Compartment syndrome nursing: recognition, assessment, and emergency interventions

Compartment syndrome is a surgical emergency in which pressure within a closed muscle compartment rises to the point where it interrupts blood flow, starving tissues of oxygen and triggering an ischemic cascade. If pressure is not relieved within 6–8 hours, muscle and nerve death become irreversible. For nurses, recognition is the intervention: by the time a physician is called, medication is drawn up, or imaging is requested, the window may have narrowed significantly. This reference page provides the clinical depth nursing students need to recognize, assess, and respond to compartment syndrome – including the NCLEX-tested distinctions that separate early, salvageable presentations from late, catastrophic ones.

Compartment syndrome occurs most often after long-bone fractures (particularly the tibia and forearm), circumferential casting complications, crush injuries, prolonged ischemia, and reperfusion events. Less commonly, it follows burns, snake envenomation, bleeding disorders, and prolonged limb compression during surgery or unconsciousness. Because the condition progresses inside an intact fascial envelope, the external appearance of the limb is often deceptively normal until the damage is already severe – making systematic neurovascular assessment and a high clinical index of suspicion the nurse’s primary tools.

Quick reference: types and thresholds

Type	Primary cause	Pressure threshold for intervention	Time to irreversible injury	Primary intervention
Acute traumatic	Long-bone fracture, crush injury, circumferential cast, post-surgical swelling	>30 mmHg absolute OR ΔP (diastolic BP − compartment pressure) ≤30 mmHg	6–8 hours from onset of ischemia	Emergency fasciotomy
Crush/rhabdomyolysis-associated	Prolonged compression, building collapse, industrial accident, positional ischemia during surgery	Same as acute traumatic; rhabdomyolysis compounds edema rapidly	6–8 hours; myoglobin release accelerates secondary injury	Fasciotomy + aggressive IV hydration, urine alkalinization
Chronic exertional (CECS)	Repetitive exercise-induced swelling in athletes (anterior leg most common)	Post-exercise pressure ≥15 mmHg at 1 minute, ≥12 mmHg at 5 minutes (Pedowitz criteria)	Resolves with rest; no acute irreversible injury unless exercise continued past tolerance	Activity modification; elective fasciotomy if conservative measures fail

Pathophysiology

Skeletal muscle and neurovascular structures are enclosed within fascial compartments – inelastic fibrous sheaths that cannot expand. Normally, intracompartmental pressure remains below 10 mmHg, well below the capillary perfusion pressure of 25–30 mmHg. When anything increases the volume of compartment contents (edema, hematoma, reperfusion fluid) or decreases compartment volume (tight cast, circumferential burn eschar, external compression), pressure rises.

As pressure climbs toward 30 mmHg, venous outflow becomes obstructed first. Blood backs up in the compartment, increasing hydrostatic pressure further and driving more fluid into the interstitium – a self-reinforcing cycle. Once intracompartmental pressure approaches or exceeds the arteriolar perfusion pressure (roughly 30 mmHg below diastolic blood pressure), arterial inflow is compromised. The resulting tissue ischemia triggers the release of histamine, bradykinin, and oxygen free radicals, which increase capillary permeability and worsen edema even further.

Muscle cells tolerate ischemia for approximately 4 hours before irreversible changes begin; complete necrosis typically occurs by 6–8 hours. Peripheral nerve fibers are somewhat more sensitive, with early dysfunction (tingling, numbness) appearing within 30 minutes of ischemia and axonal degeneration beginning around 4 hours. This timeline explains why paresthesia is an early warning sign and paralysis is late: by the time a patient cannot move their fingers or toes, structural nerve damage has already occurred.

After 12–24 hours without decompression, the dead muscle fibers undergo fibrotic replacement, producing the irreversible flexion deformity known as Volkmann ischemic contracture. In the forearm, this results in the classic “forearm and wrist flexion with finger clawing” posture that serves as a permanent reminder of a missed diagnosis.

