Pathophysiology compartment syndrome

Jump to navigation Jump to search

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammadmain Rezazadehsaatlou[2] ;


Overview

Any condition that results in an increase in compartment contents or reduction in a compartment’s volume could lead to the development of an acute compartment syndrome. When pressure is elevated capillary blood flow is compromised. Edema of the soft tissue within the compartment further raises the intra-compartment pressure, which compromised venous and lymphatic drainage of the injured area. Pressure, if further increased in a reinforcing vicious cycle, can compromise arteriole perfusion, leading to further tissue ischemia. The normal mean interstitial tissue pressure is 25 mmHg (range 20–30 mmHg), and if it is over 50–60 mmHg or below 10mmHg (or below the diastolic blood pressure minus 20–30 mmHg) functional tissue changes can occur e.g tissue necrosis. . Arteries and arterioles are stable at these pressures, however the tissues within the compartment dependent on the capillaries for nutrients suffer hypoxia. Untreated compartment syndrome mediated ischemia of the muscles and nerves lead to eventual irreversible damage and death of the tissues within the compartment.

Pathophysiology

Compartment syndrome is defined as ‘an increased pressure within a confined compartmental space decreasing the perfusion pressure to the tissue. CS is caused by increasing pressure due to the edema and/or hemorrhage within an anatomic compartment bound. Increased pressures leads to the decreased capillary perfusion pressure resulting in sensory disturbance, pain at rest, ischemia, soft tissue compromise, and subsequent necrosis, and even ischemic neuropathy and chronic neuropathic pain. CS is defined as ‘an increased pressure within a confined compartmental space decreasing the perfusion pressure to the tissue. Whenever fluid (from bleeding etc) enters into a fixed volume compartment, both the tissue and venous pressure increase then the capillary collapse with ensuing muscle leading to the nerve ischaemia. A similar reduction in capillary perfusion pressure when the compartment size changes for example during the external compression, then due to an increase in intracompartmental pressure, as well as a reduction in the arteriolar pressure.[1][2][3][4][5][6][7][8]

Pathophysiology of compartment syndrome. © 2011 American Academy of Orthopaedic Surgeons. Reprinted from the Journal of the American Academy of Orthopaedic Surgeons, Volume 19  Volkmann R. Die ischämischen Muskellähmungen und Kontracturen. Centralblatt für Chirurgie. Leipzig. 1881;8:801–83.
Pathophysiology of compartment syndrome. © 2011 American Academy of Orthopaedic Surgeons. Reprinted from the Journal of the American Academy of Orthopaedic Surgeons, Volume 19  Volkmann R. Die ischämischen Muskellähmungen und Kontracturen. Centralblatt für Chirurgie. Leipzig. 1881;8:801–83.

Two distinct types of compartment syndrome have been recognized in this regrard:

a: CS associated with trauma as seen in fractures or muscle injuries.

b: CS associated with repetitive loading or microtrauma related to physical activity (also is called exertional compartment syndrome).

Tissue perfusion is proportional to the difference between the capillary perfusion pressure (CPP) and the interstitial fluid pressure, and its evaluated as:

LBF = (PA - PV)/R

(LBF is local blood flow, PA is local arterial pressure, PV is venous pressure, and R is local vascular resistance)

Normal myocyte metabolism requires a 5-7 mm Hg of oxygen tension, which can be provided with a CPP of 25 mm Hg and an interstitial tissue pressure of 4-6 mm Hg.

Whenever in a fixed-volume compartment the fluid occurs then tissue pressure increases and venous pressure rises. When the interstitial pressure exceeds the CPP (a narrowed arteriovenous [AV] perfusion gradient), capillary collapse and muscle and tissue ischemia occur.

Skeletal muscle responds to ischemia by releasing histaminelike substances that increase vascular permeability. Plasma leaks out of the capillaries, and relative blood sludging in the small capillaries occurs, worsening the ischemia. The myocytes begin to lyse, and the myofibrillar proteins decompose into osmotically active particles that attract water from arterial blood.

References

  1. Mars M, Hadley GP (July 1998). "Raised intracompartmental pressure and compartment syndromes". Injury. 29 (6): 403–11. PMID 9813693.
  2. Frink M, Hildebrand F, Krettek C, Brand J, Hankemeier S (April 2010). "Compartment syndrome of the lower leg and foot". Clin. Orthop. Relat. Res. 468 (4): 940–50. doi:10.1007/s11999-009-0891-x. PMC 2835588. PMID 19472025.
  3. McDonald S, Bearcroft P (June 2010). "Compartment syndromes". Semin Musculoskelet Radiol. 14 (2): 236–44. doi:10.1055/s-0030-1253164. PMID 20486031.
  4. Johnston-Walker E, Hardcastle J (2011). "Neurovascular assessment in the critically ill patient". Nurs Crit Care. 16 (4): 170–7. doi:10.1111/j.1478-5153.2011.00431.x. PMID 21651657.
  5. Suzuki T, Moirmura N, Kawai K, Sugiyama M (January 2005). "Arterial injury associated with acute compartment syndrome of the thigh following blunt trauma". Injury. 36 (1): 151–9. doi:10.1016/j.injury.2004.03.022. PMID 15589934.
  6. Alexander W, Low N, Pratt G (January 2018). "Acute lumbar paraspinal compartment syndrome: a systematic review". ANZ J Surg. doi:10.1111/ans.14342. PMID 29316189.
  7. Thati S, Carlson C, Maskill JD, Anderson JG, Bohay DR (June 2008). "Tibial compartment syndrome and the cavovarus foot". Foot Ankle Clin. 13 (2): 275–305, vii. doi:10.1016/j.fcl.2008.02.001. PMID 18457774.
  8. Fulkerson E, Razi A, Tejwani N (February 2003). "Review: acute compartment syndrome of the foot". Foot Ankle Int. 24 (2): 180–7. doi:10.1177/107110070302400214. PMID 12627629.