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American Medical Association
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The American Medical Association
has several hundred thousand physician members, all of whom consider
themselves important members of their communities, hence important
members of the AMA. "The Association" maintains a large, experienced,
and frequently successful lobbying staff in Washington. It would be
wildly impractical to permit every individual member of the Association
to walk into the Washington office and give orders to the staff. Even
when individual doctors have a very good idea, and the staff members
thoroughly agree with it, it's never safe to assume the professional as
a whole agrees. And in fact, it is always possible to find some doctor
who violently disagrees, no matter what the topic.
So, a couple of centuries of experience led to a system of funneling physician opinion up to the line to the House of Delegates,
and passing it through that narrow neck of the funnel before it is
released to the Washington office as "policy". Sure, a couple of
knuckle-heads can sometimes block a good idea at the narrow neck of the
funnel, just as an occasional Leonidas can save civilization at this
Thermopylae, against a bad idea. Sometimes an idea slides all the way
through on the first try, and sometimes it is necessary to build up a
head of pressure behind it. The fundamental question before the House
of Delegates is not entirely whether a proposition is a good idea or a
bad one; an equally important question is whether it likely reflects
the prevailing viewpoint of the profession.
My first salvo in the campaign to win AMA approval for Medical
Savings Accounts was a letter to Jim Sammons, the Executive Vice
President. He wrote back promptly that he had read the Medical Savings
Account proposal three times, and still didn't understand it. Although
my opinion of him was never quite the same, he did me the favor of
demanding simplicity, to be more quotable. An IRA for Health. An IRA
plus a catastrophic policy. What's good about that? Cheaper. What makes
it cheaper? Compound interest. How does it help poor people? More
people can afford to buy something that's cheaper. Sammons said, ok, I
can live with that.
The letter to the EVP turned out to be a good idea because it
established my claim to ownership. A few months later I arrived in
Chicago with a crisp, brief zinger of an MSA proposal, only to find
that somebody from Louisiana was attending the same meeting with an
almost identical proposal, called CHIP. Mike Smith was president of the
Louisiana Medical Society, and not only had the same idea but
personally had a lot of Louisiana oil money which he freely spent on
professional packaging of his presentation. Mike and I suspiciously
circled each other like two wildcats for a few hours, but we had so
much in common that very shortly we were the best of friends, remaining
so for years until his unfortunate death. He introduced me to his
Southern friends, I introduced him to my Northern ones, and the idea
itself picked up some allies on its own merits. It had a fairly easy
time of it in the House of Delegates. However, it was referred to a
committee for polishing and deeper consideration. Six months later it
had disappointingly picked up quite a lot of unforeseen opposition,
probably after the hospital and insurance executives heard about it. It
took another six months to fight through a wall of specious argument,
but an endorsement of the Medical Savings Account did become a policy of the
AMA and the eager Washington staff was thus free to run with it.
It has remained AMA policy ever since, and the main technical
problem for its main sponsors became one of keeping the idea alive in a
House of Delegates with constantly shifting turnover. The AMA is like
the court system; it doesn't like to keep revisiting an issue that is
settled policy. Too many other members have proposals requesting
attention, so why should we go on reaffirming old matters? However, the
proposal was stalled in Congress, and for the momentum, we needed to keep
beating the drum with variations which somewhat stretched the patience
of the more senior members of the House of Delegates. To them, I
apologize, with gratitude for their tolerance.
But what was the matter with Congress? What was the matter with the
editorial page of the New York Times? I was always uneasy about a protracted debate because reducing the cost of medical care (from the
patient's point of view) was apt to translate into reduced income for
doctors. I was leading a procession of self-employed entrepreneurs into
a proposal to cut their own income for the benefit of the public; how
long could physician enthusiasm be maintained for that? I'm proud to
say the answer is at least twenty-five years.
Even in retrospect, I am a little surprised that even such
sophisticated students of medical economics could remain focused for so
long. They might have come to regard the sponsors of MSA as being on an
ego trip, or else nutty fanatics obsessed with a lost cause. Or they
might have joined the young newcomers in fearing that such determined
opposition at a national level might signify the opponents were somehow
right to oppose it. The arguments advanced by the opponents really
seemed to have very little merit, but perhaps in private, it might be
possible to sympathize with some embarrassing circumstances that
explained the vigor of the resistance without crediting its excuses.
Political debate after all, even in scientific organizations, quite
characteristically wraps venal motives in a cloak of logic and
altruism. I remained fearful for years that the House of Delegates
would shrug its shoulders and let the opponents have their way. That
they never, ever, did so was probably related to medical care being
physician home turf; where you get used to hearing a lot of dumb
arguments, but you don't have to credit them with any merit until merit
is displayed. You can tell doctors a lot of fairy tales about
architecture or investment banking perhaps, but if you talk medicine
with them, you better have your facts.