The compartments most frequently affected in clinical practice are:

Anterior leg – contains the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and the deep peroneal nerve; most commonly affected overall
Deep posterior leg – contains the flexor hallucis longus, flexor digitorum longus, and the tibial nerve; the most dangerous leg compartment because it is deep and often underappreciated
Volar forearm – contains finger and wrist flexors; affected in distal radius fractures, supracondylar fractures in children
Dorsal forearm – extensor compartment; less often involved than volar
Hand (intrinsic compartments) – burn injuries, injection injuries, snake envenomation
Thigh – femoral shaft fractures, massive hemorrhage; requires much higher pressure because of its large volume
Gluteal – prolonged positioning during surgery; often overlooked

Post-fracture development is the most common scenario encountered on NCLEX. For nurses caring for patients with tibial fractures, forearm fractures, or supracondylar humeral fractures (particularly in children), compartment syndrome must be treated as an active threat until the risk window has passed. The fractures nursing reference provides additional context on fracture classification and perioperative care.

The 6 P’s: NCLEX assessment priorities

The six classic signs of compartment syndrome – Pain, Pressure, Paresthesia, Paralysis, Pallor, and Pulselessness – appear roughly in order of their clinical timeline. This sequence is the most heavily tested topic on NCLEX questions about compartment syndrome: early signs are actionable; late signs indicate that permanent damage is already underway.

Sign	Description	Clinical significance	NCLEX priority
Pain	Severe pain that is disproportionate to the injury; unrelieved by opioid analgesics; dramatically worsened by passive stretch of muscles within the compartment	Earliest and most reliable sign. Pain out of proportion to the injury is the defining clinical feature. If a patient says their pain is 10/10 after receiving IV morphine, this should trigger an immediate neurovascular assessment and compartment syndrome workup.	Highest priority – act immediately
Pressure	Palpable firmness or tenseness of the compartment on physical exam; the affected limb segment feels "woody" or "board-like" compared to the contralateral limb	Direct sign of elevated intracompartmental pressure. May be the first objective finding when the patient is sedated or cannot communicate pain clearly. Not always prominent in deep compartments.	High priority – supports diagnosis
Paresthesia	Tingling, pins-and-needles sensation, or numbness in the sensory distribution of nerves running through the affected compartment (e.g., dorsal web space of first toe for anterior leg compartment via deep peroneal nerve)	Early ischemia signal. Peripheral nerves depolarize abnormally under ischemic conditions before they die, producing sensory changes. The appearance of paresthesia indicates that nerve function is being compromised – decompression is urgently needed to prevent progression to permanent deficit.	High priority – escalate care
Paralysis	Inability to actively move muscles in the compartment or move distal structures (inability to dorsiflex the foot in anterior leg ACS; inability to extend the wrist or fingers in volar forearm ACS)	Late sign – indicates severe ischemia and likely irreversible nerve/muscle damage. Do not wait for paralysis to intervene. On NCLEX questions asking "which finding should prompt immediate action," paralysis appearing alongside the other signs means fasciotomy cannot be delayed even one hour.	Very high priority – late, potentially irreversible
Pallor	Pale, mottled, or ashen distal skin; may be accompanied by coolness on palpation of the skin distal to the affected compartment	Late sign – indicates severe arterial compromise. Skin color changes represent markedly reduced arterial inflow, meaning the ischemic cascade is far advanced. In darker-pigmented patients, checking capillary refill time (>3 seconds) and skin temperature are more reliable than color alone.	High priority – very late sign
Pulselessness	Absent or markedly diminished pulse distal to the compartment on Doppler or palpation; loss of Doppler flow at the dorsal pedal artery in leg ACS, or the radial artery in forearm ACS	Ominous/terminal sign – vascular occlusion is complete. By the time pulses are absent, irreversible muscle and nerve death are almost certain. A common NCLEX trap: students assume "no pulse" is the earliest sign because it seems most serious. In practice, the absence of a pulse is the last sign, and limb viability may already be lost. Waiting for pulselessness to call the surgeon represents a critical nursing failure.	Highest urgency – permanent damage highly likely

The key NCLEX sequence to memorize: Pain and Paresthesia = early (act NOW). Paralysis, Pallor, and Pulselessness = late (damage may be done). Pressure is not reliably graded as early or late – it reflects compartment tension throughout the syndrome’s course.

