Acute Compartment Syndrome of the Leg

• The muscles and neurovascular structures of limbs are separated into closed noncompliant osteofascial compartments by tough unyielding fascia that limit the ability for volume expansion. 
• Blood supply to the structures within the compartment depends on the difference between the arterial and venous pressure (pressure gradient) and the local vascular resistance. 
• Any decrease in the arterial pressure or increase in venous pressure reduces the pressure gradient. 
• Increase in local vascular resistance decreases the blood flow.
• When the blood flow cannot meet the metabolic demand of the tissues, first the function ceases, if not corrected the tissue undergoes necrosis.
• Compartment syndrome develops when increase in the hydrostatic pressure within the compartment decreases the perfusion pressure, that results in cellular hypoxia, tissue ischemia, myoneural damage, muscle necrosis, permanent disability, loss of limb or even death. 
• Acute compartment syndrome (ACS) is a dreaded complication of musculoskeletal injuries.

Epidemiology

• Incidence is 3.1 per 100,000 population in the western world.
• Male to female ratio is 10:1.
• Age is the strongest factor with ACS being most common in the 2^ndand 3^rddecades.
• Most common site is the leg, followed by the forearm.
• ACS develops in 11.5% of tibial diaphyseal fractures.

History

• First described by Richard von Volkmann in 1869 in the forearm. He described the sequelae and the causative factors in 1881.
• Bardenheuer first described fasciotomy as treatment in 1906.
• Rowland attributed raised intracompartmental pressure as the cause of ischemia and its sequelae.
• Management of ACS first described by Petersen in 1888.
• Myerson described compartment syndrome of the foot in 1987. (Myerson 1987)

Etiology

• Cause may be fractures, soft tissue trauma, bleeding, extravasation or external compression.
• Up to 30% of cases occur without fracture.
• Causes may be divided into exogenous or endogenous.
• Endogenous causes are hemorrhage, edema or perivascular infusions which increase in the volume of contents within the compartment.
• Exogenous causes may be constricting casts, prolonged lithotomy positioning, drunken stupor, tight dressing etc.
• Causes
  • Trauma
  • Thermal injuries
  • Constricting casts or dressings
  • Bleeding disorders including anticoagulant therapy
  • Nephrotic syndrome
  • Rhabdomyolysis
  • Accidental extravasation of infusions or drugs such as Propofol, Iohexol etc.
  • Lithotomy positioning during surgery
  • Streptococcal infections

Pathogenesis

• Normal interstitial pressure is 8mm of mercury in adults and 10-15mm Hg in children.
• Trauma leads to inflammation which leads to vasodilation and increased capillary permeability resulting in edema which increases interstitial pressure leading to increased venous capillary pressure. The decreased perfusion pressure leads to ischemia which causes further tissue damage creating a vicious cycle with positive feedback loop.
• Ischemia leads to hypoxia and depletion of intracellular energy stores. Anaerobic metabolic pathways are activated to compensate leading to acidosis. Further reduction in the ATP production leads to shut down of sodium-potassium ATPase channels that maintain the cellular polarity and osmotic balance. Loss of cellular polarity leads to influx of chloride ions and cellular swelling. Increased cytosolic calcium accumulation causes lysosomal enzyme release and cell lysis.
• Cell lysis releases intracellular toxins, leading to microvascular damage, inflammation, increased capillary permeability, capillary leakage and increased intra-compartmental pressure. 
• Ischemia of one hour can lead to neuropraxia and axonotmesis can start developing by 4 hours. Irreversible changes start appearing by 6 hours.
• Edema is due to increased capillary permeability secondary to injury or reperfusion.

