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Avascular necrosis of knee
Other Resources UpToDate PubMed

Avascular necrosis of knee

Contributors: Ayush Parikh BS, Sandeep Mannava MD, PhD
Other Resources UpToDate PubMed

Synopsis

Avascular necrosis (AVN), also known as osteonecrosis, is a rare, progressive disease defined by bone infarction due to ischemia from vascular disruption to the bone. If left untreated, it can lead to range of motion deficits, significant pain, and end-stage arthritis in the affected joint. AVN of the knee is the second most common site of osteonecrosis and is further classified into 3 subtypes: spontaneous osteonecrosis of the knee (SONK), secondary (or idiopathic) osteonecrosis, and postarthroscopic osteonecrosis.

Classic history and presentation: SONK is the most common subtype of knee osteonecrosis. It is typically seen in patients 50 years and older and more frequently in women (3:1 ratio of women to men). The typical presentation is a middle-aged patient with acute onset of medial-sided knee pain not precipitated by trauma. In the majority of SONK patients, the classic injury is a unilateral, focal subchondral lesion of the medial femoral condyle.

Secondary or idiopathic osteonecrosis is a much rarer form of knee AVN and has notable characteristics that differentiate it from SONK. It usually affects patients younger than 45 years and frequently involves multiple lesions in both knees and other joints. It may involve both femoral condyles in addition to the epiphysis, diaphysis, and metaphysis of the affected femur and/or tibia. It is also more frequently seen in women than men. In contrast to SONK, secondary osteonecrosis progresses more gradually with pain worsening over time. The initial focus of pain is most often the femoral condyles or proximal tibia. Patients may also complain of pain in other joints due to the multifocal etiology.

Postarthroscopic AVN is the rarest form of knee osteonecrosis and is seen in up to 4% of patients after routine chondroplasty and meniscectomy. Men and women are equally affected, and onset of pain is usually 6-8 weeks after the procedure at the site of the prior injury / arthroscopy. Although the pathophysiology underlying postarthroscopic AVN is still unclear, it has been associated with postprocedural alterations in knee biomechanics. These changes may lead to increased contact pressures, insufficiency fractures, synovial fluid leakage, and eventual necrosis.

Pathophysiology: SONK is thought to occur secondary to vascular ischemia, although controversy exists over whether vascular disruption is due to subchondral insufficiency fractures or the progression of underlying osteoarthritis. In either case, the resulting reduced subchondral blood supply can lead to cellular hypoxia, membrane disruption, and necrosis. The medial condyle is particularly susceptible due to its watershed vascular supply as opposed to the lateral condyle.

Risk factors: Secondary osteonecrosis is associated with direct and indirect risk factors that lead to vaso-occlusion and ischemia without joint predilection. Direct risk factors include sickle cell disease, decompression sickness, Gaucher disease, and myeloproliferative disorders. Indirect risk factors include alcohol and tobacco abuse, chronic corticosteroid use, and obesity.

Classification systems: The Koshino classification system (stages I-IV) was first used to describe SONK disease progression and to guide treatment. However, the newer Modified Ficat and Arlet staging system (stages 0-4) is used more frequently. For secondary osteonecrosis, the Modified Ficat and Arlet staging system is the preferred classification to characterize disease progression and treatment.

Modified Ficat and Arlet staging system
  • Stage 0: radiographs and MRI do not show pathology; no clinical symptoms
  • Stage I: normal or minor osteopenia (on x-ray); edema on MRI; patient has pain, typically groin pain
  • Stage II: x-rays show mixed osteopenia and/or sclerosis and/or subchondral cysts, without any subchondral lucency, crescent sign; MRI shows geographic defect; patient has pain and stiffness
  • Stage III: radiographs and MRI show crescent sign and eventual cortical collapse; patient has pain and stiffness and may limp
  • Stage IV: radiographs and MRI show end-stage disease with evidence of secondary degenerative change; patient has pain and stiffness and may limp

Codes

ICD10CM:
M87.08 – Idiopathic aseptic necrosis of bone, other site
M87.38 – Other secondary osteonecrosis, other site

SNOMEDCT:
397758007 – Avascular necrosis of bone

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Drug Reaction Data

Below is a list of drugs with literature evidence indicating an adverse association with this diagnosis. The list is continually updated through ongoing research and new medication approvals. Click on Citations to sort by number of citations or click on Medication to sort the medications alphabetically.

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Last Reviewed:05/03/2021
Last Updated:05/31/2021
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Avascular necrosis of knee
Copyright © 2022 VisualDx®. All rights reserved.