01Approach to the Critical Patient/attcp40

Immediate recognition and time targets

›Surgical emergency recognition

›Irreversible nerve damage begins at 4 hours of ischemia

›Irreversible muscle necrosis occurs by 6 hours

›Immediate orthopedic or trauma surgery consultation at first clinical suspicion

›Do not delay consultation for confirmatory imaging or pressure measurement

›Critical alarm triggers

›Pain out of proportion to injury — the hallmark symptom

›Pain refractory to escalating analgesics — most reliable early sign

›Pain with passive stretch of involved compartment muscles

›Progressive paresthesias in first web space (deep peroneal nerve)

›Tense, woody compartment on palpation

Initial stabilization

›Immediate decompression measures

›Remove all constrictive dressings, casts, and splints immediately

›Bivalve and spread casts — do not merely split

›Position limb at heart level — elevation above heart decreases perfusion pressure

›Padding removal from beneath cast

›Resuscitation targets

›IV crystalloid resuscitation for rhabdomyolysis prevention

›Urine output target 1–2 mL/kg/hr when myoglobinuria suspected

›Emergent treatment of hyperkalemia if ECG changes present

›Calcium gluconate for cardiac membrane stabilization

›Insulin and dextrose for potassium shifting

›Analgesia

›IV opioid analgesia — do not withhold, but escalating requirements heighten suspicion

›Do not use regional anesthesia or epidural catheters in at-risk patients

›Regional anesthesia masks pain — the primary diagnostic symptom

02History/hx47

Mechanism and onset

›Causative mechanism

›Tibial shaft fractures — most common cause; ACS occurs in 1–9% of lower extremity fractures

›High-energy tibial plateau fractures and knee fracture-dislocations

›Crush injury — prolonged compression of lower extremity

›Vascular injury with reperfusion

›Burns — especially circumferential

›Prolonged immobilization — found down patient

›Iatrogenic — tight cast, dressing, or splint

›Massive fluid resuscitation

›Intravenous infiltration at lower extremity site

›Onset timeline

›Can develop minutes to hours after inciting event

›Most commonly develops within 24–48 hours of injury

›Open fractures do not exclude ACS — up to 30% of cases occur without fracture

Pain characterization

›Pain quality

›Severe, deep, unrelenting — out of proportion to injury

›Initially controlled, then becomes refractory to escalating analgesics — highly concerning

›Pain with passive stretch of muscles of involved compartment

›Anterior compartment: pain with passive plantarflexion of toes

›Lateral compartment: pain with passive inversion of foot

›Deep posterior compartment: pain with passive dorsiflexion of toes

›Superficial posterior compartment: pain with passive dorsiflexion of ankle

›Associated symptoms

›Paresthesias — especially first web space (deep peroneal nerve, anterior compartment)

›Swelling and tightness of leg

›Difficulty moving toes

03Physical Exam/exam36

Vital signs

›Hemodynamic snapshot

›Tachycardia — may indicate systemic effects of rhabdomyolysis or hemorrhage

›Hypotension — hemorrhagic shock from associated injury or severe rhabdomyolysis

›Fever — consider infectious etiology including Group A Streptococcus causing ACS

Compartment assessment

›Inspection

›Swelling — diffuse or focal compartment swelling

›Ecchymosis — underlying hematoma

›Skin changes — tense, shiny skin

›Circumferential burns or constrictive dressings

›Palpation

›Tense, firm, woody compartment — low sensitivity/specificity but raises suspicion

›Compare to contralateral uninjured limb

›Four compartments of the lower leg: anterior, lateral, superficial posterior, deep posterior

›Passive stretch provocative testing

›Anterior compartment: passive plantarflexion of toes

›Lateral compartment: passive inversion of foot

›Deep posterior compartment: passive dorsiflexion of toes

›Superficial posterior compartment: passive dorsiflexion of ankle

Neurologic exam

›Sensory assessment

›First web space sensation — deep peroneal nerve, anterior compartment involvement

