CHAPTER SYNOPSIS
Avascular necrosis (AVN) of the humeral head accounts for 5% of all shoulder arthroplasties performed. Alterations to the blood supply of the humeral head result in localized necrosis and collapse of the subchondral bone. Trauma, corticosteroid use, and systemic illness are the most common causes of AVN. Early stages can be managed with nonoperative modalities and core decompression, but later stages require arthroplasty to relieve pain. The outcomes of shoulder arthroplasty for AVN are very promising, although long-term studies are lacking at this point in time.
IMPORTANT POINTS:
- 1
Arthroplasty should be considered for a patient with AVN and stage III, IV, or V disease.
- 2
The choice between hemiarthroplasty and total shoulder replacement is often made intraoperatively based on the condition of the glenoid
- 3
Younger patients (younger than 50) may be better suited to a total shoulder arthroplasty because a high percentage will develop glenoid wear and pain after hemiarthroplasty.
- 4
Posttraumatic AVN patients may have altered anatomy and outcomes different from those with AVN of different origin.
CLINICAL/SURGICAL PEARLS:
- 1
The humeral head osteotomy should emerge precisely at the insertion of the rotator cuff.
- 2
In the case of malunited tuberosities, surgical approaches may be facilitated by greater and lesser tuberosity osteotomies.
- 3
Complete visualization of the glenoid is paramount to glenoid preparation. If exposure is difficult, an extended soft tissue release should be performed.
- 4
The anterior capsular attachment on the glenoid should be released superiorly to inferiorly.
- 5
The humeral head selected to should be the largest size possible that allows closure of the subscapularis.
CLINICAL/SURGICAL PITFALLS:
- 1
Patients with stage III disease may be better treated with arthroplasty than core decompression.
- 2
The decision for hemiarthroplasty or total shoulder arthroplasty may be made intraoperatively, but the surgeon must be prepared for both.
- 3
The version of the glenoid must be accurately determined for proper stability. If there is posterior instability, a larger humeral head may be inserted, the humeral component may be placed in less retroversion, or the posterior capsule may be plicated.
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Avascular necrosis (AVN), also known as osteonecrosis and aseptic necrosis, is a disease resulting from the temporary or permanent loss of the blood supply to the subchondral bone. Approximately 5% of all shoulder arthroplasties are performed for AVN of the humeral head. The humeral head is the second most commonly affected joint, after the femoral head, and current understanding of AVN in the humeral head is largely based on studies of AVN in the femoral head. However, unlike the femoral head, patients with AVN of the humeral head often present in later stages of the disease. Numerous factors can cause a disruption of blood supply to the humeral head and subsequent AVN, including corticosteroid treatment, trauma, dysbaric dysfunction, hemoglobinopathies, and systemic diseases such as Gaucher disease. Operative treatment options for humeral head AVN include core decompression, hemiarthroplasty, and total shoulder arthroplasty (TSA). The results of TSA for humeral head AVN have been improving and are quite encouraging.
ETIOLOGY
Central to the development of AVN is disruption of the arterial blood supply or blockage of the venous outflow tract, which results in decreased blood flow in the subchondral of bone where AVN takes place. The primary blood supply to the humeral head is through intraosseous vessels from the arcuate artery that cross the anatomic neck from the metaphysis ( Fig. 17-1 ). Arterial blood supply originates in the axillary artery anterior to the subscapularis muscle. The anterior humeral circumflex artery branches off the axillary artery 1 cm distal to the inferior border of the pectoralis major and runs along the inferior border of the subscapularis muscle. At the superolateral aspect of the bicipital groove, the artery enters the humeral head at a constant position at the proximal end of the transition from the greater tuberosity to the intertubercular groove and branches into multiple intraosseous vessels within the humeral head. Due to the intraosseous arch shape of this vessel, it is referred to as the arcuate artery. Despite the rich periosteal vascular network, there are few anastomoses once the artery courses interosseously. Injury to this primary blood supply of the humeral head with displacement of fracture fragments is the primary cause of AVN following proximal humeral fractures. In addition, a smaller vascular network arises from the posterior humeral circumflex artery. Its branches penetrate medially at the cartilage bone interface and supply a small portion of the posteroinferior humeral head as well as the posterior aspect of the greater tuberosity.
