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Fremont A. Chandler (Fig 1) was born in Chicago. After his preliminary education he enrolled in the College of Agriculture of the University of Wisconsin. After 3 years, he began taking premedical courses. After graduating from the University of Wisconsin in 1916, Chandler attended the College of Physicians and Surgeons of Columbia University where he received his medical degree in 1919. After an internship in Hartford, CT, Chandler spent 1 year at the Grenfell Hospital in St. Andrews, Newfoundland. It was here that he saw numerous patients with tuberculosis of the bone and joints and decided to become an orthopaedic surgeon. After his training at the New York Orthopaedic Dispensary and Hospital, he returned to Chicago to begin his practice in 1924.Fig 1.: Fremont A. Chandler, MD (Reprinted with permission from J Bone Joint Surg 37A:424, 1955.)In the same year, Chandler began his academic career with an appointment as an instructor on the faculty of Northwestern University. In 1943, he went to the University of Illinois, and became Professor of Orthopaedics and head of the department, a position which he held until his death. Chandler was a superb practitioner and administrator and he made important contributions to the orthopaedic community. He played an important role in the founding of the American Board of Orthopaedic Surgery and was its first secretary. In 1950, as President of the American Orthopaedic Association, he represented the society at the London meeting of the six English speaking orthopaedic associations. He served in the Army Medical Corps in World War I, and served as a member of the Naval Reserve Medical Corps between the wars. During World War II, he was a consultant to the Surgeon General. Chandler’s sudden and premature death at the age of 61 years was a great shock to his friends and associates and a great loss to the entire orthopaedic community. The classic article is typical of Chandler’s unique approach to clinical problems. In his papers and lectures he called attention to the diagnosis of aseptic necrosis of the head of the femur to the extent that for many years the condition was known as “Chandler’s Disease”. CORONARY DISEASE OF THE HIP Fremont A. Chandler, M.D. Chicago, Illinois INFARCTION of the head of the femur in the clinical sense is a group of symptoms, dominated by pain, loss of function and bony collapse caused by anoxemia and other deficiency in arterial nutrition of the head of the femur, prolonged enough to result in marked degeneration, even necrosis of bone. Its most frequent cause is abrupt obstruction, thrombosis or embolism of a large branch of the coronary artery. Two or three times as frequent in men as in women, most cases of femoral head infarction occur between 50 and 70 with fewer cases in the next, earlier and later decades. Below 40, cases are infrequent but may occur at still earlier ages, even in the 20 to 30 period. Increased recognition of mild cases is greatly increasing the incidence of the disease. The foregoing paragraphs are in no sense original but are a direct quotation of the definition and incidence of cardiac infarction taken from the 15th edition of Osler’s Medicine. The terms “cardiac” and “myocardial” have been replaced by the terms “head of the femur” and “bone.” No clearer definition of the pathologic process in the femoral head, due to circulatory failure, could be devised. The pathology of cardiac infarction is so well known to every busy surgeon, that any review is unnecessary. Too frequently cardiac coronary disease becomes the sword of Damocles, hanging over our heads as we go about our regular work. Christian, in this 15th edition of Osler, goes on to describe how cardiac infarction was recognized in autopsy examinations since the earliest periods of medical history, but that the clinical recognition of this entity is of modern times. Between 1896 and 1912, few isolated cases were diagnosed ante mortem. In 1912, James B. Herrick of Chicago aroused the medical profession to clinical recognition of coronary disease and brought the subject to its place of eminence in medical and lay thought. Compare the head of the femur with the heart and it is evident that much of the anatomy is similar. The myocardium and the cancellous bone and cartilage differ histologically, but each is composed of living cells requiring oxygenation and nutrition. The heart protrudes into its pericardial sack much in the same manner as the head of the femur protrudes into the synovia-lined capsule of the hip joint. The nutrient vessels of each are extended and have but limited anastomoses. They are, in a sense, end-arteries. The term, coronary artery, by usage, has come to mean almost exclusively the nutrient arterial channels of the heart. The term “coronary” means crown-like or encircling. We still have the term coronary ligament of the liver. When used in this sense, i. e., crown-like or encircling, it aptly applies to the circulation of the head and neck of the femur. A projection of our knowledge of the varied pathologic processes of cardiac muscle to the structures of the femoral head leads to better understanding of the pathology of the hip joint. The terms coxae malum senilis, arthrosis, aseptic necrosis, etc., are descriptive, but they fail to convey true concepts of the pathologic processes present in the femoral head. Such terms are descriptive of the terminal phases of a complex pathologic process, but they do not convey a concept of the sequence of preceding pathologic events. As in the myocardial lesion, coronary disease of the hip reflects defective circulation and inadequate nutrition of the cancellous bone of the femoral head and neck. The nutrient channels of the femoral head and neck are essentially end-arteries with limited anastomoses. Impairment of circulation, due to vascular obstruction from any cause, is followed by degenerative changes in either myocardium or bone, or in any other tissue. The degree of degeneration and the effectiveness of repair depends upon the extent of the vascular impairment and establishment of an adequate collateral circulation. If new vessels develop to sufficient size and extent, repair will be more complete. Fortunately a margin of safety exists in both myocardium and bone, but this factor diminishes with age, the presence of general vascular disease and the limits of repair. In the head of the femur, degenerative bone changes lag considerably in their manifestation, due to the very nature of the tissue involved. Degenerative changes of the femoral head, due to interrupted circulation from traumatic dislocation of the