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Acute Compartment Syndrome

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Other Names

  • Compartment Syndrome
  • Acute Compartment Syndrome (ACS)

Background

  • This page refers to acute compartment syndrome (ACS) which occurs when compartment pressure exceeds arterial pressure into compartment, typically due to trauma

History

  • Needs to be updated

Epidemiology

  • 1 to 7.3 per 100,000[1]
  • Fractures/ Trauma is most common etiology[2]
    • Accounts for 75% of cases
  • Most commonly occurs in the leg due to tibial fracture, affecting between 2-9% of fractures
  • Rhabdomyolysis may occur in nearly 1/4 of cases[1]

Introduction

Cross-section of the lower leg depicting the 4 compartments and select key structures[3]
Key structures within the lower leg compartments. The last column is alterations seen with Acute Compartment Syndrome[3]

General

  • Occurs when localized compartment pressure exceeds perfusion pressure in a closed osteofascial compartment leading to irreversible muscle and nerve damage if not treated emergently
  • Most commonly associated with fracture of the Tibia
  • Can occur in any part of upper or lower extremity where muscle is surrounded by fascia
  • Tissue perfusion represents difference between diastolic blood pressure and compartment pressure
  • This is a life threatening condition and surgical emergency[4]
    • All key structures within the compartment can be affected including muscle, nerve and vasculature
    • Delay in diagnosis or treatment can result in irreversible damage

Pathophysiology

  • General
    • Local trauma, soft tissue injury
    • Subsequent bleeding, swelling and elevated intercompartmental pressure
    • As this exceeds perfusion pressure, there is vascular occlusion
    • Muscle and neuronal ischemia
  • Arteriovenous Pressure Gradient theory (APG)[5]
    • ACS occurs when blood flow does not meet the metabolic demands of affected tissues with subsequent tissue ischemia
    • Cascade of events occur: increased inflammation, arterial spasm, disrupted capillary flow, increased osmotic pressure, proteinaceous exudate, muscle fiber swelling, and edema
    • Without intervention, cycle self propagates and contributes further to increased ICP
    • Consequently, there is continual rise in edema within the compartment enclosed in an fixed, inexpandable fascia
    • As ICP increases, tissue and venous pressure compromises capillary function with muscle and nerve ischemia occurring
    • Without surgical decompression, irreversible pressure-induced ischemia results in tissue and cellular death

Common Etiologies

  • Orthopedic[6]
  • Vascular
    • Reperfusion therapy
    • Arterial puncture or injury
    • Hemorrhage
    • Deep Vein Thrombosis
  • Soft Tissue
    • Crush injury
    • Contusion
    • Burn
    • Envenomation (Snake Bite)
  • Iatrogenic
    • Drugs (Anticoagulants)
    • Bleeding Disorders (Sickle cell)
    • Casts or Splints
    • Constrictive Dressings
    • Extravasation of drugs and fluids
    • Prolonged lithotomy positioning
    • Viral myositis
    • Diabetic muscle infarction

Anatomy of the Lower Leg

  • There are 4 compartments in the lower leg: anterior, lateral, superficial posterior, deep posterior
  • Each compartment contains specific nerves, arteries, veins, muscles and bony structures that can contribute to the clinical presentation of ACS
  • It is critical to know and understand the structures in each compartment to effectively assess and diagnose ACS

Risk Factors

  • Male > Female[7]

Differential Diagnosis

  • Variable depending on area of injury and mechanism

Clinical Features

General

  • Diagnosis is largely based on clinical exam
  • Defining feature is pain out of proportion to exam
  • Expect patient to have tender, swollen compartment(s)
    • Can be delayed up to 48 hours after inciting event
  • In polytrauma, may be missed on initial survey or due to distracting injuries
  • Early recognition is critical and requires a high index of suspicion

Classic "5/6 Ps" of Compartment Syndrome

  • General
    • Often tested on exams this way
    • Not universally present in each patient
  • Pain (early finding)
    • Severe, out of proportion to physical findings
    • Worse with passive movement (muscle extension > increased volume > increased pressure)
    • Often the presenting symptom.
  • Paresthesia (early finding)
    • Occurs in sensory distribution of affected nerve
  • Pallor
  • Paralysis: late finding
    • May occur as early as 30 minutes[8]
    • Loss of light touch often precedes limb weakness
  • Pulselessness: late finding
    • Late finding with poor prognosis
    • Arterial insufficiency is not typically present initially, both DP and PT pulses are typically palpable
    • Cap refill is brisk early
  • Poikilothermia
    • Change in temperature or presence of coolness to the affected limb

