Bone Changes in Alcoholics Raymond 0. Pierce, Jr, MD Indianapolis, Indiana
Man has consumed alcohol for its euphoric and sedative effect down through the ages. Attention in the medical literature has been primarily focused on the effects of alcohol on the nervous system and liver. In the past few years, isolated reports have appeared in the medical literature concerning the effects of alcohol on the bony skeleton. The purpose of this paper is to classify these lesions, discuss their pathophysiology, and briefly review their clinical course. The lesions discussed include osteoporosis, hip fractures, aseptic necrosis of the hip, and fat embolism. For the purpose of this discussion these lesions are divided into two groups. Group I includes the battered alcoholic syndrome. Group II includes fat embolism, both acute and chronic, and aseptic necrosis of the hip. Since the allocation of approximately $22 million for the study of alcoholism by the former Secretary of Health, Education, and Welfare, Joseph Califano, alcoholism has been accepted as a disease and the social stigma removed. This has and will allow medical science to more carefully investigate some of the effects of alcohol on various organ systems. Much attention has been given to the economic effect of alcohol by people in industry. It has been found that absenteeism can be reduced and work production greatly increased if employee alcoholic problems are better understood and handled. Alcohol-related accidents are the leading cause of deaths in the 15-24-year-old group. The true incidence of alcoholism in the general population is not known. Therefore, it would be most difficult to know the incidence of alcohol-related conditions. Although studied extensively, there are still major gaps in our knowledge about how alcohol actually affects the nervous system. The purpose of this article is to bring to the attention of the practitioner the common bone changes found in alcoholic patients, in hope that From the Department of Orthopaedic Surgery, Wishard Memorial Hospital, Indianapolis, Indiana. Requests for reprints should be addressed to Dr. Raymond 0. Pierce, Jr, Department of Orthopaedic Surgery, Wishard Memorial Hospital, 960 Locke Street, Indianapolis, IN 46202.
if these lesions are recognized early more appropriate treatment can be afforded.
Pathophysiology We believe that the bony changes associated with alcoholism occur by two different mechanisms. The first causes changes which result in the loss of structural integrity of bones. The second has to do with changes in fat metabolism. It is not clear if these changes are a result of chance or a primary metabolic defect. Clinical correlation seems to point to the latter. Whether these changes are associated with cirrhosis of the liver strictly on a nutritional basis or represent a primary defect is not known. The changes that occur in bone following the ingestion of alcohol are not necessarily timerelated. Acute fat embolism and aseptic necrosis of the hip may occur after a short period of alcoholic indulgence. Other lesions such as osteoporosis and early hip fracture may occur in patients who have consumed large amounts of alcohol over a long period of time.
Pathophysiology-Group I The mechanism whereby the integrity of the bony skeleton is lost in chronic alcoholism is not known. However, once these changes occur, they
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 12, 1979
result in clinical conditions such as osteoporosis and the battered alcoholic syndrome. Saville1 probably was one of the first to note the similarity between structural bone changes found in the alcoholic and in postmenopausal osteoporotic women. Saville pointed out that the possible mechanism for the production of osteoporosis in the alcoholic was calcium deficiency. A study by Smith2 in 1941 found that secretions of adrenal cortical steroids in rats which had been fed alcohol were definitely increased. To our knowledge, no study has been done to determine if bone changes found in alcoholics are the result of a muscle or protein deficiency. Kalbflesch et a13 reported in 1963 the results of clinical studies in alcoholic patients. They found that the administration of alcohol to normal and alcoholic subjects caused an increase in the diuresis of magnesium and calcium. Snell4 in 1971 reported to the AOA on a paper entitled, "The chronic alcoholic and his fractures." He observed that the fracture pattern found in alcoholics was at least 20 years older than actual ages of people studied. He also stated that any hip fractures occurring in a patient under 50 years old should be suspected as being secondary to alcoholism. In spite of the mechanism described above, numerous other investigators feel that the structural changes in the body skeleton occur strictly on a nutritional basis. 1213
Figure 1. X-rays taken at the time of initial visit to medical clinic showing a nonunion of a humeral (left) and femoral neck fracture (right)
than non-alcoholic patients. Currently an investigation is in progress at this institution to corroborate this. Jones in 19689 reported on the triad of alcoholism, fat embolism, and avascular necrosis of the hip, and suggested that this may be a new syndrome. He studied 30 cases and found 77 aseptic lesions, 55 of which occurred in the femoral head. Of 19 patients having histologic studies, systemic embolic fat was found in nine. In two additional patients, fat was found in the resected femoral head. He concluded from these findings that the alcoholic-induced fatty liver was probably the common source of continuous or intermittent low grade showers of fat emboli. Patients in his series showed abnormal liver function tests.