›Lateral foot sensation — superficial peroneal nerve, lateral compartment

›Plantar surface sensation — tibial nerve, posterior compartments

›Motor assessment

›Extensor hallucis longus strength — deep peroneal nerve, anterior compartment

›Dorsiflexion strength — anterior compartment

04Differential Diagnosis/ddx40

Life-threatening diagnoses

›Acute arterial ischemia

›ICD-10 I74.3 — embolism and thrombosis of arteries of lower extremities

›Pallor, pulselessness, and paralysis more characteristic than in ACS

›Check ankle-brachial index and Doppler pulses

›Urgent vascular surgery consultation

›Necrotizing fasciitis

›ICD-10 M72.6

›Erythema, fever, systemic toxicity, crepitus

›Rapidly progressive skin changes out of proportion to injury

›Urgent surgical debridement required

›Septic arthritis with adjacent myositis

›Fever, leukocytosis, joint involvement

›Imaging and aspiration required

Common mimics

›Deep vein thrombosis

›ICD-10 I82.4

›Swelling and pain but typically less severe

›No pain with passive stretch maneuvers

›Compression ultrasound to confirm

›Cellulitis

›ICD-10 L03.1

›Erythema, warmth, tenderness

›No passive stretch pain

›No tense compartment

›Fracture pain without compartment syndrome

›Expected post-fracture pain should improve with immobilization, not worsen

›Pain trajectory trending down reassuring

05Laboratory Tests/lt37

Rhabdomyolysis and muscle injury panel

›Creatine kinase

›Elevated with muscle necrosis — serial monitoring recommended

›CK greater than 5000 U/L associated with increased acute kidney injury risk

›Peak CK timing typically 24–72 hours post-injury

›Trend to confirm resolution with treatment

›Serum myoglobin

›Elevated with muscle breakdown

›Correlates with renal injury risk

›Myoglobin clears faster than CK — serial CK more useful for monitoring

›Urinalysis

›Myoglobinuria: dipstick positive for blood without RBCs on microscopy

›Urine color: dark brown, tea-colored, or cola-colored

›Specific gravity and concentration assessment

Electrolytes and metabolic panel

›Basic metabolic panel

›Hyperkalemia — life-threatening, released from necrotic muscle

›Serum potassium greater than 6.0 mmol/L requires emergent treatment

›Metabolic acidosis — lactic acid from ischemic muscle

›Elevated creatinine indicating renal compromise

›Phosphate — elevated with rhabdomyolysis

›Calcium — may be low (sequestered into necrotic muscle)

Coagulation and hematologic labs

›Complete blood count

›Baseline hemoglobin for operative planning

›Leukocytosis may suggest infectious etiology

›Coagulation studies

›INR and aPTT if anticoagulant use or coagulopathy suspected

06Diagnostic Tests/dt65

Scoring Systems

›Delta pressure threshold

›Delta P = Diastolic blood pressure minus compartment pressure

›Delta P less than 30 mmHg — fasciotomy indicated (preferred over absolute thresholds)

›Preferred threshold: superior specificity over absolute pressure alone

›Class I recommendation from American College of Surgeons Best Practices Guidelines

›Absolute pressure thresholds

›Compartment pressure greater than 30 mmHg — traditionally cited threshold

›Compartment pressure greater than 45 mmHg — threshold used by some centers

›Absolute thresholds of 30–45 mmHg have low specificity and may lead to unnecessary fasciotomies

›Normal compartment pressure: approximately 8 mmHg in adults, 10–15 mmHg in children

›Clinical scoring systems

›No validated composite clinical score exists for ACS diagnosis

›ACS is primarily a clinical diagnosis in the awake, alert patient

›Pressure measurement indicated when clinical exam is equivocal or unobtainable

Intracompartmental Pressure Measurement

›Stryker device technique

›Indicated when clinical exam is equivocal or unobtainable (obtunded, sedated, pediatric, regional anesthesia)