hip, may be delayed weeks or even months, both clinically and roentgenologically. The same time lag is present in air embolism, thrombosis, fracture, infection of the hip joint or in any other vascular obstruction. In the presence of general vascular disease, the margin of safety diminishes and the probability of the completeness of repair is less. Repair in bone is a slow process, so well and aptly described by Phemister as “creeping substitution.” The possibility of regaining normal function in the head of the femur, as in the heart, depends upon the completeness of repair. When the magnitude of the compression forces and torque, acting through the head of the femur, is taken into consideration, the importance of complete healing is obvious. In a recent article Inman states that the torque at the hip in abduction in males is 10.00 ± .86 × body weight. In females it is 9.4 ± .97 × body weight. He also states that the pressure on the femoral head when the pelvis is horizontal is 2.4–2.6 × the body weight. This is due to the action of the hip abductors countering the forces at the center of gravity which is medial to the hip joint. In its embryologic development, the head and neck of the femur protrude into the synovia-lined capsular cuff of the hip joint. This cuff is shorter posteriorly than in its anterior aspect. The articular surface of the femoral head migrates anteriorly and posteriorly, incorporating a portion of the capsule to form the ligamentum teres. Evidence of this is present in reptiles where the reflected ligament persists and in many humans where a distinct retinaculum is encountered. The arterial supply of the femoral head and neck are found in the ligamentum teres, the folds of synovia encircling the femoral neck and in the nutrient channels of the cancellous bone. Some vessels penetrate the epiphyseal plate, others enter the capital epiphysis at its margins. With closure of the epiphysis more blood supply comes from the femoral neck proper. The trochanteric area of the femur is supplied by freely anastomosing arteries forming the cruciate anastomosis. The medial and lateral circumflex branches of the profunda connect with the inferior and superior gluteal arteries encircling the trochanteric area and capsule of the hip joint. Small perforating branches penetrate the capsule, lie in folds of synovia and enter the margin of the femoral head. These branches, to a degree, may be considered end-arteries, for their anastomoses are, at best, limited. The acetabulum and ligamentum teres derive their arterial supply from the posterior branch of the obturator artery and the acetabular branch of the medial circumflex artery. Anastomoses between the ligamentum teres and the femoral neck are very limited but do exist in some specimens. Several years ago S. W. Chandler reported observations of the blood vessels of 114 ligamenta teres in subjects averaging 48 years of age. Four were relatively avascular. Eight showed many small vessels. In 16 the vessels were obliterated or sclerosed; 86 had vessels .4–.2 mm. in diameter and 50 1.5-.4 mm. in diameter. These variations of the patency of the vessels of the round ligament are important, for they indicate the limitations of possible anastomoses in many hips. Venous channels parallel the arterial supply and normally are adequate. The possibility of embarrassment of circulation through the vessels lying in the synovial folds of the femoral neck by increased joint pressure, caused by effusion, must be kept in mind. The patency of these vessels is diminished by pressure from without. This possibility was suggested by me in 1936. The clinical application of this “coronary disease” concept of hip joint pathology is wide. As the function of the head and neck of the femur is impaired by inadequate blood supply and the resulting lack of nutrition and oxygenation, a series of degenerative changes ensue. These may be of the mildest degree or of major import, with corresponding loss of hip function. The femoral head loses its ability to resist the tremendous stresses of weight-bearing and muscle action and collapses in varying degrees. The loss of contour alone introduces an unending series of additional stresses, with further loss of function and increasing pain. When the nutritive insult is severe, little repair follows and necrosis is complete. Should this insult be less in degree, repair occurs. This is a slow process and rarely advances to complete restoration of the bony contour of the femoral head. The objectives of therapy in “coronary disease of the hip” are the restoration of the functions of weight-bearing and of normal movement at this articulation. Reduction of the “load” by reduction in body weight and the use of crutches or traction is indicated. General nutrition should be optimum. Attempts to improve the local circulatory deficiency should be considered. These consist of multiple drilling of the femoral neck to aid revascularization. This gives only a limited promise of improvement. Implantation of adjacent muscle into the neck of the femur as an additional source of blood supply has been advocated by Walter Stuck of San Antonio, Texas. Alteration of the mechanics of the hip joint by osteotomy, reconstruction of the hip (Whitman) or cup arthroplasty, offer a means of preserving the function of motion. In selected cases, normal function may be attained, but too frequently the result falls short of what we might hope to accomplish. Sacrifice of the motion of the hip joint by some form of hip fusion operation is probably the best solution in unilateral cases. The best technic is the erasement of the hip joint combined with massive iliac grafts and internal fixation. Bony fusion is dependent upon new bone formation across the joint line. Because of the very nature of the bone at this area, obstacles are encountered and fusion is difficult to accomplish. The hip is fixed in a position facilitating sitting as well as walking. Consideration of the flexibility of the lumbar spine must not be overlooked. The many and varied operative approaches designed to alleviate the dysfunction of the hip joint which results from disturbances of nutrition, reflect the complexity of this problem. SUMMARY In many respects the sequence of degenerative pathologic changes following impairment of the circulation in the head and neck of the femur parallels similar processes encountered in cardiac coronary disease. It is hoped that the concept of “coronary disease of the hip” will afford a better understanding of many of the pathologic processes encountered in the head and neck of the femur.
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