Humeral head necrosis 

                                       Dr. KS Dhillon

Osteonecrosis of the humeral head is a disorder that involves osteocytes and the marrow. It is characterized by bone death. Osteonecrosis of the humeral head may be atraumatic or traumatic. Osteonecrosis of the humeral head can result in the collapse of the humeral head articular surface and joint destruction. Since the glenoid is less constrained it can therefore accept greater deformity of the humeral head. The scapula can compensate for some of the glenohumeral motion loss due to the osteonecrosis.

Traumatic osteonecrosis occurs due to disruption of the blood supply to the head caused by fracture or dislocation of the proximal humerus [1].  Atraumatic osteonecrosis involves abnormalities of humeral head blood flow. There are multiple etiologies but corticosteroid therapy is the most commonly reported cause. Atraumatic osteonecrosis can be bilateral and multifocal. Osteonecrosis is considered multifocal when three or more joints are involved. The femoral and humeral head are most often affected [2].

Disease prevention is important. Most cases can be treated successfully without surgical intervention. In other patients, prosthetic replacement may be necessary. Early identification of disease progression is important to treat symptomatic disease in the early stages, thereby avoiding arthroplasty.

Anatomy

The main blood supply to the head of the humerus is from the ascending branch of the anterior humeral circumflex artery. It enters the humeral head through the bicipital groove. A small amount of collateral flow is provided by the posterior humeral circumflex artery which pierces the rotator cuff attachments. The collateral flow about the proximal humerus is minimal. The intraosseous blood supply to the head comes from the arcuate artery.

Pathophysiology

The insult that initiates the avascular necrosis differ on the basis of causation. Fracture dislocation of the shoulder causes traumatic disruption of the proximal humeral vasculature. There are several theories of steroid-induced disease [3]. One of the proposed theories is that increased intraosseous fat cell size results in increased intraosseous pressure and fat embolism. Alcohol abuse also appears to work in a similar manner as steroids. Dysbarism causes cell death via air bubbles leading to congestion and ischemia. In patients with sickle cell disease, the sickled red blood cells cause infarcts in the subchondral bone.

Following the initial insult, the pathogenesis of the disease is the same, regardless of the cause. Death of the cells and marrow occurs. During the healing phase, the necrotic tissue is removed by bone resorption. Bone resorption leads to the weakening of the bone. The forces across the subchondral plate of the weakened bone result in microfractures and subsequent collapse. Progressive deformity of the humeral head causes changes in the glenoid leading to osteoarthritis of the shoulder joint. 

Etiology

Traumatic humeral head osteonecrosis results from disruption of the blood flow of the humeral head due to proximal humeral fracture or dislocation. There are a growing number of case reports that report shoulder osteonecrosis following arthroscopic rotator cuff surgery [4].   

There are multiple causes of atraumatic osteonecrosis. These include: 

• Steroid use

• Alcohol abuse

• Dysbarism

• Hemoglobinopathies

• Coagulopathies

• Gaucher disease

• Connective tissue disorders

• Idiopathic disorders [3,5].

 Adults with sickle cell disease are at higher risk for shoulder osteonecrosis if hip osteonecrosis is present or if they have the SC or S Beta genotype [6]. 

Epidemiology

The traumatic form of osteonecrosis has been reported in up to 34% of 3-part fractures and 90% of 4-part fractures of the proximal humerus, as well as nearly all fractures of the anatomic neck. The incidence of atraumatic osteonecrosis of the humeral head is difficult to determine. However, it occurs less often than in the hip. 

The traumatic form of shoulder osteonecrosis can occur at any age. The atraumatic form usually occurs in patients aged between 20-60 years. 

Clinical presentation

The presentation depends on etiology. Pain is usually poorly localized and severe. Rest pain and night pain are present. Pain increases with activity. The joint movements are preserved in the early stages of the disease. Following subchondral collapse, crepitation and locking are present. When arthritis sets in the joint movements are reduced.

Laboratory Studies

Laboratory studies are usually not necessary for the diagnosis of osteonecrosis. Tests can however be utilized to identify inciting factors, such as:

• Sickle cell disease in African Americans

• Lipid profile to reveal if there is underlying hyperlipidemia

• Thrombotic disorders - Protein S and protein C deficiencies, factor V Leiden disease

Imaging Studies

The diagnosis can be established in most of the cases by radiography. Essential radiographic views include anteroposterior (AP), and axillary views.

When humeral head osteonecrosis is suspected but the x-rays are normal magnetic resonance imaging (MRI) is the diagnostic modality of choice. MRI has sensitivity and specificity greater than 98% for humeral head osteonecrosis [7]. The extent of humeral head necrosis on MRI is a good predictor of future collapse of the humeral head [8].

A bone scan [7] can be useful when the disease is suspected clinically but is not apparent on radiographs. It is not commonly used because of the high success rate with MRI. 

Tomography can be useful in stage II disease to further define the lesion. 

Biopsy 

A biopsy can be performed at the time of surgery. The diagnosis is usually made based on clinical and radiographic findings.