›Measure within 5 cm of the fracture site

›Measure all four compartments of the lower leg

›Multiple measurements in each compartment recommended

›Continuous ICP monitoring

›Sensitivity 94%, specificity 98% in one study

›Valuable in sedated or obtunded patients

›Not yet standard practice in most centers

›Near-infrared spectroscopy (NIRS)

›Noninvasive tissue oxygenation monitoring

›Most promising noninvasive modality under investigation

›Awaiting clinical trial validation — not yet standard of care

›Walters et al. (Journal of Trauma and Acute Care Surgery, 2019): state-of-the-art review of noninvasive diagnostics

MRI

›MRI indications and limitations

›Not routinely indicated in acute compartment syndrome

›May show muscle edema on T2 and STIR sequences

›Should NOT delay treatment or surgical consultation

›May be useful in chronic exertional compartment syndrome post-exercise

›MRI findings in ACS

›T2 hyperintensity within involved muscle compartments

›Loss of normal muscle architecture in advanced necrosis

›Subcutaneous edema overlying affected compartments

CT

›CT indications

›Plain CT of extremity: identifies fracture morphology and associated injuries

›Does not diagnose compartment syndrome directly

›CT angiography

›Indicated if arterial injury is suspected as the etiology

›Differentiate ACS from acute arterial ischemia as primary diagnosis

›High sensitivity and specificity for arterial occlusion or transection

›CT angiography should not delay surgical consultation when ACS is strongly suspected

›Plain radiography as first line

›X-ray of affected extremity — first-line imaging to identify fractures

›Tibial shaft fractures: most common cause of ACS

›Identify associated fibula fractures, plateau fractures, or dislocations

›Imaging should never delay clinical assessment or surgical consultation

Ultrasound

›Point-of-care ultrasound limitations

›Limited diagnostic utility for ACS itself

›Cannot reliably measure intracompartmental pressure

›No evidence-based threshold for fasciotomy based on ultrasound findings

›Ultrasound applications in ACS workup

›Compression ultrasound to exclude DVT as alternative diagnosis

›Identify subcutaneous hematoma contributing to compartment compression

›Doppler for vascular injury assessment — differentiate from arterial occlusion

›Soft tissue assessment for necrotizing fasciitis features (thickening, gas, fluid)

›ECG in rhabdomyolysis

›Indicated if hyperkalemia is suspected from muscle necrosis

›Peaked T waves — early hyperkalemia

›Widened QRS — severe hyperkalemia

›Sine wave pattern — pre-arrest hyperkalemia

›Bradycardia with wide complex — emergent treatment required

07Disposition/dispo24

Admission indications

›Universal admission requirement

›All confirmed or suspected ACS cases require admission — surgical emergency

›Discharge is never appropriate when ACS is under active consideration

›Clinical suspicion alone is sufficient to mandate hospital admission

Level of care

›ICU admission criteria

›Rhabdomyolysis with acute kidney injury

›Serum creatinine greater than 1.5 times baseline or oliguria

›Hyperkalemia with ECG changes

›Metabolic acidosis with hemodynamic instability

›Hemodynamic instability from hemorrhage or systemic inflammation

›Post-fasciotomy monitoring if ICU-level comorbidities present

›Operative suite — emergent

›Confirmed ACS: immediate transfer to operating room for fasciotomy

›Do not await morning operating room time — this is a nighttime emergency

›Time to fasciotomy directly correlates with functional outcome

Transfer criteria

›Transfer indications

›Fasciotomy capability not available at presenting facility — emergent transfer

›Accept no more than 2–3 hours in transit if ACS is diagnosed

›Stabilize with IV fluids, analgesia, and cast removal prior to transfer

›Transfer with active surgical consultation at receiving facility pre-arranged

Observation and high-risk monitoring

›Serial observation pathway

›High-risk patients (tibial fractures, crush injuries): serial exams every 1–2 hours for 24–48 hours