Assessment and diagnosis

Neurovascular checks

Neurovascular assessment frequency depends on risk level:

High-risk patients (post-tibia fracture, post-casting, post-crush injury, post-forearm fracture, post-fasciotomy to monitor for recurrence): every 1 hour
Moderate-risk (post-surgical limb, post-reduction): every 2 hours for the first 24 hours
Lower-risk: every 4 hours or per unit protocol

Each check must document: skin color, skin temperature, capillary refill time, sensation in nerve distribution, motor function (active toe/finger movement), pulse quality, pain level, and response to passive stretch.

Passive stretch test

The passive stretch test exploits the fact that ACS pain is dramatically worsened by stretching the muscles within the involved compartment:

Anterior leg compartment: passively dorsiflex the toes → this stretches the extensor muscles in the anterior compartment → significant pain is a positive test
Volar forearm: passively extend the fingers and wrist → this stretches the flexor muscles → pain in the volar forearm is positive
Deep posterior leg: passively dorsiflex the foot (same maneuver, different sensation location – pain in the calf rather than the dorsum)

Passive stretch pain is widely considered the most sensitive early sign of ACS, more reliable than paresthesia in well-sedated patients.

Intracompartmental pressure measurement

Formal pressure measurement is performed when clinical signs are equivocal, when the patient cannot communicate (unconscious, intubated, pediatric), or when the clinical picture needs objective confirmation before surgical decision-making.

Devices used:

Stryker STIC device – the most commonly used bedside tool; a small catheter is inserted directly into the compartment and connected to a pressure transducer
Arterial line manometer – arterial line setup repurposed for compartment measurement; less common but available in most ICUs
Wick or slit catheter – research/specialized settings; provides continuous monitoring

Normal intracompartmental pressure is less than 10 mmHg. Two thresholds guide fasciotomy decisions:

Absolute pressure >30 mmHg – action threshold
ΔP ≤30 mmHg – where ΔP = (diastolic blood pressure) − (compartment pressure). This is the preferred threshold in hemodynamically unstable patients: a patient with a diastolic BP of 50 mmHg and a compartment pressure of 25 mmHg has a ΔP of only 25 – below the threshold despite the compartment pressure appearing “acceptable” by the absolute standard alone.

Laboratory workup in crush-associated ACS

When compartment syndrome follows crush injury or prolonged ischemia, rhabdomyolysis is a co-occurring process that requires parallel management. Key labs:

Creatine kinase (CK): rises within hours of muscle injury; levels >1,000 U/L are concerning, >5,000 U/L indicate significant rhabdomyolysis, >10,000 U/L carry high AKI risk
Myoglobin (urine and serum): myoglobin filters rapidly into urine, producing the classic dark brown or tea-colored urine of myoglobinuria
BUN/creatinine: rising values indicate early renal involvement – the myoglobin is precipitating in renal tubules
Urinalysis with microscopy: positive for blood on dipstick (myoglobin triggers heme reaction) but no red cells on microscopy – a dissociation that is classic for rhabdomyolysis
Potassium: crush injury releases massive intracellular potassium; hyperkalemia can be immediately life-threatening, particularly in cardiac patients

The rhabdomyolysis nursing reference covers the renal management pathway in detail. When AKI develops secondary to myoglobinuria, the AKI nursing reference provides the full nursing management framework.

Imaging

Imaging is generally not useful for diagnosing acute compartment syndrome. Pressure measurement and clinical signs are the definitive tools.

X-ray: useful for fracture characterization and confirming injury context; does not measure compartment pressure
MRI: the only imaging modality with meaningful utility; shows edema and necrosis within compartments; used primarily for chronic exertional compartment syndrome diagnosis and for post-fasciotomy complications assessment. Not appropriate for acute ACS because it delays treatment.
Duplex ultrasound: can demonstrate absent arterial flow in late ACS; again, not appropriate to delay surgery waiting for this

Nursing interventions

Once compartment syndrome is suspected, nursing action precedes physician notification – not the other way around. The following interventions are performed on clinical judgment while simultaneously escalating to the surgical team.