Staging

Ficat and Arlet have staged osteonecrosis of the humeral head [9] :

Stage I - Normal

Stage II - Cystic and/or osteosclerotic lesions are seen. The humeral head contour is normal.

Stage III - There is subchondral collapse or crescent sign

Stage IV - There is narrowing of the joint space. Secondary osteoarthritic changes such as cysts, marginal osteophytes, and destruction of cartilage,

of the glenoid fossa and the glenohumeral head are seen. 

Treatment

Depending on the stage of the disease and the symptoms, the treatment of humeral head osteonecrosis varies. An important initial step is eliminating the inciting factor if and when it is recognized. Treatment often can be delayed or is not required because the shoulder is a non–weight bearing joint. When there is severe pain and/or mechanical symptoms, conservative and surgical options are available. The presence of infection or severe systemic disease may preclude surgical intervention.

Medical Care

Removal of the offending agent is the first line of treatment. Nonsurgical options are often more successful in cases of shoulder osteonecrosis because the shoulder is a non–weight-bearing joint. Physical therapy that includes modalities for pain control and range of motion exercises with muscle strengthening is helpful in all stages, particularly in stage I and stage II of the disease.

Alendronate is known to prevent a collapse of the femoral head caused by osteonecrosis. Its effectiveness in treating osteonecrosis of the shoulder is not known.

Surgical Care

Core decompression is performed in the early stage of the disease before the collapse of the head. The surgical procedure involves surgical drilling into the area of dead bone near the joint. This reduces pressure, allows for increased blood flow, and slows or stops bone and/or joint destruction. It allows bone healing. 

In 90% of cases of stage I and stage II disease core decompression have shown good and excellent results [10,11]. Core decompression can also be successful in stage III disease. There is, however, a 30% failure rate requiring subsequent arthroplasty in stage 3 disease. There is failure with core decompression in all cases of stage IV or V disease. The procedure is palliative only [12].  Harreld et al [13] have described an alternative technique of decompression utilizing multiple passes of a small-diameter (3-mm) drill in a percutaneous fashion. 

Mesenchymal stem cell grafting is also effective in treating posttraumatic shoulder osteonecrosis. A prospective randomized clinical study by Hernigou et al [14] of 50 patients with post-traumatic shoulder osteonecrosis compared the results of mesenchymal stem cell grafting of the humeral head versus simple core decompression. They found that after more than a decade of follow-up, the rate of collapse was significantly lower in the group treated with stem cells. Arthroscopic debridement of chondral lesions can be performed. Arthroscopy has no effect on the disease process. It may be helpful in dealing with mechanical symptoms. 

In patients with advanced-stage disease a hemiarthroplasty or total shoulder arthroplasty can be done depending on the condition of the glenoid [15,16,17]. A 90% success rate has been reported for hemiarthroplasty and total shoulder arthroplasty in advanced-stage disease. Most of them regain full movements of the shoulder [15,17]. Surface replacement arthroplasty also is an option [18,19].

Hemiarthroplasty has had a longer follow-up. Schoch and colleagues recommend that hemiarthroplasty should be considered in patients with atraumatic osteonecrosis of the humeral head with preserved glenoid cartilage [20]. 

Schoch et al [21] compared the outcome of 37 hemiarthoplasties with 46 total shoulder replacements performed for post-traumatic osteonecrosis of the humeral head after conservative treatments failed. They found that hemiarthroplasties provided improvements in range of motion and total shoulder replacement provided superior pain relief with better patient reported satisfaction.  

Core decompression is performed as follows:

The patient is placed in the beach-chair position with the arm over the edge of the table. A small incision is made in the lateral deltoid. Under image intensification guidance, a K-wire is inserted into the necrotic lesion, and a cannulated drill is used to take a core of bone. If the drilling technique is used multiple passes are made into the lesion with a small-diameter drill (usually 3.2 mm) under image intensification.

Arthroscopy can be used for intraarticular debridement. Articular cartilage flaps can be debrided, loose bodies removed, and selective capsular release can be performed.

Hemiarthroplasty involves the placement of a humeral head prosthesis, usually through a deltopectoral approach. 

For total shoulder arthroplasty, several prostheses are available. The glenoid is resurfaced with an all-polyethylene component. Total shoulder arthroplasty is required in individuals with stage IV disease.

When surface replacement arthroplasty is carried out the humeral head is resurfaced partially or completely with a metal component.

Postoperatively immediate range of motion (ROM) exercises can be initiated. Patients who had core decompression are started on immediate passive ROM exercises, with active ROM as tolerated. After full ROM is achieved, strengthening exercises can be started.

Following hemiarthroplasty and shoulder arthroplasty, immediate passive ROM exercises can be initiated. External rotation is limited to 45° for 6 weeks to allow for healing of the subscapularis. Active ROM can be started as tolerated. Strengthening is usually started 6 weeks after surgery.

Complications

Complications following surgery are rare. Common surgical complications include infection and neurovascular injuries. 

When core decompression is carried out care must be taken to avoid injury to the axillary nerve anteriorly. Penetration of the humeral head during core decompression should be avoided.

Complications with arthroplasty include prosthetic loosening, dislocation, and intraoperative fracture. 