Clinical Condition
Osteoporosis
Figure 2XX-rays taken at earlier date showing a fracture of proximal right humerus (left) and distal right radius (right)
Pathophysiology-Group 11 The pathophysiology of Group II is the result of abnormal fat metabolism. Whether this is associated with cirrhosis of the liver, found in chronic alcoholics, is not known. It has been shown experimentally that when blunt trauma is applied to the fatty liver, showers of embolic fat can be demonstrated in the systemic circulation.;) Lynch" studied 200 adult and 68 pediatric autopsies where a total of 73 (27.2 percent) showed intravascular fat 1214
emboli. He advanced the theory that fat embolism was a major factor in alcoholic psychosis, and that in some cases it could lead to sudden death. Jones and Sakovith7 were able to demonstrate intra-osseous embolic fat experimentally in rabbits followiilg injections of lipids. Kimble8 reported a case, confirmed by autopsy, of a 35-year-old chronic alcoholic who died from fat embolism. Clinically, we believe that alcoholics who undergo acute traumatic episodes are more apt to suffer fat embolism
Osteoporosis per se or osteopenia is not a too infrequent finding in the elderly white female patient. However, when a black female or any male patient has osteoporosis, other metabolic problems should usually be ruled out. Osteoporosis per se usually is not symptomatic. Attention is usually directed to this either when a fracture occurs following minimal trauma or when a patient is x-rayed for some other reason. The association of osteoporosis and hip fractures, compression fractures of the spine, or fractured distal radius are well known. Most authorities feel that this triad of fractures, although not occurring concomitantly, is usually the result of a decrease in bone mass. Because of the decreased incidence of hip, wrist, or vertebral body fracture in the black female, any black female with any of the above fractures should be studied for alcoholism. Hip fractures occurring in any race at an early age should be suspected of being secondary to alcoholism.
Battered Alcoholic Syndrome The term "battered alcoholic syndrome" was coined by Oppenheim'0 in 1977. A person fits into this syndrome if three distinct fractures in different
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 12, 1979
stages of healing can be demonstrated. The clinical significance of this syndrome. is fairly obvious. Any patient with fractures in various stages of healing should be suspected of being an alcoholic and his/her alcoholism should be treated as well as the orthopedic problem. Any alcoholic who presents with a fracture should be carefully followed and protected in order to try to prevent the occurrence of this syndrome. Case Report M.M. was a 64-year-old white, female who came to the medical clinic complaining of "blacking-out" spells. Her examination at that time revealed that she had a deformity of her left hip and left shoulder (Figure 1). She could not recall any traumatic episodes that may have caused the lesions. She admitted to social drinking. She was able to walk with one cane and used the left upper extremity without too much difficulty. She was admitted to the medical service where she had a complete metabolic workup. All her laboratory work was normal. She was transferred to the orthopedic service for definite care of her hip and shoulder. A review of her medical records revealed that she had been seen on several occasions in the Emergency Room complaining of pain in numerous extremities following falls. The record further indicated that she had a drinking problem (Figures 2 and 3).
Fat Embolism-Acute The clinical course of acute fat embolism is well known by most physicians treating trauma patients. The fat embolism syndrome usually occurs in young male patients who have received major trauma. Clinically, this syndrome usually occurs within the first few days following trauma. Changes in sensorium and pulmonary symptoms are the most common presenting symptoms. Laboratory findings include a decrease in arterial oxygen and hemoglobin, lipiduria, and changes in the platelets. It has been our observation that alcoholics hospitalized following acute traumatic episodes are apt to demonstrate the above symptoms. Because they are known alcoholics they are usually treated for delirium tremens. It has been our observation that when alcoholic patients are admitted to other services delirium tremens usually occur later.