Intervention	Rationale	Timing/priority
Remove all constrictive dressings, splints, and circumferential casts immediately	Cast padding and splint wrapping reduce the space available for swelling; each layer removed may reduce compartment pressure by 5–10 mmHg. Bivalving a cast (cutting it longitudinally on two sides) and spreading it open reduces pressure further. This is a nursing action that does not require a physician order in most facilities – nurses have a duty to respond to imminent tissue ischemia.	First priority – do this before calling the physician
Position limb at heart level – never elevated	Elevation reduces arterial perfusion pressure to the ischemic compartment, worsening inflow. This is the opposite of what nurses do for edema, DVT, and most orthopedic post-op care. Heart-level positioning (flat, neutral) maintains the maximum available arterial pressure gradient. This is a high-yield NCLEX distinction.	Immediate – do simultaneously with cast removal
Do NOT apply ice or cold therapy	Cold causes vasoconstriction, further reducing arterial inflow to already-ischemic tissue. Ice is standard for acute musculoskeletal injuries but is contraindicated in suspected compartment syndrome.	Immediate – stop any cold therapy in progress
Supplemental oxygen	Maximizes oxygen delivery to ischemic tissue by increasing the dissolved oxygen content of blood reaching the affected compartment. Use non-rebreather mask to deliver FiO2 as high as clinically appropriate.	Immediate
IV access and fluid resuscitation	Large-bore IV access supports resuscitation, blood product administration if hemorrhage is present, and IV analgesia. In crush-associated ACS with rhabdomyolysis, aggressive crystalloid resuscitation (normal saline or LR at 1–1.5 L/hour initially) is required to prevent myoglobin precipitation in renal tubules and maintain urine output ≥200–300 mL/hour.	Immediate; titrate based on clinical response
Pain management with opioids	IV opioid analgesia is appropriate – this is a genuinely painful emergency. The critical nursing assessment point is that opioid administration does not eliminate ACS pain; persistent severe pain despite opioids strengthens the diagnosis, not weakens it. Adequate analgesia should be provided while monitoring for the persistence of pain as a diagnostic signal.	Early; do not withhold adequate analgesia
Neurovascular monitoring q15–30 minutes	Once ACS is suspected, monitoring frequency increases to every 15–30 minutes, documenting all 6 Ps plus capillary refill time and digital pulse oximetry (if available). Any deterioration is immediately reported. This frequent monitoring provides both clinical data and a timeline record for surgical decision-making.	Ongoing until surgical decision made
Prepare for emergency fasciotomy	Fasciotomy is the definitive treatment for ACS. Nursing preparation includes: obtaining surgical consent with the provider present, establishing an additional large-bore IV, patient NPO status, foley catheter insertion (especially if rhabdomyolysis – precise urine output monitoring is critical), type and screen or crossmatch, pre-operative documentation and medication reconciliation.	Concurrent with above – delay increases injury
Notify the surgical team	ACS requires orthopedic or vascular surgical consultation for definitive management. The escalation call should include: the affected compartment, current neurovascular status (pain, sensation, motor function, pulse quality), compartment pressure if measured, vital signs, and a direct statement – "I am concerned this is acute compartment syndrome."	As soon as clinical suspicion is formed – do not wait for all 6 Ps to be present

The trauma and emergency nursing reference covers the broader framework for emergency assessment and surgical preparation that applies here.

Fasciotomy nursing care

Fasciotomy is the definitive surgical treatment for acute compartment syndrome. The procedure involves making longitudinal incisions through the overlying skin and fascia to decompress all compartments in the affected limb segment. For the lower leg, this typically means four-compartment release through two incisions; for the forearm, both volar and dorsal incisions are required.

The defining feature of post-fasciotomy wounds

Fasciotomy wounds are left open – this is non-negotiable. Attempting primary closure immediately after fasciotomy would simply recreate the pressure problem the surgery was designed to solve. The wound remains open for 48–72 hours while edema resolves, then undergoes delayed primary closure or split-thickness skin grafting if direct closure is not possible due to excessive tissue swelling.

This open-wound status requires specific nursing management and clear patient and family education. Many patients (and families) are alarmed to see a large open wound on their limb following “leg surgery.” Proactive education about why the wound is open and what the closure plan looks like is a key nursing role during the post-operative period.