References

1. Patel S, Colaco HB, Elvey ME, Lee MH. Post-traumatic osteonecrosis of the proximal humerus. Injury. 2015 Jun 19. 

2. El Gamal TA, El-Bakoury A, Hawkins A, Ed AlTayeb Mussa M, Er Ahmed Sweed T, Eh Samir Ansara S. Bilateral Osteonecrosis of the Femoral and Humeral Heads after Short Term Corticosteroid Therapy. A Case Study. Ortop Traumatol Rehabil. 2016 Mar 23. 18 (2):187-190.

3. Cruess RL. Experience with steroid-induced avascular necrosis of the shoulder and etiologic considerations regarding osteonecrosis of the hip. Clin Orthop Relat Res. 1978 Jan-Feb. 86-93.

4. Keough N, Lorke DE. The humeral head: A review of the blood supply and possible link to osteonecrosis following rotator cuff repair. J Anat. 2021 Nov. 239 (5):973-982.

5. Cushner MA, Friedman RJ. Osteonecrosis of the Humeral Head. J Am Acad Orthop Surg. 1997 Nov. 5(6):339-346.

6. Hernigou P, Hernigou J, Scarlat M. Shoulder Osteonecrosis: Pathogenesis, Causes, Clinical Evaluation, Imaging, and Classification. Orthop Surg. 2020 Oct. 12 (5):1340-1349.

7. Mont MA, Ulrich SD, Seyler TM, Smith JM, Marker DR, McGrath MS, et al. Bone scanning of limited value for diagnosis of symptomatic oligofocal and multifocal osteonecrosis. J Rheumatol. 2008 Aug. 35(8):1629-34. 

8. Sakai T, Sugano N, Nishii T, Hananouchi T, Yoshikawa H. Extent of osteonecrosis on MRI predicts humeral head collapse. Clin Orthop Relat Res. 2008 May. 466(5):1074-80.

9. Ficat RP, Arlet J. Necrosis of the femoral head. Hungerford DS. Ischemia and necrosis of bone. Baltimore, MD: Williams & Wilkins; 1980. 171-82.

10. LaPorte DM, Mont MA, Mohan V, Pierre-Jacques H, Jones LC, Hungerford DS. Osteonecrosis of the humeral head treated by core decompression. Clin Orthop Relat Res. 1998 Oct. 254-60. 

11. Mont MA, Maar DC, Urquhart MW, Lennox D, Hungerford DS. Avascular necrosis of the humeral head treated by core decompression. A retrospective review. J Bone Joint Surg Br. 1993 Sep. 75(5):785-8.

12. Soohoo NF, Vyas S, Manunga J, Sharifi H, Kominski G, Lieberman JR. Cost-effectiveness analysis of core decompression. J Arthroplasty. 2006 Aug. 21(5):670-81.

13. Harreld KL, Marulanda GA, Ulrich SD, Marker DR, Seyler TM, Mont MA. Small-diameter percutaneous decompression for osteonecrosis of the shoulder. Am J Orthop (Belle Mead NJ). 2009 Jul. 38 (7):348-54.

14. Hernigou P, Hernigou J, Scarlat M. Mesenchymal stem cell therapy improved outcome of early post-traumatic shoulder osteonecrosis: a prospective randomized clinical study of fifty patients with over ten year follow-up. Int Orthop. 2021 Oct. 45 (10):2643-2652.

15. Feeley BT, Fealy S, Dines DM, Warren RF, Craig EV. Hemiarthroplasty and total shoulder arthroplasty for avascular necrosis of the humeral head. J Shoulder Elbow Surg. 2008 Sep-Oct. 17(5):689-94.

16. Smith RG, Sperling JW, Cofield RH, Hattrup SJ, Schleck CD. Shoulder hemiarthroplasty for steroid-associated osteonecrosis. J Shoulder Elbow Surg. 2008 Sep-Oct. 17(5):685-8. 

17. Tauber M, Karpik S, Matis N, Schwartz M, Resch H. Shoulder arthroplasty for traumatic avascular necrosis: predictors of outcome. Clin Orthop Relat Res. 2007 Dec. 465:208-14.

18. Raissp, Kasten p, Baumann F, Moser M, Rickert M, Loew M. Treatment of osteonecrosis of the humeral head with cementless surface replacement arthroplasty. JBJS(Am). Feb 2009. 91(2):340-9. 

19. Uribe JW, Botto-van Bernden A. Partial humeral head resurfacing for osteonecrosis. J Shoulder Elbow Surg. Sept-Oct 2009. 18(5):711-6.

20. Schoch BS, Barlow JD, Schleck C, Cofield RH, Sperling JW. Shoulder arthroplasty for atraumatic osteonecrosis of the humeral head. J Shoulder Elbow Surg. 2016 Feb. 25 (2):238-45.

21. Schoch BS, Barlow JD, Schleck C, Cofield RH, Sperling JW. Shoulder arthroplasty for post-traumatic osteonecrosis of the humeral head. J Shoulder Elbow Surg. 2016 Mar. 25 (3):406-12.