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Achilles Tendon Rupture

Also known as: Tendo Achilles rupture

Achilles tendon rupture is complete or partial disruption of the Achilles tendon, usually occurring approximately 2 to 6 cm proximal to its calcaneal insertion in an area with relatively limited blood supply.

The classic patient is a recreational athlete aged approximately 30 to 50 years who suddenly pushes off, jumps or changes direction.

Predisposing factors include:

  • Chronic Achilles tendinopathy
  • Increasing age
  • Fluoroquinolone exposure
  • Corticosteroid exposure
  • Diabetes
  • Previous rupture

The key modern management principle is that both operative repair and high quality accelerated functional nonoperative rehabilitation are valid treatments for an acute midsubstance rupture. When modern functional rehabilitation is used, functional outcomes and rerupture differences are substantially smaller than with historical prolonged casting.

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Management sections cite the guideline they came from. Atlas supports clinical judgement rather than replacing it; verify against current national guidance and the patient in front of you.

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Chronic Osteomyelitis

Chronic osteomyelitis is persistent bone infection characterised by devascularised infected bone, biofilm, impaired local perfusion and recurrent inflammation.

The defining pathological structures are:

Sequestrum

A fragment of necrotic devascularised bone separated from viable bone.

Systemic antibiotics penetrate it poorly because it has no functioning blood supply.

Involucrum

Reactive new bone formed around the infected sequestrum.

Cloaca

An opening through involucrum allowing pus to drain externally.

Sinus tract

A chronic tract communicating infected bone with the skin.

Longstanding sinus tracts rarely undergo malignant transformation into squamous cell carcinoma, termed a Marjolin ulcer.

Cierny Mader classification

This classification combines anatomical disease extent with host physiology.

Anatomical type

Type I: Medullary

Infection is confined predominantly to the medullary canal.

Examples include infected intramedullary devices and selected haematogenous infections.

Type II: Superficial

Infection involves the cortical surface without full thickness cortical involvement.

Often associated with a soft tissue wound.

Type III: Localised

Full thickness cortical infection with a localised cavity, but the remaining bone is mechanically stable after adequate debridement.

Type IV: Diffuse

Circumferential or extensive bone involvement producing or threatening structural instability.

Frequently requires major reconstruction.

Physiological host

A host

Normal systemic and local healing capacity.

B host

Healing is compromised.

BL

Local compromise, for example:

  • Severe scarring
  • Poor soft tissue envelope
  • Venous stasis
  • Radiation fibrosis
  • Local vascular insufficiency

BS

Systemic compromise, for example:

  • Malnutrition
  • Diabetes
  • Renal disease
  • Smoking
  • Immunosuppression

BLS

Both local and systemic compromise.

C host

The morbidity of attempted curative treatment is greater than the burden of the disease itself.

In such patients, suppressive treatment, palliation or occasionally amputation can be preferable to complex salvage.