Post-fasciotomy nursing priorities

Wound care:

Wet-to-dry dressings or negative pressure wound therapy (wound VAC) are the most common approaches to fasciotomy wound management
Wound VAC therapy reduces edema, promotes granulation tissue formation, and helps manage wound exudate – it also keeps the wound contained and reduces infection risk
Dressing changes should be documented with wound dimensions (length, depth, width), tissue quality (granulation, slough, eschar), exudate type and amount, and surrounding skin condition
The wound assessment reference provides the full framework for wound documentation and staging

Edema monitoring:

Document limb circumference at a fixed anatomical landmark daily to track edema resolution
Edema is expected to peak 24–48 hours post-injury, then begin declining; failure to resolve raises concern for recurrent elevated pressure or infection
Elevate the limb only AFTER fasciotomy (not before) – once compartments are open and pressure is decompressed, standard elevation to reduce edema is appropriate and encouraged

Infection surveillance:

Open wounds in traumatic and crush injury patients carry significant infection risk
Monitor wound edges for erythema, warmth, induration, and purulent exudate
Monitor systemic signs: fever, rising WBC, tachycardia
Pre-existing muscle necrosis provides an ideal medium for anaerobic bacterial growth – gas-forming organisms (Clostridium) must be considered if wound odor is present or tissue appears necrotic despite fasciotomy

Pain management:

Post-fasciotomy pain management requires opioid analgesics, NSAIDs (if renal function permits), and often regional nerve blocks (popliteal nerve block for anterior compartment releases)
Pain should decrease significantly after fasciotomy; persistent or worsening pain post-operatively suggests incomplete decompression, recurrent pressure, or wound complications

Rehabilitation:

Physical therapy involvement begins early – passive range of motion during the open-wound phase prevents contracture formation
Occupational therapy involvement is particularly important for upper extremity fasciotomies where hand function is the primary rehabilitation goal
Patient and family education covers: expected wound appearance, dressing change participation, functional rehabilitation timeline, signs of wound complications to report

Burns involving electrical injury can produce a similar fascial compartment problem, typically managed with escharotomy (incision through burned skin) or fasciotomy; the burns nursing reference covers this parallel in the context of circumferential burn care.

Complications

Complication	Mechanism	Nursing monitoring
Volkmann ischemic contracture	Prolonged ischemia causes myocyte death and fibrotic replacement of muscle tissue. In the forearm, this produces irreversible flexion deformity: the forearm pronates, the wrist flexes, and the fingers claw into flexion. In the leg, claw toe and equinus foot deformity develop. Once established, contracture is only partially reversible with surgery.	Document baseline range of motion immediately post-injury; monitor for progressive loss of passive extension; report new or worsening contracture to surgical team; ensure PT/OT involvement starts in the acute phase
Rhabdomyolysis-associated AKI	Myoglobin released from necrotic muscle cells is filtered at the glomerulus, precipitates in renal tubules in the acidic environment of concentrated urine, and causes direct tubular toxicity plus mechanical obstruction. Serum creatinine rises, urine output falls, and urine darkens to brown or cola-colored.	Strict hourly urine output (target ≥200 mL/hr with aggressive IVF); document urine color with each void or hourly if foley in place; monitor serial CK, BUN, creatinine, and potassium; report rising creatinine, falling urine output, or urine darker than amber immediately
Wound infection and sepsis	Necrotic muscle is an ideal bacterial medium. Open fasciotomy wounds are exposed to hospital flora. Immunocompromised patients, diabetic patients, and those with crush injuries face the highest risk. Gas-forming organisms (Clostridium perfringens) can cause gas gangrene in contaminated traumatic wounds.	Monitor wound for erythema, warmth, purulent exudate, unusual odor, or tissue that looks necrotic despite decompression; daily temperature trending; CBC for rising WBC; blood cultures if fever develops; report gas in soft tissue on imaging immediately (gas gangrene is a surgical emergency)
Reperfusion injury	Restoration of blood flow to ischemic tissue triggers a burst of oxygen free radicals from mitochondria and activated neutrophils. This worsens local tissue injury, increases capillary permeability, and can contribute to systemic inflammatory response. Clinically, patients may experience increased pain and swelling transiently after fasciotomy.	Monitor for worsening rather than improving pain and swelling in the first 4–6 hours post-fasciotomy; document vital signs for SIRS criteria (fever, tachycardia, elevated WBC); the expected trajectory after fasciotomy is improvement – clinical deterioration should prompt reassessment
Nerve and vessel injury during fasciotomy	Surgical incisions in anatomically constrained compartments carry risk of inadvertent nerve or vessel injury. The saphenous nerve (medial leg fasciotomy incision), deep peroneal nerve, and superficial peroneal nerve are at particular risk in lower extremity releases.	Baseline neurological exam documentation before surgery is critical for post-operative comparison; post-fasciotomy, assess sensation in all nerve distributions for the affected limb; new sensory deficits after surgery may indicate intraoperative nerve injury vs. pre-existing ischemic damage
Amputation	Delayed diagnosis, inadequate decompression, or extensive crush injury may result in non-viable limb with irreversible muscle and vascular necrosis. Amputation is the last resort when limb salvage is anatomically or physiologically not possible.	Document neurovascular status serially; if limb remains pulseless and motor-paralyzed 24–48 hours post-fasciotomy, report to surgical team for reassessment; provide psychological support for patients facing limb-loss discussions; involve social work and rehabilitation teams early in high-risk presentations

