable pulse does not exclude compartment syndrome — frequent MCQ trap.
• Rhabdomyolysis labs: raised CK, hyperkalaemia, myoglobinuria → AKI.

Mnemonics

• The 6 Ps: Pain (out of proportion), Paraesthesia, Pallor, Paralysis, Pulselessness, Poikilothermia (cold). Remember the first two are early/reliable; the last three are late/ominous.
• "Pain, Pressure, Paralysis" — the order in which compartment syndrome unfolds.
• Leg compartment nerves — "ALL the Deep, Superficial, Posterior": Anterior–deep peroneal, Lateral–superficial peroneal, deep posterior–tibial.

Rapid revision

1. Acute compartment syndrome = pressure in a closed osteofascial space exceeds perfusion → ischaemic necrosis; time to fasciotomy decides outcome (irreversible by ~6 h).
2. Commonest cause overall = tibial shaft fracture; commonest forearm cause in children = supracondylar humerus fracture.
3. Open fractures do not protect against it; tight casts are a common precipitant.
4. Earliest/most reliable signs = pain out of proportion and pain on passive stretch; paraesthesia is the first nerve sign.
5. Pulselessness, pallor, paralysis = late, ominous—never wait for them; pulse may be present even in established disease.
6. Investigation of choice = intracompartmental pressure measurement (Stryker needle), especially in the unconscious patient.
7. Fasciotomy if ICP > 30 mmHg, or ΔP (diastolic − compartment pressure) < 30 mmHg; normal pressure 0–10 mmHg.
8. Pre-op: split cast & dressings to skin, keep limb at heart level (do not elevate or ice), correct hypotension, give oxygen.
9. Leg has 4 compartments; anterior most affected (deep peroneal nerve → foot drop), deep posterior most often missed.
10. Forearm volar (flexor) compartment most affected; FDP and FPL are the watershed muscles damaged first.
11. Late sequela = Volkmann's ischaemic contracture → claw hand; graded by Tsuge classification.
12. Systemic danger = rhabdomyolysis → hyperkalaemia + myoglobinuric AKI; manage with IV fluids, treat hyperkalaemia, monitor renal function.