Musculoskeletal clinical topic of the month – Exercise Induced Avascular Necrosis of the Hip

Avascular Necrosis (AVN) of the hip joint

Avascular necrosis of the femoral head is a type of osteonecrosis and is due to disruption of blood supply to the proximal femur. It must be carefully considered in those patients presenting with hip pain +/- associated risk factors. It can occur due to a variety of causes, either traumatic or atraumatic in origin.

AVN of the femoral head is a debilitating disease, and musculoskeletal professionals must be aware of patients with potential risk factors. If caught early enough, aggressive treatment can slow the rate of necrosis. Sadly, patients often present too late and surgical intervention is usually required.

Pathophysiology of AVN

Pathophysiology of AVN

The majority of the blood supply to the head of the femur comes from the medial and lateral circumflex branches of the profunda femoris, which itself is a branch of the femoral artery (the profunda femoris is the deep penetrating branch of the upper thigh). The medial and lateral circumflex femoral arteries anastomose to form a ring around the neck of the femur, from which many small arteries branch off to perfuse the femoral head. Because of limited collateral circulation, disruption of the blood supply to the head of the femur can lead to ischemia and subsequent necrosis. If restoration of blood supply does not occur promptly, this will lead to the progressive death of osteocytes followed by the collapse of the articular surface, and eventually by degenerative arthritis.

Traumatic Femoral head AVN

Large injury or insult to the hip joint (e.g. trauma, dislocation), can acutely disrupt the blood supply to the femoral head causing AVN. This mechanism is well described in orthopaedic literature and common in elderly patients or those with medical co-morbidities.

What is less considered, is how repetitive hip joint loading from sport (contact sport and running in particular) can also lead to similar patterns of AVN and bone destruction. This may be due to repetitive micro-trauma, with microtrabecular and/or subchondral injury triggering an avascular necrotic process.

Non-Traumatic Femoral head AVN

AVN can also occur from medical and biochemical issues without any history of trauma. Examples of these cases can include;

  • Chronic steroid use
  • Chronic alcohol use
  • Smoking
  • Coagulopathy
  • Medication e.g. steroids, bisphonates
  • Medical treatments e.g. renal transplant, radiation therapy
  • Viral illness (now reported cases post COVID) (https://casereports.bmj.com/content/14/7/e242101)

Clinical history

HClinical history;

  • 46-year-old man presented to LBSM with a 6 month history of right buttock discomfort, mild in severity 3/10
  • Prior to attending, had received therapy treatment for sciatica and nerve root impingement with neural release techniques and manual therapy
  • With no progression made, therapist began treating for deep gluteal syndrome with particular bias to Piriformis release and stretching
  • Patient noticed that gait pattern had changed, with people beginning to comment that patient was “swaying or waddling”

Past Medical history;

  • BMI 37
  • Non-smoker
  • Poorly controlled asthmatic – Blue and Brown inhaler, taken antibiotics and prednisolone rescue packs four times this year
  • Previously good bone health

Social history;

  • Works in financial services
  • Alcohol consumption acutely increased due to return to work in office, 10-15 units most days of the week

Clinical examination;

  • Waddle gait pattern with lack of swing through right hip
  • Marked reduction in IR/ER and flexion range of both hips R>L
  • Mild pain only on quadrant testing of both hips and on deep squat R>L
  • Mild external rotation of right foot
  • Trigger pointing throughout QL, gluteals and hamstrings bilaterally

Next steps

  • Hip joint pathology suspected so MRI pelvis and hips organised

Imaging

Left image – MRI T2 weighted coronal sequence showing oedema throughout femoral head and neck and joint effusions bilaterally, with right worse than left.

Right image – MRI T1 weighted coronal sequence showing femoral head infarcts bilaterally and destruction of femoral head. Findings are in keeping with AVN bilaterally R>L.

Screenshot 2021 12 02 at 08.17.44 Musculoskeletal clinical topic of the month - Exercise Induced Avascular Necrosis of the Hip

Diagnosis

Bilateral femoral head and neck avascular necrosis (right worse than left) due to excessive loading patterns, high BMI, high alcohol consumption and multiple steroid use for poorly controlled asthma.

Management

Rehabilitation

First 8 weeks

  • Strict bilateral lower limb offloading through use of wheelchair, to stop progression of AVN
  • To use crutches when walking is necessitated
  • Patient given pool based rehab to complete 3-4 times a week
  • No land based rehab in first rehab phase
  • Strict working from home conditions to avoid unnecessary loading

8-12 weeks

  • Land based rehab with no impact training
  • Slow progression to improve range of movement of both hip joints with no forced passive movements e.g. hip mobilisations.

12 weeks+

  • Return to unaided walking
  • No further impact activity or contact sport conducted

Medical

  • Cessation of alcohol consumption with help from therapist
  • Patient given the option of bilateral hip replacement from outset in LBSM surgical MDT
  • Calorie and nutritional intake optimised to help reduce weight
  • Referred for Lung Function Tests and asthma medication optimised to avoid long term use of steroids
  • Repeat MRI at 12 weeks shows no further progression of AVN and improvement of oedema, but significant residual hip joint destruction bilaterally
  • Pain levels significantly improved but gait pattern remains abnormal
  • Patient opted to delay hip replacement due to symptom improvement, but advised to have bilateral THR within the next 10 years

Patient Self monitoring tools

  • LBSM pain and symptom diary
  • LBSM load monitoring diary

Key Summary – AVN of the hip

  • Hip joint pain can often present as deep seated gluteal pain (beware of diagnosing Piriformis syndrome without prior investigation)
  • In patients who may be subjected to potential hip joint repetitive micro-trauma (e.g. endurance runners, contact sports, military personal), AVN must be considered
  • AVN is not necessarily overtly painful, due to cellular death and nerve ending destruction
  • Always consider alcohol consumption and smoking as strong risk factors for developing AVN
  • Although already necrotic bone cannot heal, the rate of AVN can be considerably slowed with appropriate offloading and medical intervention
  • Priority is to preserve as much healthy bone as possible as this will also improve surgical outcomes if replacement is considered at a later stage
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