The development of AKI following crush-associated compartment syndrome is one of the most clinically significant complications to manage. Orthopedic conditions complicated by prolonged hospitalization also carry risk of osteomyelitis in patients with compromised soft tissue and open wounds – the osteomyelitis nursing reference covers the infectious complications of orthopedic injuries.

NCLEX tips

Pain out of proportion to the injury + unrelieved by opioids = suspect acute compartment syndrome immediately. This is the single highest-yield fact for NCLEX. If a patient with a casted tibia fracture rates their pain 9/10 after IV morphine, the next nursing action is neurovascular assessment and physician notification – not another dose of pain medication.
Passive stretch pain is the most sensitive early sign. Passive dorsiflexion of the toes causing significant pain in the anterior leg compartment is positive – more reliable than paresthesia in patients whose baseline sensation may be affected by medications or pre-existing neuropathy.
Paresthesia = early ischemia; paralysis = late, likely irreversible. Tingling or numbness in the sensory distribution of the nerve within the compartment (e.g., the first web space of the foot for the deep peroneal nerve) is an early warning. Loss of motor function means structural nerve damage has begun.
Never elevate a limb with suspected ACS. This is the most commonly tested NCLEX trap. Elevation is standard for sprains, DVT, post-op orthopedic care, and virtually every other limb injury – but in compartment syndrome, elevation reduces arterial perfusion pressure and worsens ischemia. Position the limb at heart level.
Never apply ice. Cold causes vasoconstriction, worsening ischemia. Ice is contraindicated in suspected compartment syndrome despite being standard for acute musculoskeletal injury.
Remove casts and constrictive dressings first; then notify the physician. This is a nursing action requiring clinical judgment, not a physician order. Removing the constrictive element may be the intervention that saves the limb. The physician is called simultaneously or immediately after, not before.
Fasciotomy threshold: compartment pressure >30 mmHg OR ΔP ≤30 mmHg. ΔP = diastolic BP minus compartment pressure. A patient with diastolic BP of 50 mmHg and a compartment pressure of 28 mmHg has a ΔP of 22 – well below the threshold – and needs fasciotomy even though the absolute pressure seems acceptable. NCLEX may present a BP and a compartment pressure and ask whether fasciotomy is indicated.
Absent pulse is a LATE, ominous sign – not the first sign. A common misconception is that pulselessness is the hallmark of compartment syndrome. In fact, by the time the pulse disappears, the damage is often irreversible. Waiting for absent pulses before acting = nursing failure.
Crush injury → monitor CK and urine color for rhabdomyolysis and AKI. Any patient with prolonged muscle compression should have serial CK measurements and urine output documented with color description. Dark urine (tea-colored or cola-colored) + dipstick positive for blood + no red cells on microscopy = myoglobinuria = rhabdomyolysis.
Post-fasciotomy wounds are left open. Immediate closure would recreate the pressure problem. The wound is left open 48–72 hours, then closed by delayed primary closure or skin grafting. Patients and families need explicit education about why the wound is open and what to expect.
Neurovascular checks every 1 hour minimum for high-risk patients. Post-tibial fracture, post-casting, post-crush, and post-fasciotomy patients require hourly neurovascular assessment. If a student sees “every 4 hours” as an NCLEX option for a patient with a fresh tibia fracture in a cast, that answer is wrong.
Chronic exertional compartment syndrome resolves with rest. CECS typically presents as bilateral aching or tightness in the anterior lower legs during running or cycling, consistently resolving within 15–30 minutes of stopping exercise. The diagnosis is confirmed by measuring post-exercise compartment pressures (Pedowitz criteria). This is a clinical and NCLEX differentiator from acute traumatic ACS.
In ACS, the limb feels firm or tense on palpation. The compartment pressure sign (the second P) is detectable by palpation – the limb segment feels “woody” or unusually hard compared to the contralateral side. This is particularly useful in unresponsive patients where pain cannot be assessed.
Electrical burns can cause compartment syndrome requiring fasciotomy. Electrical injury causes deep muscle necrosis that may not be apparent on external inspection. This can create compartment syndrome that presents hours after the burn event – requiring the same assessment and intervention framework as traumatic ACS.