Disruption of the humeral head blood supply can be thought of as either a macrovascular insult, such as a traumatic event, or microvascular insult, which occurs with corticosteroid use, dysbarism, and hemoglobinopathies. The subchondral area of bone where AVN occurs is highly vulnerable to small changes in vascularity. Arterioles become sinusoids and make a 180-degree turn to return to the intraosseous circulation. Disruption of these small arterioles can occur by either thrombotic or embolic events, circulating fat, nitrogen bubbles, and abnormally shaped red blood cells that occur in hemoglobinopathies. The risk factors for developing AVN of the humeral head are summarized in Table 17-1 .
| Risk Factor | Proposed Trigger |
|---|---|
| Trauma | Disruption of blood supply |
| Corticosteroid use | Increased intraosseous pressure, fat emboli |
| Sickle cell disease | Embolic blockade of sinusoids |
| Gaucher disease | Emboli, local cytotoxicity |
| Alcohol abuse | Fat embolism |
| Dybarism | Air emboli, local vasoactive substances released |
| Connective tissue disorders | Small vessel injury, thromboplastin release |
| Radiation injury | Small vessel injury |
| Pancreatitis | Fat emboli |
| Pregnancy | Fat emboli |
| Idiopathic | Unknown |
Trauma
Interruption of the blood supply to the humeral head dramatically increases the risk of developing AVN. This can occur with a fracture/dislocation of the proximal humerus, as well as with surgery. Four-part fractures of the proximal humerus are associated with the highest prevalence of AVN due to the disruption of the anterior and posterior humeral circumflex arteries from the humeral head.
The incidence of AVN following three- and four-part fractures of the proximal humerus varies considerably in the literature, from as low as 5% to as high as 50%. Surgical fixation of these fractures varies as well, from percutaneous transosseous fixation to formal open reduction internal fixation with plates and screws. Despite the minimally invasive nature of transosseous suture fixation, the incidence of AVN was 7% (11 of 165 patients), with four patients developing complete collapse of the humeral head. With the advent of locking plate technology, there has been renewed interest in open reduction internal fixation of complicated three- and four-part fractures. Despite the presence of AVN, clinical outcomes after fracture fixation have been reported to be good. Wijgman et al. examined the outcomes of cerclage or T-plate fixation in 60 patients over 10 years. Thirty-seven percent of the patients developed AVN, although more than 75% of these patients still had good subjective outcomes at time of the study. A similar study in 34 patients with proximal humeral fractures with articular involvement had a 35% incidence of AVN, with 2 patients requiring shoulder replacement. The incidence of AVN with intramedullary nails seems similar to that seen following plate fixation. Linhart et al. followed 97 patients after antegrade intemedullary nailing of a proximal humerus fracture. Two percent were identified with complete AVN; an another 6% had partial AVN of the humeral head. Despite improved techniques of operative fixation, AVN following proximal humerus fractures remains common. This is likely due to the initial insult, rather than method of fixation, because the rate of AVN following trauma is high regardless of fixation type. Regardless, total shoulder arthroplasty after the development of posttraumatic AVN presents a challenge because factors such as malunion, nonunion, scarring, failed hardware, and infection may be present at the time of arthroplasty. These all may have an impact on intraoperative technique as well as postoperative outcomes following total shoulder arthroplasty.
Corticosteroids
Corticosteroid use is the most commonly reported cause of nontraumatic AVN. Originally described in 1957, the number of cases rose dramatically as the indications for larger dose corticosteroid therapies increased. Recently, as the systemic complications of high-dose steroid treatment have become well known and administration has become more judicious, the incidence of AVN has decreased from more than 25% to less than 5%.
The mechanism of corticosteroid-induced AVN is not entirely elucidated. There are two predominant theories—the first based on local alterations to bone, the second based on embolic events that result in disruptions in blood flow to the humeral head. Studies of AVN in the femoral head have documented an increase in the intraosseous fat-cell size, with increased intraosseous pressure in animal studies, as well as in clinical studies, supporting the first theory. Recent animal studies have also shown a decrease in osseous blood flow during administration of high-dose methylprednisolone, supporting the first theory. The embolic theory is based on changes in fatty metabolism brought about by corticosteroid therapy. With corticosteroid administration, there is altered fat metabolism resulting in fatty changes in the liver. Fat can subsequently embolize to multiple different sites including bone, resulting in focal cell death. The second theory is supported by cadaveric studies that demonstrate embolized fat in subchondral vessels. Most likely, corticosteroids result in AVN due in part to both increased intraosseous pressure and embolic events from altered fatty metabolism.