Vicious Cycle of pathogenesis

Clinical Features

• Compartment syndrome should be suspected in awake patients with unrelenting and increasing pain not responding to standard dose of analgesics, pain on passive stretch, paresthesia and paresis.
• Classically the symptoms are described as 5 P’s. 
  • Pain
  • Pallor
  • Pulselessness
  • Paresis
  • Paresthesia
• Griffiths described the 4 P’s in 1948; pain, pain on stretch, paresthesia and paresis (Griffiths 1948). Pulselessness and pallor were added later.
• The classically described pulselessness is absent as the systolic blood pressure usually remains above the compartment pressure even in the late stages.
• Pain which is persistent and increasing is the earliest and most common sign.
• Pain on passive stretching of involved muscles is the most sensitive sign.
• In the leg, anterior compartment is most commonly involved followed by the lateral compartment.
• In children, the presentation is by 3 A’s
  • Anxiety
  • Agitation
  • Analgesic need that continuously rises
• Compartment syndrome should be ruled out in unconscious patients with persistent tachycardia if there is no other cause or hypotension.
• Risk factors that increase the likelihood of ACS are high velocity injury, systemic hypotension, younger age and obtunded patients.
• Multiple injury patients with hypotension and hypoxia are more susceptible to compartment syndrome.
• Other injuries more susceptible to compartment syndrome are vascular injuries with peripheral ischemia, high velocity injuries, crush injuries, and comminuted proximal tibial fractures.
• Patients on anticoagulants are at high risk of ACS after injury.
• More common in the young due to relatively thick and inelastic fascia.
• Age between 12-29 years is the strongest predictor for ACS. 
• Fractures of the tibia and fibula are 4 times more likely develop in comparison to all other fractures.
• 36% of cases are due to tibial shaft fractures followed by soft tissue injury (23%), distal end radius #s (10%), forearm diaphyseal #s (8%) and crush syndrome (8%). (McQueen 2000)

Diagnosis

• Diagnosis may be made by clinical examination or by measurement of compartment pressure or tissue oxygenation.
• Diagnosis is unconscious patients’ needs compartment pressure monitoring.
• Compartment pressure measurement by infusion technique was described by Whitesides in 1974 (Whitesides 1974). 
• Compartment pressure measurement techniques
  • Whitesides infusion technique
  • Matsen’s continuous infusion and monitoring technique
  • Mubarak wick catheter technique
  • Stick technique
  • Fine wire transducer technique
  • Weiner fibro-optic transducer tip catheter technique
• Some of the available catheters are the following
  • Slit catheter
  • Solid-state transducer intra-compartmental catheter (STIC)
  • Transducer tipped catheter
  • 18G needle with arterial-line transducer
• Arterial line transducers with side-port needles, slit catheters and self contained measuring systems are most accurate. (Keudell 2015)
• Monitoring of ICP by slit catheter technique has a sensitivity of 94% and specificity of 98% when pressure gradient (∆P) of 30mm Hg is used for diagnosis.

Compartment Pressure Measuring Technique

• Compartment pressure should be measured within 5 cm of the fracture and pressure within all 4 compartments of the leg should be measured. 
• Proper technique which includes proper positioning of the catheter within the compartment, proper setup of devices, proper zeroing is essential for correct measurement of intra-compartmental pressure. Otherwise catastrophic errors are likely. 
• The landmarks for insertion of needle for compartment pressure measurement are as follows.
  • Superficial posterior compartment- In the posterior midline of calf.
  • Deep posterior compartment- 1 cm posterior to posteromedial border of tibia.
  • Anterior compartment- 2 cm lateral to the tibial crest.
  • Lateral compartment- Directly over the fibula.
• Diagnosis is made if the difference between compartment pressure and diastolic pressure (∆P) is less than 30mm (McQueen 1996) or if the intra-compartmental pressure is above 30mm of Hg (Whitesides 1975).
• Recently 35% false positive rate was reported when compartmental pulse pressure of <30mm Hg on single measurement was used in patients with acute fractures with no clinical evidence of compartment syndrome. (Whitney 2014)

Treatment

• Timely diagnosis and dermatofasciotomy is essential to ensure optimum outcomes.
• Initial treatment consists of removal of circumferential dressings and elevation of the limb to the level of heart.
• The limb should not be elevated in impending compartment syndrome as it further reduces pressure gradient.
• Techniques of fasciotomy
  • Dermatofasciotomy
  • Percutaneous fasciotomy
• Percutaneous fasciotomy is contraindicated in trauma patients
• Techniques of dermatofasciotomy
  • Mubarak’s 2-incision, 4-compartment fasciotomy
  • Matsen’s parafibular 4-compartment fasciotomy
  • Fibulectomy-fasciotomy
• Fibulectomy-fasciotomy is contraindicated in trauma patients.
• Mubarak’s 2-incision, 4-compartment fasciotomy of leg
  • Medial incision for release of deep and superficial posterior compartments made 2 cm posterior to the posteromedial border of tibia. Incise from proximal tibia to the musculotendinous junction of Achilles tendon. Protect saphenous nerve and vein. Incise fascia to release superficial posterior compartment. Elevate the soleus from the medial border of tibia to expose the deep posterior compartment and release the fascia.
  • Lateral incision for release of anterior and lateral compartments made 2 cm anterior to the fibular head. Incise from fibular head to the distal fibula Protect superficial peroneal nerve distally. Elevate the anterior flap. Incise fascia to release anterior compartment anterior to the anterior intermuscular septum. Elevate the posterior flap, incise the fascia along the posterior border of fibula to release the lateral compartment.
• Matsen’s parafibular dermatofasciotomy.
• After fasciotomy, the viability of the muscle should be ascertained by the 4 C’s: Color, Consistency, Contractility and Capacity to bleed.
• The wound left open and spring sutures placed to progressively close the wound.
• Patient returned to operation theatre at 48 hours to reassess the wound. 
• Fasciotomy increases the duration of hospital stay, escalates the costs, increases the chance of infection and interferes with fracture healing.
• Recently the need for release of all four compartments in all patients have been questioned and an algorithmic approach consisting of selective release of compartments have been put forward. (Tornetta 2016)
• Tornetta 2016 algorithm advises measurement of diastolic BP preoperatively, measurement of ICP, fasciotomy of anterior and lateral compartments, measurement of ICP of posterior compartments and medial incision if the pressure difference with diastolic BP (∆P) is less than 30mm Hg and to avoid release if ∆P is more than 30mm Hg. Close post-operative monitoring by clinical examination every 2 hours is necessary. They did not recommend this algorithm in centres with no facility to monitor the intracompartmental pressure in the post-operative period. 