Figure 3. X-ray of dorsal spine showing old compression fracture which had been treated (left). X-ray of distal ulna showing fracture (right). Also shows healing distal radial fracture
Fat Embolism-Chronic Some may doubt that this syndrome actually exists. We feel that some of the symptoms exhibited by alcoholics may indeed result from this syndrome rather than alcoholic psychosis. Chronic alcoholics with cirrhosis of the liver are apt to have recurrent showers of fat embolism. These may present either with pulmonary or cerebral symptoms. Any patient who is a known alcoholic and has symptoms of this nature should be hospitalized for appropriate studies. It should be remembered that when embolism occurs it may involve any organ.
A vascular Necrosis of the Hip Avascular necrosis 6f the hip has many causes. When a patient has this lesion, all known causes of avascular necrosis should be ruled out. These causes include trauma, steroid ingestion, elevated uric acid, and blood disorder. Bonfigilio'1 studied x-rays from 1,410 patients, 705 of which were from
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 12, 1979
alcoholics and 200 from normal subjects. The incidence of avascular necrosis was found to be no greater in the alcoholic. Hungerford,12 however, using pressure studies of the upper femur, found that there was a definite increase in avascular necrosis in chronic alcoholics. In our series at Wishard Hospital, we have found that most people, in the age range of approximately 29-50 years, with avascular necrosis usually are alcoholics. The patient usually complains of vague hip pain and usually gives a vague history of trauma. Physical findings as well as routine x-rays are usually negative. If special x-rays or pressure studies are done, the diagnosis can be made when alcohol is the etiological agent. The incidence of both hips eventually being involved may be as high as 80-90 percent. When the diagnosis is first made, early treatment is mandatory in order to obtain satisfactory results. The following is a brief medical report of a case of avascular necrosis of the hip secondary to alcoholism. 1215
Figure 5. AP of pelvis showing Phemister grafts in place in femoral head and a fracture in upper femur
Figure 4. AP of right hip showing early avascular necrosis of the hip
Case Report J.D.L. was a young male patient who presented himself complaining of pain in his hip. The pain had been present for several months. He denied any traumatic episodes involving his right hip. The pain was constant, deep, and aching, and was located in the anterior aspect of his hip; it was worse with activity and only partially relieved by rest. Physical examination revealed that he walked with a limp favoring his right hip. Examination of the right hip revealed normal range of motion; however, there was pain at the extremes of motion. Following hospitalization, his laboratory work, which included blood chemistries and hematological parameters, was essentially negative. Plain x-rays of the hip revealed early avascular necrosis (Figure 4). Following his hospitalization, he was carried to surgery where a Phemister bone graft of his hip was performed. Histological studies of the core specimen was consistent with avascular necrosis. Postoperatively, he did well and was discharged on crutches. He returned to the emergency room approximately three weeks following his discharge complaining of acute pain in his hip. He stated that he was jogging when he had the onset of pain in his hip (Figure 5). 1216
Discussion Chronic alcoholism presents, in addition to its social and economic problems, certain medical problems. We are beginning to see more and more orthopedic problems in people who are alcoholics. It is essential that these lesions be sought because early treatment in these disorders affords a better prognosis. When these lesions are found and treatment is instituted, one should be aware that alcoholics, as a group, are not too reliable. This is well pointed out by the second citation. Karlstrom'3 studied the management of tibial fractures in alcoholics and mentally disturbed patients and suggested that alcoholics should be treated for a longer period of time than other patients. With the increase in medical interest in alcoholism, we hope that more can be learned about these patients' other medical problems and that better medical care can be given. All the lesions discussed in this paper can be found in people who are not alcoholics. We do notX infer that if one of these lesions is found that the patient be accused of being an alcoholic before other causes are ruled out. A case may be made that the lesions found in alcoholics may not be due to underlying bone changes, but to the alcoholic being more apt to injure him-