Multiple studies of AVN following corticosteroid use support the theory that high-dose corticosteroid administration is a key factor in the development of AVN. However, not all patients who receive high-dose corticosteroids develop AVN, and no studies to date have been able to clearly identify risk factors for development of AVN in this patient population. The effect of short-term high-dose corticosteroid therapy is not clear in the literature either. AVN has been described after a short course of corticosteroids for arthritic exacerbations, cancer, and lupus. Conversely, Wing et al. conducted a prospective cohort study to determine if large doses of corticosteroid following spinal cord injury resulted in an increased incidence of AVN in either the femoral or humeral head. Magnetic resonance imaging (MRI) was used to screen 59 spinal cord–injured patients 6 months after administration of high-dose methylprednisolone and found no cases of AVN in either the humeral or femoral heads. One critical difference may lie in the fact that the spinal cord patients had no underlying systemic illness, which may increase the likelihood that the patient has a susceptible blood supply to the subchondral bone following short-term high-dose corticosteroid treatment.
Hemoglobinopathies and Systemic Diseases
Worldwide, sickle cell disease and associated hemoglobinopathies are believed to be the most common cause of AVN. In sickle cell disease, deoxygenation of the blood causes polymerization of the abnormal hemoglobin, resulting in alteration of the shape of the red blood cells. The cells become stiff and sickled in shape and can become caught in the small subchondral arterioles. Evidence of humeral head AVN has been found in up to 28% of patients with sickle cell disease, with shoulder function decreased in 64% of these patients. In one series, humeral head involvement was more common than femoral head involvement in adults with sickle cell disease. Evaluation of these patients can be difficult because many patients have pain secondary to bone infarcts, osteomyelitis, and septic arthritis. Treatment of sickle cell disease with bone marrow transplant is very successful in treating the systemic aspect of the disease and has been shown to reverse the AVN seen in the humeral head in one case report.
Gaucher diesase is a lysosomal storage disease with autosomal recessive heritage pattern. Although an uncommon cause of humeral head AVN, it represents approximately 1% of all cases of AVN of the humeral head and approximately 5% of all atraumatic cases in one case series of 150 patients. The disorder is a result of a deficiency in the glucocerebrosidase hydrolase enzyme, which allows an accumulation of sphingolipid in macrophages. These large, lipid-filled macrophages, known as Gaucher cells, infiltrate the bone marrow and result in increased intraosseous pressure. In addition, angiospasm is induced by a release of cytotoxic chemicals from damaged macrophages. Similar to other systemic illnesses, AVN occurs most commonly in the hip, followed by the humeral head in Gaucher disease. In a retrospective review of 51 patients with Gaucher disease, 15 patients were found to have at least one site of AVN, and 8 had humeral head involvement. A prior splenectomy markedly increased the rate of AVN in this study. Treatment of Gaucher disease with alglucerase, a replacement enzyme, has potential to reverse the systemic effects of the disease in the hematopoietic system, but there are no clear data on the effects on AVN.
Systemic lupus erthematosus (SLE), rheumatoid arthritis, vasculitis, and other connective tissue disorders have been associated with the development of AVN of the humeral head. However, because most of these patients have been treated with corticosteroids, the pathogenesis is quite complicated and the precise etiology is obscure. Rascu et al. followed a cohort of 280 SLE patients over a 10-year period. Only seven developed symptomatic AVN, two of which occurred years after discontinuation of corticosteroid therapy. It is likely that both the corticosteroid administration and the vascular inflammation that is central to these connective tissue disorders result in the higher incidence of AVN in this patient population.