Evaluation

The Stryker intra-compartmental pressure monitor system[3]

Imaging

  • Radiographs to evaluate for fracture

Compartment Pressure Testing

  • If possible, measure all 4 compartments
    • Compare to contralateral limb
  • Normal
    • < 20 mm Hg generally considered "normal"
    • Normal resting limb compartment pressure is 0 to 4 mm Hg
    • It may increase up to 10 mm Hg physiologically with exertion
  • Pathologic
    • Lack of clear diagnostic criteria
    • Compartment pressure > 30 may be pathologic
    • Must be taken in clinical context
    • Within 8 hours at 30 mm Hg, nerve conduction is disrupted
    • Higher pressures accelerate damage to compartment pressure structures
  • Delta pressure may be more accurate
    • Diastolic pressure - compartment pressure
    • Delta pressure less than or equal to 30 mm Hg is considered diagnostic
  • If clinical index of suspicion is high, surgical intervention may be indicated regardless of compartment pressure measurements

Laboratory

  • Evaluate for muscle injury, including Rhabdomyolysis
    • Creatinine Kinase
    • Urinalysis
  • Metabolic panel
    • Check postassium, kidney function

Management

Nonoperative

  • Decision to manage acute compartment nonoperatively should be made by surgical team
  • Cast, splint and any compression dressing should be immediately removed which can reduce ICP by up to 65%[9]
  • Serial examinations should be performed
  • Elevation of extremity no higher than the level of the heart facilitates venous drainage, reduces edema and maximize tissue perfusion
  • Avoid knee flexion (can limit circulation) and dorsiflexion (limit perfusion of deep posterior compartment)

Fasciotomy

  • Should not be delayed if clinical suspicion high or diagnosis confirmed
    • >8 hours of ischemia associated with permanent injury

Rehabilitation and Return to Play

Rehabilitation

  • Needs to be updated

Return to Play/Work

  • Guided by patients primary recovery
  • No clear guidelines

Prognosis and Complications

Acute Complications

Chronic Complications


See Also

Internal

External


References

  1. 1.0 1.1 McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. Who is at risk? J Bone Joint Surg Br. 2000;82:200–203
  2. Mauser N, Gissel H, Henderson C, Hao J, Hak D, Mauffrey C. Acute Lower-leg Compartment Syndrome. Orthopedics. 2013;36:619–624.
  3. 3.0 3.1 3.2 Pechar, Joanne, and M. Melanie Lyons. "Acute compartment syndrome of the lower leg: a review." The Journal for Nurse Practitioners 12.4 (2016): 265-270.
  4. Donaldson J, Haddad B, Khan WS. The pathophysiology, diagnosis and current management of acute compartment syndrome. Open Orthop J. 2014;8:185–193.
  5. Murdock M, Murdoch MM. Compartment syndrome: a review of the literature. Clin Podiatr Med Surg. 2012;29:301–310. viii.
  6. Konstantakos EK, Dalstrom DJ, Nelles ME, Laughlin RT, Prayson MJ. Diagnosis and management of extremity compartment syndromes: an orthopaedic perspective. Am Surg. 2007;73:1199–1209.
  7. Mauser N, Gissel H, Henderson C, Hao J, Hak D, Mauffrey C. Acute lower-leg compartment syndrome. Orthopedics. 2013;36:619–624.
  8. Bowyer MW. Compartment Syndrome. In: Gahtan V, Costanza MJ, editors. Essentials of Vascular Surgery for the General Surgeon. Springer; New York: 2014. pp. 55–69.
  9. Garfin SR, Mubarak SJ, Evans KL, Hargens AR, Akeson WH. Quantification of intracompartmental pressure and volume under plaster casts. J Bone Joint Surg Am. 1981;63:449–453.
Created by:
John Kiel on 24 June 2019 13:59:56
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Last edited:
1 May 2024 22:37:22
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