self. We cannot argue this point, but we do think that the findings referred to earlier in this paper certainly point out that the lesions have a high incidence in alcoholic patients. Literature Cited 1. Saville PD: Changes in bone mass with age and alcoholism. J Bone Joint Surg 47 (3):492-498, 1965 2. Smith J: The effect of alcohol on the ascorbic acid and cholesterol of the rat. J Clin Endoc 11:792-797, 1951 3. Kalbflesch JM, Lindeman RD, Ginn HE, et al: The effects of ethanol administration on urinary excretion of magnesium and other electrolytes in alcoholic and normal subjects. J Clin Invest 42:1471-1475, 1963 4. Snell W: The chronic alcoholic and his fractures. J Bone Joint Surg 53A:1655, 1971 5. Owens G, Northington BA: Liver lipid as a source of post-traumatic embolic fat. J Surg Research 11(4):283-284, 1962 6. Lynch MJ, Raphael S, Dixon T: Fat embolism in chronic alcoholics. AMA Arch Path 67:68-79, 1959 7. Jones JP, Sakovich L: Fat embolism of bone: A roentgenographic and histological investigation with the use of intra-arterial lipiodol, in rabbits. J Bone Joint Surg 48:149-164, 1966 8. Kimble ST: Fatal nontraumatic fat embolism in an alcoholic. Med Ann Dist Col 30(5):283-287, 1961 9. Jones JP, Jamerson R, Engleman EP: Alcoholism, fat embolism and avascular necrosis. J Bone Joint Surg 50(5):1065-1069, 1968 10. Oppenheim WL: The battered alcoholics syndrome. J Trauma 7(11):850-856,1978 11. Smith K, Bonfigilio M, Dolan K: Roentegenographic search for avascular necrosis of the head of the femur in alcoholics and normal adults. J Bone Joint Surg 59:391-396, 1977 12. Hungerford DS, Zizic TM: Alcoholism associated ischemic necrosis of the femoral head. Clin Orthoped 130:144-152, 1978 13. Karlstrom G, Olerud S: The management of tibial fractures in alcoholics and mentally disturbed patients. J Bone Joint Surg 56(4):730-734, 1974
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 12, 1979
Man has consumed alcohol for its euphoric and sedative effect down through the ages. Attention in the medical literature has been primarily focused on the effects of alcohol on the nervous system and liver. In the past few years, isolated reports have appeared in the medical literature concerning the effects of alcohol on the bony skeleton. The purpose of this paper is to classify these lesions, discuss their pathophysiology, and briefly review their clinical course. The lesions discussed include osteoporosis, hip fractures, aseptic necrosis of the hip, and fat embolism. For the purpose of this discussion these lesions are divided into two groups. Group I includes the battered alcoholic syndrome. Group II includes fat embolism, both acute and chronic, and aseptic necrosis of the hip. Since the allocation of approximately $22 million for the study of alcoholism by the former Secretary of Health, Education, and Welfare, Joseph Califano, alcoholism has been accepted as a disease and the social stigma removed. This has and will allow medical science to more carefully investigate some of the effects of alcohol on various organ systems. Much attention has been given to the economic effect of alcohol by people in industry. It has been found that absenteeism can be reduced and work production greatly increased if employee alcoholic problems are better understood and handled. Alcohol-related accidents are the leading cause of deaths in the 15-24-year-old group. The true incidence of alcoholism in the general population is not known. Therefore, it would be most difficult to know the incidence of alcohol-related conditions. Although studied extensively, there are still major gaps in our knowledge about how alcohol actually affects the nervous system. The purpose of this article is to bring to the attention of the practitioner the common bone changes found in alcoholic patients, in hope that From the Department of Orthopaedic Surgery, Wishard Memorial Hospital, Indianapolis, Indiana. Requests for reprints should be addressed to Dr. Raymond 0. Pierce, Jr, Department of Orthopaedic Surgery, Wishard Memorial Hospital, 960 Locke Street, Indianapolis, IN 46202.
if these lesions are recognized early more appropriate treatment can be afforded.