Complications

• Delayed or missed diagnosis may lead to complications such as renal failure, ischemic contractures and limb loss.
• Cause of delayed or missed diagnosis
  • Unconscious or inebriated patients
  • Regional or general anesthesia
  • Polytrauma
  • Soft tissue injuries
  • Inexperience
  • Over-reliance on clinical symptoms and signs
• Complications of delayed or missed diagnosis
  • Muscle necrosis and contractures
  • Permanent neurological deficit
  • Infection
  • Chronic pain
  • Amputation
  • Death
• The side effects or complications of fasciotomy are muscle weakness, chronic venous insufficiency, adherent scars, impaired sensation, ulceration, increases in duration of hospitalization and costs and the delay in definitive treatment.

Recent Advances

• Newer diagnostic tools include the following.
  • Near-infrared spectroscopy (NIRS) uses differential light reflection and absorption characteristics to estimate the proportion of hemoglobin saturated with oxygen 2-3 cm below the skin. It is currently FDA approved for noninvasive continuous monitoring of pressure in the intracranial and somatic tissues. Skin pigmentation and thickness of subcutaneous fat may interfere with NIRS. 
  • Radio-frequency identification implants are minimally invasive devices with sensors to measure pressure, oxygenation etc. that are microfabricated into silicon substrate.  It uses RFID technology to transmit the data collected.
• Newer methods to reduce pressure
  • Methods to decrease intramuscular pressure
    • Anti-inflammatory drugs like indomethacin
    • Ultrafiltration catheters as treatment- Tissue ultrafiltration by insertion of small diameter hollow fibers into the compartment, connected to suction to remove interstitial fluid to reduce compartment pressure.
    • Foot pumps
    • Mannitol
    • Diuretics
    • Decompression by dorsal skin fenestration or pie crusting in compartment syndrome of foot.
  • Improving tissue oxygenation
  • Free radical scavengers 
  • Small-volume resuscitation with hypertonic saline.