›Pressure measurement if exam becomes equivocal

›Continuous intracompartmental pressure monitoring in sedated patients

08Treatment/t57

Immediate non-operative interventions

›Decompression of external constraints

›Remove circumferential dressings, casts, and splints immediately

›Bivalve cast along its full length and spread padding apart

›Loosen any circumferential bandages or wound VAC dressings

›Position limb at heart level — not elevated above heart

›Fluid resuscitation for rhabdomyolysis

›Normal saline (0.9% NaCl) IV — preferred for initial resuscitation

›Target urine output 1–2 mL/kg/hr to clear myoglobin

›Avoid hypotonic fluids in severe hyperkalemia

›Sodium bicarbonate — alkalinize urine to prevent myoglobin precipitation in renal tubules

›Sodium bicarbonate 50–100 mEq IV bolus, then infusion

›Add to IV fluid if pH less than 7.0 or myoglobinuria present

›Target urine pH greater than 6.5

Hyperkalemia management

›Cardiac membrane stabilization

›Calcium gluconate 1–2 g (10 mL of 10% solution) IV over 5–10 minutes

›Indicated immediately for ECG changes from hyperkalemia

›Onset in 1–3 minutes, duration 30–60 minutes

›Repeat every 30 minutes as needed

›Potassium shifting

›Regular insulin 10 units IV with dextrose 50 g (50 mL of 50% dextrose) IV

›Onset 20–30 minutes, duration 4–6 hours

›Monitor blood glucose every 30 minutes

›Sodium bicarbonate 50 mEq IV if severe acidosis coexists

›Shifts potassium intracellularly

›Less effective in dialysis patients

›Albuterol 10–20 mg nebulized for additional potassium shift

09Special Populations/sp42

Pregnancy

›Physiologic considerations

›Plasma volume expansion — may dilute CK and myoglobin readings

›Supine hypotension syndrome — affects limb perfusion assessment

›Increased risk of DVT in pregnancy — key differential consideration

›Management modifications

›Four-compartment fasciotomy remains standard of care regardless of gestational age

›General anesthesia preferred over neuraxial in ACS setting — avoids masking symptoms

›Obstetric consultation required for operative planning

›Fetal monitoring during operative procedure if viable gestational age

›Medication safety

›IV opioids — use lowest effective dose; neonatal opioid effects if near delivery

›Sodium bicarbonate — safe in pregnancy for rhabdomyolysis alkalinization

›NSAIDs — avoid in third trimester (premature ductus arteriosus closure)

Geriatric

›Age-related physiologic changes

›Decreased pain perception — may not manifest classic pain out of proportion

›Attenuated tachycardia response — hemodynamic changes may be blunted

›Baseline peripheral neuropathy — may obscure paresthesia as diagnostic finding

›Reduced renal reserve — lower threshold for AKI from rhabdomyolysis

›Modified thresholds

›Lower delta P threshold consideration in frail patients with lower baseline diastolic pressures

›Higher vigilance for ACS in anticoagulated patients following falls

›Serial pressure monitoring strongly recommended when exam unreliable

›Medication modifications

›Opioid dosing: reduce by 25–50% and titrate cautiously

›Renal function-guided fluid resuscitation — avoid volume overload

›Careful electrolyte monitoring given reduced renal reserve

10Background/b61

Epidemiology

›Incidence and demographics

›Incidence approximately 3.1 per 100,000 per year in general population

›Strong male predominance: male to female ratio 10:1

›Highest incidence in young males aged 20–35 years

›Athletes represent a subgroup with unique risk (Farah et al., Clinics in Sports Medicine, 2023)

›Anatomic distribution

›Lower leg is the most common location for ACS

›Anterior compartment most frequently affected within the lower leg

›Four compartments of the lower leg: anterior, lateral, superficial posterior, deep posterior

›Etiology distribution

›Tibial shaft fractures — most common cause

›ACS occurs in 1–9% of all lower extremity fractures

›Up to 30% of ACS cases occur without fracture

›Rhabdomyolysis found in 44% of traumatic ACS patients (Tsai et al., Annals of Plastic Surgery, 2015)