Pathophysiology We believe that the bony changes associated with alcoholism occur by two different mechanisms. The first causes changes which result in the loss of structural integrity of bones. The second has to do with changes in fat metabolism. It is not clear if these changes are a result of chance or a primary metabolic defect. Clinical correlation seems to point to the latter. Whether these changes are associated with cirrhosis of the liver strictly on a nutritional basis or represent a primary defect is not known. The changes that occur in bone following the ingestion of alcohol are not necessarily timerelated. Acute fat embolism and aseptic necrosis of the hip may occur after a short period of alcoholic indulgence. Other lesions such as osteoporosis and early hip fracture may occur in patients who have consumed large amounts of alcohol over a long period of time.
Pathophysiology-Group I The mechanism whereby the integrity of the bony skeleton is lost in chronic alcoholism is not known. However, once these changes occur, they
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 12, 1979
result in clinical conditions such as osteoporosis and the battered alcoholic syndrome. Saville1 probably was one of the first to note the similarity between structural bone changes found in the alcoholic and in postmenopausal osteoporotic women. Saville pointed out that the possible mechanism for the production of osteoporosis in the alcoholic was calcium deficiency. A study by Smith2 in 1941 found that secretions of adrenal cortical steroids in rats which had been fed alcohol were definitely increased. To our knowledge, no study has been done to determine if bone changes found in alcoholics are the result of a muscle or protein deficiency. Kalbflesch et a13 reported in 1963 the results of clinical studies in alcoholic patients. They found that the administration of alcohol to normal and alcoholic subjects caused an increase in the diuresis of magnesium and calcium. Snell4 in 1971 reported to the AOA on a paper entitled, "The chronic alcoholic and his fractures." He observed that the fracture pattern found in alcoholics was at least 20 years older than actual ages of people studied. He also stated that any hip fractures occurring in a patient under 50 years old should be suspected as being secondary to alcoholism. In spite of the mechanism described above, numerous other investigators feel that the structural changes in the body skeleton occur strictly on a nutritional basis. 1213
Figure 1. X-rays taken at the time of initial visit to medical clinic showing a nonunion of a humeral (left) and femoral neck fracture (right)
than non-alcoholic patients. Currently an investigation is in progress at this institution to corroborate this. Jones in 19689 reported on the triad of alcoholism, fat embolism, and avascular necrosis of the hip, and suggested that this may be a new syndrome. He studied 30 cases and found 77 aseptic lesions, 55 of which occurred in the femoral head. Of 19 patients having histologic studies, systemic embolic fat was found in nine. In two additional patients, fat was found in the resected femoral head. He concluded from these findings that the alcoholic-induced fatty liver was probably the common source of continuous or intermittent low grade showers of fat emboli. Patients in his series showed abnormal liver function tests.
Clinical Condition
Osteoporosis
Figure 2XX-rays taken at earlier date showing a fracture of proximal right humerus (left) and distal right radius (right)
Pathophysiology-Group 11 The pathophysiology of Group II is the result of abnormal fat metabolism. Whether this is associated with cirrhosis of the liver, found in chronic alcoholics, is not known. It has been shown experimentally that when blunt trauma is applied to the fatty liver, showers of embolic fat can be demonstrated in the systemic circulation.;) Lynch" studied 200 adult and 68 pediatric autopsies where a total of 73 (27.2 percent) showed intravascular fat 1214
emboli. He advanced the theory that fat embolism was a major factor in alcoholic psychosis, and that in some cases it could lead to sudden death. Jones and Sakovith7 were able to demonstrate intra-osseous embolic fat experimentally in rabbits followiilg injections of lipids. Kimble8 reported a case, confirmed by autopsy, of a 35-year-old chronic alcoholic who died from fat embolism. Clinically, we believe that alcoholics who undergo acute traumatic episodes are more apt to suffer fat embolism
Osteoporosis per se or osteopenia is not a too infrequent finding in the elderly white female patient. However, when a black female or any male patient has osteoporosis, other metabolic problems should usually be ruled out. Osteoporosis per se usually is not symptomatic. Attention is usually directed to this either when a fracture occurs following minimal trauma or when a patient is x-rayed for some other reason. The association of osteoporosis and hip fractures, compression fractures of the spine, or fractured distal radius are well known. Most authorities feel that this triad of fractures, although not occurring concomitantly, is usually the result of a decrease in bone mass. Because of the decreased incidence of hip, wrist, or vertebral body fracture in the black female, any black female with any of the above fractures should be studied for alcoholism. Hip fractures occurring in any race at an early age should be suspected of being secondary to alcoholism.