Whenever my colleagues would privately draw me aside and ask why in
the world a lot of people were so resistant to the MSA, I had to tell
them I was not entirely certain. However, it was notable that three
groups had important things to lose, and would probably fight to
preserve them. The Medical Savings Account threatened the
eighty-year-old pricing preferences between hospitals and insurance
companies. Secondly, it threatened the sixty-year-old preferential
healthcare pricing for members of organized labor. And finally, the
politicians who were so anguished about the uninsured population might
possibly be more interested in preserving the grievance than achieving
its solution.
I can never remember a private conversation of this sort that didn't
satisfy the doctor who asked the question. And I also never met a
representative of health insurance, hospital administration or
organized labor who would admit any truth to it.
The present problem with
PSYCHIATRY can be summarized as follows: At the suggestion of the American Hospital Association, Congress introduced the DRG system of paying for inpatients by diagnosis, rather than itemized services. It worked well except for psychiatry, where the diagnosis usually implies little relation to the later costs it generates, so an exception was made. The dual system of payment created loopholes which unfortunately overpaid psychiatric hospitals and were described as exploitation. Congress over-reacted in a way that was unsustainable, and essentially all of the psychiatric hospitals of the nation were forced to close. This is not a history for anyone to be proud of, and the lack of outcry is also a disappointment. However, after twenty years without reform, evidently, nothing is going to be done without an outcry.
CONVENE BLUE RIBBON COMMISSION TO REPAIR PSYCHIATRIC INPATIENT CARE. The 1983 BRA switched hospital inpatient reimbursement to payment by diagnosis (DRG). Abuse of the psychiatric exclusion then led to "corrective" legislation which has essentially reduced American's psychiatric inpatient care to an underfunded national disappointment. The problem is not an easy one, so a commission should devise a workable methodology for psychiatric hospitals, relying neither on present approaches nor on DRG. But overpayment is a better outcome than no care at all. Homeless people sleeping in cardboard boxes on downtown steam grates are the consequence any visitor to the area can observe at night after the commuters go home. Psychiatric social workers readily recognize their daytime patients in the boxes.
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Daniel Blain, M.D.
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Daniel Blain, M.D. (1898-1981) was just about the most important psychiatrist in America. He was the Physician in Chief of the Institute of the Pennsylvania Hospital at 49th and Market, the first and in many ways the most prestigious psychiatric hospital before it was closed. Before that, he was the first Medical Director of the American Psychiatric Association, itself the first (1844) medical society in America. His fame rested on organizing the disorganized psychiatry of the Veteran's Administration into a chain of advanced "Dean's Hospitals", a huge and very important achievement. Before that, he had achieved considerable fame as the man who took the dilapidated State Psychiatric Hospitals with a reputation as "snake pits" and made them a respectable part of the medical community. And before that, he had been born in China as the son of missionaries. As a matter of fact, even before that, he was a descendant of General Mercer of Revolutionary War fame.
Dan was an outstanding example of the peculiar fact that Psychiatry was dominated by social upper crust psychiatrists in Philadelphia for a very long time. In fact, Benjamin Rush of the 8th Street branch of the Pennsylvania Hospital is known in some circles as the "Father of Psychiatry", while in other circles he is known for signing the Declaration of Independence. That isn't true in other cities, and it definitely isn't true in New York City, where the psychoanalytic school of Sigmund Freud took that city by storm, and essentially drove every other school of psychiatric thought out of town, out of medical schools, out of psychiatric hospitals. The famous sixteen-year psychoanalysis of Woody Allen is an example of the extremes of that fad. Every profession has petty civil wars of that sort, best left undiscussed in public. But in the case of psychiatry, it was indirectly a material contributor to the present disappearance of inpatient psychiatry, and the related appearance of lots of homeless people on steam grates. Let me give a biased view of what is a massive human tragedy, which someone else can "rectify" if he chooses.
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APA
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It starts with a Budget Reconciliation Act of the 1980s, which brought us the DRG (Diagnosis-related) system of paying for hospitalized patients. The idea was that appendicitis resulted in essentially 7 days in the hospital, give or take a couple of days, and the bills for admission for appendectomy were for more or less the same amount. If you had fifty or a hundred cases a year in your hospital, the high bills balanced the low bills, and the overall hospital reimbursement was essentially the same without itemizing the bandages and whatnot. Congress bought this package, and after it got going, just about all hospital bills were reimbursed at one of three hundred prices, the cost to the government was the same, and there was a whole lot less bookkeeping and accounting cost. It was a success, except for a few cases where the costs did not closely line up with the diagnosis, and psychiatric hospitals were where they concentrated. So, psychiatric hospitals were excluded, and psychiatric bills skyrocketed. This experience has been carelessly cited as an example of the evils of payment by service ("fee for service"), when in fact the duration of psychiatric hospitalization is related to features of the condition, like danger of suicide, rather than the diagnosis itself. Psychiatric leadership at the time contained many in a subset of physicians who did not think much of inpatient psychiatry in the first place and even less of lobbying, and they underestimated the severity of the assault on the specialty. Apparently, no workable formula for pricing inpatient psychiatry has since been brought forward to be approved by a Congress which is more accustomed to getting its lobbying in the form of one-liners. And would you believe it, psychiatric inpatient care soon disappeared.
