Congestive syndrome arthrogenes I87.2-

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Synonym(s)

Arthrogenic congestion syndrome; Arthrogenic venous stasis syndrome

History
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Schmeller 1990 - First describer of the Circulus vitiosus s. Figure. Unfavourable mutual influence of venous congestion and reduced or eliminated joint mobility.

Definition
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Most severe complication of chronic venous insufficiency (CVI) with/ without existing varicosis and/or post-thrombotic syndrome.

Classification
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Regarding pathophysiology, 2 forms of the arthrogenic congestive heart failure syndrome can be distinguished.

  • a) The arthrogenic congestion syndrome, which occurs as a consequence of severe chronic venous insufficiency. In advanced venous disease (from clinical stage 4), there are changes in the skin and subcutaneous fatty tissue. It is a progressive inflammatory reaction that turns into a sclerosing process. In the further course of the disease, the fasciae become involved, leading to dermatolipofasciosclerosis. As a consequence, the ligamentous apparatus of the upper ankle joint is also affected. The degenerative remodelling of the joint structures and the Achilles tendon can lead to the increasing restriction of movement and even to complete fixation of the upper ankle joint in the toe position. In addition, the presence of a painful leg ulcer itself contributes to the formation of a fixed pointed foot by keeping the foot in plantar flexion. In the worst case, joint motility in the upper ankle joint is 0 - 40 - 40° (dorsal extension - 0 - plantar flexion). As the upper ankle joint stiffens, the calf muscles atrophy. This results in the loss of the functionality of the most important venous pump, namely the crural venous pump. The ankle pump as well as the muscle pump of the powerful M. triceps surae from the superficial flexor box and the muscle pumps of the deep flexors (M. tibialis posterior, M. flexor digitorum longus, M. flexor hallucis longus) lose their function. The fixed pointed foot also causes a recurvature of the knee joint in an upright and walking patient. The recurvation presses the veins at the level of the knee joint against the head of the tibia and constricts them. This additionally impairs the venous outflow. As a result of the increasing venous congestion, the disease situation worsens and further tissue damage occurs, which promotes the development, maintenance and expansion of chronic ulcerations. This vicious circle, in which venous congestion on the one hand and joint motility - especially in the upper ankle joint - on the other hand influence each other unfavourably as pathophysiological processes, was already aptly described by Schmeller in 1990. Characteristically, cuff ulcers and necroses form in the course of the disease.
  • b) The arthrogenic congestion syndrome, which occurs in primarily venous healthy patients as functional venous insufficiency in disorders of the venom-muscle pump of the leg. The mobility in the upper ankle joint seems to be of particular importance here. However, movement disorders of the knee, the lower ankle joint as well as hollow and flat foot also have an influence on the venous outflow.

Occurrence/Epidemiology
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There are no reliable epidemiological data on arthrogenic congestion syndrome

From the Bonn Vein Study it is known that approx. 3.6% of the population are in clinical CEAP stages C4a to C6 and are therefore at immediate risk of developing an arthrogenic congestion syndrome

Epidemiological data on arthrogenic congestion syndrome at the bottom of a movement restriction without prior CVI are not available

Etiopathogenesis
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  • progressive inflammatory reaction in the context of venous hypertension, which changes into a sclerosing process
  • in the further course it comes to the inclusion of skin, subcutis and fasciae. Dermatolipofasciosclerosis develops.
  • As a consequence, the ligamentous apparatus of the upper ankle joint is involved, the joint structures and the Achilles tendon are remodeled until they are completely fixed in the toe position

Clinical features
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  • all signs of severe CVI may be present:
    • Hyperpigmentations
    • Dermatolipofasciosclerosis
    • Atrophie blanche
    • ulcerations, usually very resistant to therapy, often of large extension
  • in severe cases, chronic venous compartment syndrome, possibly

Diagnosis
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Diagnosis can usually be made on the basis of the following three symptoms:

  • ulcus cruris that is refractory to therapy and/or other signs of severe CVI
  • fixed toe
  • atrophic calf muscles

Duplex sonographic diagnosis is useful to verify or exclude underlying venous outflow disorders (varicosis or thrombosis or postthrombotic syndrome).

General therapy
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  • if possible reactivation/ promotion of mobility in the ankle joint
  • symptomatic compression therapy with high resting pressure and high material strength/ low elasticity
  • if necessary, supplementary intermittent compression therapy using equipment
  • Pain therapy to avoid a somewhat relieving posture/ pointed foot position
  • in case of underlying varicosis or postthrombotic syndrome whenever possible causal therapy of the same with improvement of the venous outflow situation
  • biomechanical stimulation (NOT for pacemakers, severe heart disease, neurological disease, osteoporosis, metal implants)
  • Ultima ratio - removal of the fascia cruris as well as the ulcer cruris with adjacent sclerotic tissue, subsequent covering with graft - e.g. en-bloc resection according to Homans, surgery according to Hach
  • postop. Fitting of orthopedic shoes to ensure mobility, no compression therapy, contrast relaxation, muscle stretching according to Janda, repeated contractions

Literature
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  1. Doerler M et al (2013). Venous leg ulcer caused by obesity-associated dependency syndrome Case report and discussion of the pathogenesis and treatment. Phlebology 42: 205-208.

  2. Frendel A et al. (2015). The arthrogenic congestion syndrome. Phlebology 44:215-217

  3. Gallenkemper G et al (1995) Venous function in dorsal extension and plantar flexion of the foot - a photoplethysmographic examination series. Phlebology 24: 139-43.
  4. Gallenkemper G et al. (1996) Rabe E, Kreysel HW. Venous outflow during passive compression of various regions of the foot and lower leg as well as during active and passive dorsal extension in the ankle joint. Phlebology 25: 89-94.

  5. Hach W (2003) The arthrogenic congestion syndrome. Vascular surgery 8: 227-233
  6. Hach W et al (1983) The arthrogenic congestion syndrome. Vasa 12: 109-16.

  7. Hach W (2006) Venous surgery. Stuttgart: Schattauer, 2nd edition 304-306.

  8. Kugler C et al (1999) Strunk M, Rudofsky G. Effect of impaired joint mobility on venous pump function of the healthy lower limb, a phlebodynamometric analysis. Phlebology 28(1): 16-22.
  9. Lentner A (1994) Mobility in the upper and lower ankle joint in advanced chronic venous insufficiency. Phlebology 23: 149-55.

  10. Ludwig M et al (2010) Vascular medicine in clinic and practice - guideline-oriented angiology, vascular surgery and interventional radiology. Stuttgart: Thieme, 2nd edition, 283-284.
  11. Nüllen H et al (2010) Arthrogenic congestion syndrome In: T Noppeney, H Nüllen Diagnosis and therapy of varicosis. Springer Medicine Publishing House Heidelberg S 213 -214
  12. Reich-Schupke S (2016) Why can compression therapy be useful for immobility? vasomed 28:278-283
  13. Schmeller W (1990) The arthrogenic congestion syndrome. Ankle joint changes in chronic venous insufficiency, Berlin: Diesbach Verlag
  14. Uhl JF et al (2012) Static foot disorders: a major risk factor for chronic venous disease? Phlebology 27:13-18.

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Please ask your physician for a reliable diagnosis. This website is only meant as a reference.

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Last updated on: 29.10.2020