Battered Alcoholic Syndrome The term "battered alcoholic syndrome" was coined by Oppenheim'0 in 1977. A person fits into this syndrome if three distinct fractures in different
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 12, 1979
stages of healing can be demonstrated. The clinical significance of this syndrome. is fairly obvious. Any patient with fractures in various stages of healing should be suspected of being an alcoholic and his/her alcoholism should be treated as well as the orthopedic problem. Any alcoholic who presents with a fracture should be carefully followed and protected in order to try to prevent the occurrence of this syndrome. Case Report M.M. was a 64-year-old white, female who came to the medical clinic complaining of "blacking-out" spells. Her examination at that time revealed that she had a deformity of her left hip and left shoulder (Figure 1). She could not recall any traumatic episodes that may have caused the lesions. She admitted to social drinking. She was able to walk with one cane and used the left upper extremity without too much difficulty. She was admitted to the medical service where she had a complete metabolic workup. All her laboratory work was normal. She was transferred to the orthopedic service for definite care of her hip and shoulder. A review of her medical records revealed that she had been seen on several occasions in the Emergency Room complaining of pain in numerous extremities following falls. The record further indicated that she had a drinking problem (Figures 2 and 3).
Fat Embolism-Acute The clinical course of acute fat embolism is well known by most physicians treating trauma patients. The fat embolism syndrome usually occurs in young male patients who have received major trauma. Clinically, this syndrome usually occurs within the first few days following trauma. Changes in sensorium and pulmonary symptoms are the most common presenting symptoms. Laboratory findings include a decrease in arterial oxygen and hemoglobin, lipiduria, and changes in the platelets. It has been our observation that alcoholics hospitalized following acute traumatic episodes are apt to demonstrate the above symptoms. Because they are known alcoholics they are usually treated for delirium tremens. It has been our observation that when alcoholic patients are admitted to other services delirium tremens usually occur later.
Figure 3. X-ray of dorsal spine showing old compression fracture which had been treated (left). X-ray of distal ulna showing fracture (right). Also shows healing distal radial fracture
Fat Embolism-Chronic Some may doubt that this syndrome actually exists. We feel that some of the symptoms exhibited by alcoholics may indeed result from this syndrome rather than alcoholic psychosis. Chronic alcoholics with cirrhosis of the liver are apt to have recurrent showers of fat embolism. These may present either with pulmonary or cerebral symptoms. Any patient who is a known alcoholic and has symptoms of this nature should be hospitalized for appropriate studies. It should be remembered that when embolism occurs it may involve any organ.
A vascular Necrosis of the Hip Avascular necrosis 6f the hip has many causes. When a patient has this lesion, all known causes of avascular necrosis should be ruled out. These causes include trauma, steroid ingestion, elevated uric acid, and blood disorder. Bonfigilio'1 studied x-rays from 1,410 patients, 705 of which were from
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 12, 1979
alcoholics and 200 from normal subjects. The incidence of avascular necrosis was found to be no greater in the alcoholic. Hungerford,12 however, using pressure studies of the upper femur, found that there was a definite increase in avascular necrosis in chronic alcoholics. In our series at Wishard Hospital, we have found that most people, in the age range of approximately 29-50 years, with avascular necrosis usually are alcoholics. The patient usually complains of vague hip pain and usually gives a vague history of trauma. Physical findings as well as routine x-rays are usually negative. If special x-rays or pressure studies are done, the diagnosis can be made when alcohol is the etiological agent. The incidence of both hips eventually being involved may be as high as 80-90 percent. When the diagnosis is first made, early treatment is mandatory in order to obtain satisfactory results. The following is a brief medical report of a case of avascular necrosis of the hip secondary to alcoholism. 1215