›Acute kidney injury in 39% of ACS patients with rhabdomyolysis (Tsai et al., 2015)

›Complications and outcomes

›Contractures: ankle and foot drop

›Foot drop from deep peroneal nerve injury

›Sensory neuropathy — chronic deficit

›Amputation — rare but devastating if delayed

›Chronic venous insufficiency — most common long-term complication of fasciotomy

›Lower quality-of-life scores even after timely fasciotomy compared to controls

Pathophysiology

›Mechanism of injury

›Increased pressure within closed fascial compartment

›Decreased tissue perfusion from elevated compartment pressure

›Ischemia leads to cellular injury and edema

›Edema further increases compartment pressure — positive feedback cycle

›Threshold: perfusion pressure falls when compartment pressure approaches diastolic blood pressure

›Nerve and muscle ischemia timeline

›Irreversible nerve damage begins as early as 4 hours of ischemia

›Irreversible muscle necrosis occurs by 6 hours of ischemia

›Critical window: fasciotomy within 6 hours of onset prevents permanent damage

›Delay beyond 12–24 hours: substantially worse outcomes

›Rhabdomyolysis cascade

›Muscle necrosis releases myoglobin, potassium, phosphate, and creatine kinase

›Myoglobin precipitates in renal tubules — direct tubular toxicity

›Tubular cast formation from myoglobin-Tamm-Horsfall protein binding

›Renal vasoconstriction from hypovolemia and direct myoglobin effect

›Hyperkalemia from cell lysis — cardiac arrhythmia risk

›Compartment anatomy

›Anterior compartment: tibialis anterior, extensor digitorum longus, extensor hallucis longus, peroneus tertius; deep peroneal nerve; anterior tibial artery

›Lateral compartment: peroneus longus and brevis; superficial peroneal nerve; no major artery

›Superficial posterior compartment: gastrocnemius, soleus, plantaris; sural nerve

›Deep posterior compartment: tibialis posterior, flexor digitorum longus, flexor hallucis longus; tibial nerve; posterior tibial artery

Therapeutic Considerations

›Evidence base for fasciotomy threshold

›Delta P less than 30 mmHg preferred over absolute pressure thresholds

›American College of Surgeons Best Practices Guidelines (2015) — Class I recommendation for fasciotomy based on delta P

›Absolute pressure thresholds of 30–45 mmHg have low specificity and lead to unnecessary fasciotomies

›JAMA Surgery systematic review (Mortensen et al., 2019): reviewed diagnostic modalities — clinical exam plus pressure measurement remains gold standard

›Fasciotomy timing evidence

›Fasciotomy within 6 hours: significantly better functional outcomes

›Fasciotomy after 12 hours: substantially increased rates of infection, amputation, and disability

›Long B et al. (Journal of Emergency Medicine, 2019): comprehensive EM management review

›Pharmacovigilance evidence

›FAERS analysis (Kong et al., Expert Opinion on Drug Safety, 2025): approximately 100 drugs associated with compartment syndrome reports

›Median onset of drug-associated ACS: 45 days

›Anticoagulants most prominent drug class contributing to ACS risk

›Noninvasive monitoring development

›Near-infrared spectroscopy — most promising noninvasive technology

›No validated noninvasive diagnostic modality currently replaces clinical exam and ICP measurement

›Walters et al. (Journal of Trauma and Acute Care Surgery, 2019): state-of-the-art review of noninvasive modalities

11Patient Discharge Instructions/pdi29

copy discharge instructions

›Discharge instructions for compartment syndrome of the leg

›You were treated for a condition where pressure built up inside the muscles of your leg

›This is a serious emergency — if it recurs or worsens, return to the emergency department immediately