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Pennsylvania Hospital
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That's right, if someone in your family needs psychiatric hospitalization, I wouldn't know where to tell them to get it -- at any price. From considerably overpaying for psychiatry inpatients to paying scarcely anything for them, this little change of the regulations caused every psychiatric hospital I know of by name, to close. It helped balance some state budgets, but it also was a considerable factor in filling the steam grates of American cities with people who sleep on cardboard boxes. And what it illustrates is that this is what political society always seemed to do, before Dan Blain and a small group of upper-crust psychiatrists were temporarily able to shame them into something better. In fact, if there is any tattered remnant of good inpatient psychiatric care left in America today, it is in the Veterans Hospitals that Dan was able to straighten out.
Dan Blain will probably eventually be bypassed as a curiosity, like his wife. She was a Wister Logan Blain, descended from families who ruled Philadelphia a hundred years before even General Mercer came along. So the Blain couple lived on an enormous farm plot, centered at 20th and Olney right next to LaSalle University, which is built on their property. It also contains the Peale House, where Charles Willson Peale lived as the elected president of the rebel faction of the American Revolution. Peale didn't know what he was supposed to do, so he resigned and painted portraits of people. The Blains enjoyed keeping a cow on their land, the last cow in Philadelphia, and the LaSalle students enjoyed stealing the cow and leaving it on the top floor of a dormitory, for laughs. Meanwhile, the Blain couple had cocktail parties on their front porch for visiting dignitaries. They usually wore blue jeans, and Mrs. Blain, the absolute Queen of Philadelphia society, was occasionally observed to pour vodka into her glass of beer. That sort of background may well have been useful when psychiatry needed to be built up and humanized, but it became a liability when the rest of inpatient psychiatry failed to appreciate what was knocking on its door.
SKELETAL TRAUMA IN CHILDREN:
DIAGNOSTIC AND THERAPEUTIC CONSIDERATIONS
MARY STUART FISHER AWARD LECTURE
Alvin H. Felman, M.D.
Professor of Radiology & Pediatrics
The University of Florida at Jacksonville
Address reprints:
Alvin H. Felman, M.D.
Department of Radiology
University Hospital
655 West 8th Street
Jacksonville, FL 32209
INTRODUCTION
I would like to thank the members of the Pennsylvania Radiological Society for inviting me to share in this marvelous celebration of Mary Fisher’s career in Radiology. Also, I want to express my thanks to this organization for recognizing the work that Mary has done over the years, and for consecrating, so to speak, what we, her former students, have known for so many years; namely that she is, indeed, entitled to be counted among the great radiologists of Philadelphia, of Pennsylvania, and indeed well beyond.
It is not my purpose to enlarge upon Mary’s career or her accomplishments. This singular honor that you have bestows says more than I or anyone could possibly say. Perhaps, however, I might add a few personal observations to this occasion form the standpoint of one who has known and worked with Mary.
She would arrive punctually each day in either 1953 Chevy or a large black Checker; either of which could defeat any Philadelphia weather system. Her day-long stint at her view box was interrupted almost ritualistically at five minutes to 12 each day for a trip to the hell vending machines where she purchased a package of peanut butter or cheeses crackers and soft drink which she consumed during the noon conference. At the end of each day, Mary disappeared into New Jersey where she cared for her children and husband George, but she could always be counted upon to be back at PGH for the evening conferences, ORP or other scheduled events.
Dr. George Fisher, known in some circles as the “Duke of Harrisburgâ€, is a fine physician and an author in his own right. According to Mike Huckman, a former resident, Mary was known as the Duchess of Altoona, a little apparently arising from some historic ties to British royalty.
I think it might be interesting to read part of a letter that I received from Dr. David Baker, Chairman of the Department of Radiology at Columbia. I wrote and asked Dave if he could uncover some past history of Mary Stuart, who was, I thought, a medical student at Columbia in the late 1940s and possibly also a radiology resident. He wrote me as follows:
“Dear Al:
Dashiell Hammett, Agatha Christine, Dorothy Sayers, and Dr. Arthur Conan Doyle collaborated and have finally found a picture of Dr. Fisher which I have made into a slide and I am sending to you. We had no record of Dr. Fisher as a resident but we were able to find Mary Stuart Blakely as a medical student who graduated in 1948. She interned at the Massachusetts General Hospital in 1949 and started her radiology residency here on October 1, 1949. She was appointed by Dr. Rose Golden. She wrote to Dr. Golden on July 30th, 1949 from Venice where she was spending the summer with her parents. The letter on July 30th noted that her address in Paris to the middle of August would be American Express Company, in Edinburgh until the end of August and in London through the first week in September. Sounds like a nice summer. A letter from Dr. Loeb to Dr. Golden on September 7 states that Dr. Blakely was the number one student in her class and was offered an internship at the Presbyterian Hospital but preferred erred acceptance at Massachusetts General where she went. While she was in medical school she won the Jane way Prize and was apparently an outstanding student. Her internship recommendations are equally glowing. Her record then became a little bit sparse.