References

1. von Keudell AG, Weaver MJ, Appleton PT, et al. Diagnosis and treatment of acute extremity compartment syndrome. Lancet. 2015;386:1299–1310.
2. McQueen MM, Duckworth AD, Aitken SA, et al. The estimated sensitivity and specificity of compartment pressure monitoring for acute compartment syndrome. J Bone Joint Surg Am. 2013;95:673–677. 
3. Sanjit R. Konda, Benjamin S. Kester, Nina Fisher, BS, Omar A. Behery, Alexander M. Crespo, Kenneth A. Egol. Acute Compartment Syndrome of the Leg. J Orthop Trauma 2017;31:S17–S18. 
4. Whitesides TE, Heckman MM. Acute compartment syndrome: update on diagnosis and treatment. J Am Acad Orthop Surg. 1996;4:209–218.
5. Manjoo A, Sanders D, Lawendy A, et al. Indomethacin reduces cell damage: shedding new light on compartment syndrome. J Orthop Trauma. 2010;24:526–529.
6. Bariteau JT, Beutel BG, Kamal R, et al. The use of near-infrared spectrometry for the diagnosis of lower-extremity compartment syndrome. Orthopedics. 2011;34:178.
7. Volkmann R: Die Krankheiten der Bewegungsorgane [Diseases of the musculoskeletal system], in von Pitha FR, Billroth T, eds: Handbuch der allgemeinen und speziellen Chirurgie. Stuttgart, Germany: Ferdinand Enke, 1865, vol 2, pp 234–920.
8. Volkmann R: Krankenheiten der Bewegungsorgane. In Pitha, Billroth (eds): Handbuch der Chirurgie, Erlangen, 1869:846.
9. Volkmann R: Die ischaemischen Muskellahmungen and Kontrakturen, Zentralb Chir 8:801-803, 1881.
10. Bardenheuer L: Die ischamische Kontraktur und Gangran als Folge der Arterienverletzung, Leuthold’s Gedenkscrift 2:87, 1906.
11. Rowland SRP: Volkmann’s contracture, Guys Hosp Gaz 24:87, 1910.
12. Whitesides TE, Haney TC, Morimoto K, Harada H: Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop Relat Res 1975;113:43-51.
13. McQueen MM, Court-Brown CM: Compartment monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.
14. Whitney A, O’Toole RV, Hui E, et al: Do one-time intracompartmental pressure measurements have a high false-positive rate in diagnosing compartment syndrome? J Trauma Acute Care Surg 2014;76(2):479-483.
15. Paul Tornetta III, Brian L Puskas, Kevin Wang. Compartment syndrome of the leg associated with fracture: An algorithm to avoid releasing the posterior compartments. 
16. Arvind G von Keudell, Michael J Weaver, Paul T Appelton, Donald S Bae, George S M Dyer, Marilyn Heng, Jesse B Jupiter, Mark S Vrahas. Diagnosis and treatment of acute extremity compartment syndrome. Lancet 2015; 386: 1299–1310.
17. McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. Who is at risk? J Bone Joint Surg Br 2000; 82: 200–03.
18. Myerson M. Acute compartment syndromes of the foot. Bull Hosp Jt Dis Orthop Inst. 1987;47:251–261.
19. Griffiths DL. The management of acute circulatory failure in an injured limb. J Bone Joint Surg Br. 1948;30:280–298.
20. Cascio BM, Wilckens JH, Ain MC, Toulson C, Frassica FJ. Documentation of acute compartment syndrome at an academic health-care center. J Bone Joint Surg Am. 2005;87:346–350.
21. Whitesides TE, Jr., Haney TC, Harada H, Holmes HE, Morimoto K. A simple method for tissue pressure determination. Arch Surg. 1975;110:1311–1313.
22. Matsen FA 3rd: Compartmental Syndromes, Orlando, Fla, Grune & Stratton, 1980. 
23. Mubarak SJ, Hargens AR, Owen CA, et al: The wick catheter technique for measurement of intramuscular pressure: a new research and clinical tool, J Bone Joint Surg Am 58:1016-1020, 1976. 
24. Weiner G, Styf J, Gershuni D: Effect of ankle position and a plaster cast on intramuscular pressure in the human leg, J Bone Joint Surg Am 76:1476-1482, 1994.

Further Reading

1. Crespo AM, Manoli A III, Konda SR, Egol KA: Development of Compartment Syndrome Negatively Impacts Length of Stay and Cost After Tibia Fracture. J Orthop Trauma 2015;29(7):312-315.
2. O’Toole RV, Whitney A, Merchant N, et al: Variation in diagnosis of compartment syndrome by surgeons treating tibial shaft fractures. J Trauma 2009;67(4):735-741.
3. Boody AR, Wongworawat MD: Accuracy in the measurement of compartment pressures: A comparison of three commonly used devices. J Bone Joint Surg Am 2005;87(11):2415-2422.
4. Large TM, Agel J, Holtzman DJ, Benirschke SK, Krieg JC: Interobserver variability in the measurement of lower leg compartment pressures. J Orthop Trauma 2015;29(7):316-321.
5. Tharakan SJ, Subotic U, Kalisch M, Staubli G, Weber DM: Compartment pressures in children with normal and fractured forearms: A preliminary report. J Pediatr Orthop 2015.
6. Mubarak SJ, Owen CA: Double-incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg Am 1977;59(2):184-187.
7. Poon H, Le Cocq H, Mountain AJ, Sargeant ID: Dermal fenestration with negative pressure wound therapy: A new technique for managing soft tissue injuries associated with high-energy complex foot fractures. J Foot Ankle Surg 2016;55(1):161-165.
8. Odland RM, Schmidt AH: Compartment syndrome ultrafiltration catheters: Report of a clinical pilot study of a novel method for managing patients at risk of compartment syndrome. J Orthop Trauma 2011;25(6):358-365.