›Activity restrictions

›Elevate your leg above heart level when resting to reduce swelling

›Do not place weight on the affected leg until cleared by your surgeon

›No strenuous activity, exercise, or sports until cleared by orthopedic surgery

›Follow up with orthopedic surgery within 48–72 hours of discharge

›Cast and splint care

›If you have a cast or splint: do not get it wet

›Do not insert objects inside the cast

›If the cast feels too tight or painful, loosen the elastic wrap immediately

›If you cannot loosen the wrap, return to the emergency department right away

›Warning signs — return to emergency department immediately

›Worsening pain that is not controlled by your pain medications

›Pain that is much worse than expected for your injury

›Numbness or tingling in the foot or toes

›Inability to move your toes or foot

›Foot or leg feels very tight, hard, or swollen

›Swelling that is rapidly worsening

›Dark brown, tea-colored, or cola-colored urine

›Decreased urination or no urine output

›Fever greater than 38.5 C (101.3 F)

›Skin changes over the leg: blistering, black discoloration, or open wound

›Post-fasciotomy specific instructions

›Your surgical wounds will be left open initially — this is intentional and necessary

›Keep wound dressings clean and dry between dressing changes

12References/r19

Guidelines and key sources

›American College of Surgeons guidelines

›Davis ML, Della Rocca GJ, Brenner M, et al. Best Practices in the Management of Orthopaedic Trauma. American College of Surgeons, 2015

›Primary source for four-compartment fasciotomy technique, delta P threshold, and positioning guidance

›Bernard A, Oyler DR, Anglen JO, et al. Best Practices Guidelines for Acute Pain Management in Trauma Patients. American College of Surgeons, 2020

›Landmark reviews

›von Keudell AG, Weaver MJ, Appleton PT, et al. Diagnosis and Treatment of Acute Extremity Compartment Syndrome. Lancet 2015; doi:10.1016/S0140-6736(15)60827-7

›Long B, Koyfman A, Gottlieb M. Evaluation and Management of Acute Compartment Syndrome in the Emergency Department. Journal of Emergency Medicine 2019; PMID 30685220

›Mortensen SJ, Vora MM, Mohamadi A, et al. Diagnostic Modalities for Acute Compartment Syndrome of the Extremities: A Systematic Review. JAMA Surgery 2019; doi:10.1001/jamasurg.2019.1050

›Surgical technique evidence

›Neal M, Henebry A, Mamczak CN, Ruland R. The Efficacy of a Single-Incision Versus Two-Incision Four-Compartment Fasciotomy of the Leg: A Cadaveric Model. Journal of Orthopaedic Trauma 2016; PMID 26709816

›Chang G, Fram B, Krieg JC. Single-Incision 4-Compartment Fasciotomy of the Lower Leg: Safe, Effective, and Advantageous. Orthopedics 2020; PMID 32271928

›Outcomes and rhabdomyolysis data

›Tsai WH, Huang ST, Liu WC, et al. High Risk of Rhabdomyolysis and Acute Kidney Injury After Traumatic Limb Compartment Syndrome. Annals of Plastic Surgery 2015; PMID 25785380

›Fernandez JJ, Smith SR. Traumatic Rhabdomyolysis: Crush Syndrome, Compartment Syndrome, and the Found Down Patient. JAAOS 2024; PMID 38109720

›Pharmacovigilance and specialized sources

›Kong W, Shu Y, Tang J, Wan J, Yang X. Compartment Syndrome Associations With Drugs: A Pharmacovigilance Study of the FAERS. Expert Opinion on Drug Safety 2025; PMID 38966913

›Walters TJ, Kottke MA, Hargens AR, Ryan KL. Noninvasive Diagnostics for Extremity Compartment Syndrome Following Traumatic Injury: A State-of-the-Art Review. Journal of Trauma and Acute Care Surgery 2019; PMID 31246908

›Farah O, Farah G, Mumuni S, Volchenko E, Hutchinson MR. Acute Compartment Syndrome in the Athlete. Clinics in Sports Medicine 2023; PMID 37208063

›Balogh ZJ, Butcher NE. Compartment Syndromes From Head to Toe. Critical Care Medicine 2010; PMID 20724877

Evidence & Review

Evidence & Review