Figure 5. AP of pelvis showing Phemister grafts in place in femoral head and a fracture in upper femur
Figure 4. AP of right hip showing early avascular necrosis of the hip
Case Report J.D.L. was a young male patient who presented himself complaining of pain in his hip. The pain had been present for several months. He denied any traumatic episodes involving his right hip. The pain was constant, deep, and aching, and was located in the anterior aspect of his hip; it was worse with activity and only partially relieved by rest. Physical examination revealed that he walked with a limp favoring his right hip. Examination of the right hip revealed normal range of motion; however, there was pain at the extremes of motion. Following hospitalization, his laboratory work, which included blood chemistries and hematological parameters, was essentially negative. Plain x-rays of the hip revealed early avascular necrosis (Figure 4). Following his hospitalization, he was carried to surgery where a Phemister bone graft of his hip was performed. Histological studies of the core specimen was consistent with avascular necrosis. Postoperatively, he did well and was discharged on crutches. He returned to the emergency room approximately three weeks following his discharge complaining of acute pain in his hip. He stated that he was jogging when he had the onset of pain in his hip (Figure 5). 1216
Discussion Chronic alcoholism presents, in addition to its social and economic problems, certain medical problems. We are beginning to see more and more orthopedic problems in people who are alcoholics. It is essential that these lesions be sought because early treatment in these disorders affords a better prognosis. When these lesions are found and treatment is instituted, one should be aware that alcoholics, as a group, are not too reliable. This is well pointed out by the second citation. Karlstrom'3 studied the management of tibial fractures in alcoholics and mentally disturbed patients and suggested that alcoholics should be treated for a longer period of time than other patients. With the increase in medical interest in alcoholism, we hope that more can be learned about these patients' other medical problems and that better medical care can be given. All the lesions discussed in this paper can be found in people who are not alcoholics. We do notX infer that if one of these lesions is found that the patient be accused of being an alcoholic before other causes are ruled out. A case may be made that the lesions found in alcoholics may not be due to underlying bone changes, but to the alcoholic being more apt to injure him-
self. We cannot argue this point, but we do think that the findings referred to earlier in this paper certainly point out that the lesions have a high incidence in alcoholic patients. Literature Cited 1. Saville PD: Changes in bone mass with age and alcoholism. J Bone Joint Surg 47 (3):492-498, 1965 2. Smith J: The effect of alcohol on the ascorbic acid and cholesterol of the rat. J Clin Endoc 11:792-797, 1951 3. Kalbflesch JM, Lindeman RD, Ginn HE, et al: The effects of ethanol administration on urinary excretion of magnesium and other electrolytes in alcoholic and normal subjects. J Clin Invest 42:1471-1475, 1963 4. Snell W: The chronic alcoholic and his fractures. J Bone Joint Surg 53A:1655, 1971 5. Owens G, Northington BA: Liver lipid as a source of post-traumatic embolic fat. J Surg Research 11(4):283-284, 1962 6. Lynch MJ, Raphael S, Dixon T: Fat embolism in chronic alcoholics. AMA Arch Path 67:68-79, 1959 7. Jones JP, Sakovich L: Fat embolism of bone: A roentgenographic and histological investigation with the use of intra-arterial lipiodol, in rabbits. J Bone Joint Surg 48:149-164, 1966 8. Kimble ST: Fatal nontraumatic fat embolism in an alcoholic. Med Ann Dist Col 30(5):283-287, 1961 9. Jones JP, Jamerson R, Engleman EP: Alcoholism, fat embolism and avascular necrosis. J Bone Joint Surg 50(5):1065-1069, 1968 10. Oppenheim WL: The battered alcoholics syndrome. J Trauma 7(11):850-856,1978 11. Smith K, Bonfigilio M, Dolan K: Roentegenographic search for avascular necrosis of the head of the femur in alcoholics and normal adults. J Bone Joint Surg 59:391-396, 1977 12. Hungerford DS, Zizic TM: Alcoholism associated ischemic necrosis of the femoral head. Clin Orthoped 130:144-152, 1978 13. Karlstrom G, Olerud S: The management of tibial fractures in alcoholics and mentally disturbed patients. J Bone Joint Surg 56(4):730-734, 1974
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 12, 1979