Dysbarism
Dysbarism, or decompression sickness, also known as Caisson disease, usually occurs in scuba divers or undersea workers subject to compressed air environments. Originally described in 1890, the first reports of Caisson disease affecting bone were in the 1940s and 1950s as undersea construction of bridges and tunnels with compressed air increased dramatically in Europe. The compressed air environment causes nitrogen, which is normally dissolved within the bloodstream, to form embolic air bubbles within the vascular system. In addition, a release of vasoactive substances promotes vasoconstriction and local ischemia, although the mechanism is not clearly understood. The incidence of dysbaric AVN may be high in professional divers: Lesions consistent with early AVN were identified in 27 of 39 proximal humeri studied in 23 professional scuba divers.
Alcoholism
Alcoholism is a likely under-reported cause of nontraumatic AVN of the humeral head. The mechanism of alcohol-induced AVN is likely similar to that of corticosteroids. Prolonged alcohol use results in fatty changes in the liver, with subsequent release of fat into the circulation. Increased intraosseous pressure and alterations in the architecture of the bone marrow have also been implicated.
Other Causes
Many other disease processes have been implicated in the development of AVN, including pancreatitis, vascular disease, pregnancy, hemophilia, chronic renal failure, smoking, hyperlipidemia, diabetes, Cushing disease, and gout. In many patients, there is no identifiable risk factor, and their cause is described as idiopathic. Despite the multiple etiologies of atraumatic AVN, the underlying cause remains similar: Any event that decreases the blood supply to the subchondral bone either via an embolic or local phenomenon can result in subchondral necrosis and progression of AVN.
CLASSIFICATION SYSTEM
Classification of humeral head AVN can be via either plain radiographs or MRI ( Fig. 17-2 ). The most common and applicable classification system is based on a modification of the Ficat-Arlet classification of AVN in the femoral head, originally described in 1968 and modified in 1980. Cruess adapted this classification to the humeral head, and it has since become the most widely used ( Table 17-2 ). This classification system is based on the appearance of the shoulder on plain anteroposterior (AP) radiographs and has been found to have a high level of intra- and interobserver reliability.
| Modified Ficat Stage | Symptoms | Findings on Plain Radiographs | MRI Findings |
|---|---|---|---|
| I | None | Normal | “Double-line” sign |
| IIA | None | Diffuse or localized osteoporosis or sclerosis of the humeral head | Uniform loss of signal |
| IIB | None or pain with activity | Crescentic subchondral line formation, segmental flattening of the humeral head | Uniform loss of signal |
| III | Pain with activity | Break in the articular cartilage from one end of the affected area to another; formation of the “crescent sign” | Crescent sign |
| IV | Pain at rest | Loss of joint space with collapse of the humeral head | Joint effusion, progressive collapse |
| V | Pain at rest | Progression to glenohumeral arthritis with degenerative changes on either side of the joint | Extensive collapse, changes present in glenoid |
Stage I disease is characterized by no radiographic changes on plain films. Rather, changes can only be detected with MRI. MRI changes during stage I demonstrate a clear demarcation between living and dead bone. The bone marrow, which is normally high in T1-weight images, appears to have bands of low signal intensity in the osteonecrotic areas. This “double-line” sign appears as a high signal area inside a band of low signal ( Fig. 17-3 ). These bands are thought to represent reactive bone at the margins of the necrotic bone.
Stage IIA is marked with increased subchondral sclerosis along the superior central portion of the humeral head with evidence of bony remodeling and focal subchondral osteolysis. The sphericity of the humeral head remains intact in stage IIA disease. Stage IIB radiographs demonstrate crescentic subchondral line formation, with subtle segmental flattening of the humeral head that may be best visualized on external or internal rotation views of the humeral head ( Fig. 17-4 ). The MRI during stages IIA and IIB demonstrates a uniform loss of signal intensity within the necrotic area.
Stage III disease presents with the “crescent sign,” which represents collapse of the subchondral bone through a necrotic and partially revascularized area of bone that extends to the joint. The fragment becomes sclerotic, and there is loss of sphericity of the humeral head ( Fig. 17-5 ). Despite the significant subchondral osseous abnormalities, the articular surface often remains intact in stage III AVN. Clinical symptoms, including mechanical catching and locking, may begin in this stage. Similar to the radiographs, the crescent sign can be seen with MRI on this stage.
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