Practice questions

Question 1

A patient in the emergency department has a left tibial fracture stabilized with a long-leg cast 3 hours ago. The patient rates pain as 9/10, states their toes are “tingling,” and reports the pain is not responding to IV morphine given 30 minutes ago. The left foot is warm and dorsalis pedis pulse is 2+ on Doppler. Which of the following actions should the nurse take first?

A. Administer a second dose of IV morphine and reassess in 30 minutes B. Elevate the left leg above the level of the heart to reduce swelling C. Apply ice to the left lower leg to decrease inflammation D. Remove the cast and notify the orthopedic surgeon immediately

Answer: D. The clinical picture – pain disproportionate to injury, unrelieved by opioids, with new paresthesia in a freshly casted tibial fracture – is acute compartment syndrome until proven otherwise. Removing the cast is the first nursing action; physician notification occurs simultaneously. Option A is wrong because opioid-unresponsive pain in this context is a diagnostic signal, not a pain management problem. Option B is wrong because elevation reduces arterial perfusion in ACS. Option C is wrong because vasoconstriction from cold worsens ischemia.

Question 2

A nurse is caring for a patient admitted after a building collapse with crush injury to both lower extremities. The patient’s diastolic blood pressure is 55 mmHg. Intracompartmental pressure measurement of the right anterior leg compartment reads 30 mmHg. Which interpretation is most accurate?

A. No intervention is needed because the compartment pressure is below the 30 mmHg threshold B. Fasciotomy is indicated because the ΔP equals 25 mmHg, which is below the threshold of 30 C. Fasciotomy is not indicated because the absolute pressure is at the threshold, not above it D. The pressure reading should be repeated in 1 hour before making a clinical decision

Answer: B. The ΔP = diastolic BP (55) − compartment pressure (30) = 25 mmHg. This falls below the threshold of 30 mmHg, indicating that arterial perfusion pressure is dangerously close to being overcome by compartment pressure. Fasciotomy is indicated regardless of the fact that the absolute pressure of 30 mmHg is at – not exceeding – the absolute threshold. In a hemodynamically compromised patient, ΔP is the more important metric. Option D is wrong because in a crush injury patient with ΔP of 25, a 1-hour delay risks irreversible tissue injury.

Question 3

A patient is 18 hours post-fasciotomy for acute compartment syndrome of the left leg. The nurse notes the wound remains open with moist saline dressings in place, significant edema of the left lower leg, and mild serosanguineous drainage. The patient asks why the wound is not sutured closed. Which response by the nurse is most accurate?

A. “The surgeon was not able to complete the procedure and will close it tomorrow.” B. “The wound will close on its own over the next few days without any further intervention.” C. “The wound is intentionally left open to prevent pressure from building up again as swelling resolves.” D. “Leaving the wound open is a precaution in case infection develops that needs to be drained.”

Answer: C. Post-fasciotomy wounds are intentionally left open to allow edema resolution and prevent re-elevation of compartment pressure. Closing the wound immediately would recreate the constrictive environment that caused the injury. Delayed primary closure or skin grafting occurs typically at 48–72 hours once edema has sufficiently resolved. Option B is incorrect because wounds of this size do not close by secondary intention without intervention. Option D describes a rationale that is partially true regarding infection access but is not the primary reason for leaving the wound open.