The letter concludes with reference to the fact that Mary left Columbia for Bethesda and Washington and changed her name to Dr. Fisher in the interval.
I hope that this provides a little better insight into the background of your honored radiologist of the year.
GROWTH PLATE INJURIES
The growing skeleton is at risk for epiphyseal and apophyseal growth plate injuries; these constitute approximately 15% of all the fractures in children. Both structural and functional differences exist between epiphyses and apophyses. Epiphyses, located at the ends of the long bones, are usually involved with articulations of joints. Their corresponding growth plates or physics are responsible for longitudinal bone growth and are composed primarily of cartilage and proliferation of cartilage cells. In addition to providing for growth, the epiphyseal physes function as resilient zones that resist forces of compression that occur in the running, jumping, and general play of growing children and adolescents.
Apophyses, in contrast to epiphyses, constitute promontories and excrescences of bone and function primarily as points of attachments for individual muscles or muscle groups. Their corresponding physes are less involved with growth but are organized to resist forces of tension that result from the contraction of muscles and the pull of ligaments. Apophyseal growth plates contain less proliferating cartilage and more fibro-collagen strands that bridge the physes, helping to prevent avulsion.
I EPIPHYSEAL INJURIE
Injuries to epiphyseal growth plates are usually benign and heal without serious sequelae. However, certain types of trauma may cause damage to the proliferating cartilage cells with inhibition of growth, bony bridging across the growth plate, significant deformity, and functional impairment. The extent of these sequelae depends upon a variety of factors, chief among which are the extent of the original injury, location of the fracture, the future growth potential of the extremity, age of the patient, and ease and accuracy of the fracture reduction.
The Salter-Harris classification of fracture through the physes is useful in predicting the future growth arrest and other deformities. Ogden has proposed a more extensive scheme that takes into account several variations of the original Salter-Harris injuries and adds four additional types. (1) (Fig. 1) His classification illustrates serval rare injuries, occurring at birth or in the first two years that may have disabling consequences. Notable among these are types 1C and 2D where delayed growth arrest may occur as a result of damage to potential growth cartilage cells that are not as yet involved in the epiphyseal growth mechanism. Late epiphyses bar fusion become manifest when the epiphyseal growth plate expands to include the previously injured area.
Type 2 injuries are the most common overall and represent the most frequent type of physical separation in children over 10 years of age. Whereas these fractures usually heal without deformity, certain circumstances increase this risk. Damage to the growth plate, not present at the origin of the injury, may result from the act of reduction if the muscles a ligament are not relaxed. The undulation of the growth plate, especially of the distal femur, distal tibia, and proximal humerus make these areas especially vulnerable. In addition, the free metaphyseal fragments of Ogden type 2B may interfere with normal reduction.
Type 3 injuries occur most often when the physical growth plate is partially closed and invariably extend into the joint. Type 4 and 5 injuries are often associated with localized growth arrest and angular deformity despite the accurate reduction. Early definitive radiographic diagnosis and prognosis of this injury are often difficult or impossible leaving the clinician no choice but to treat expectantly. Sequential film studies may show relatively normal growth for serval years following which angular deformity may ensue.
With the development of the surgical technique for correcting partial growth plate closure, it is most imperative that these injuries be discovered and treated before the onset of serious deformity. (2, 3) Initial leg length measurements using accepted orthoroentgenographic technique should be obtained shortly after the initial injury. Thereafter, these measurements should be repeated at the at three to six-month intervals, depending upon the growth plate phase, in order to evaluate possible growth arrest. It should be remembered that the fractured bones, especially those of the lower extremities often heal with overgrowth and subsequent elongation. Hence, the failure of an injured bone to grow more rapidly than the comparison normal (bone) should be suspect for early epiphyseal growth arrest. (Fig.2)
When premature fusion of a growth plate occurs, surgical excision of the bony bar and insertion of one of a variety of materials (silastic, cranioplasty, etc.) is the accepted method of treatment. Radiological “mapping†of these abnormalities is necessary in order to evaluate the surgical approach and prognosis. Multidirectional tomography at 0.5 cm intervals in the frontal and lateral planes is used to map the size and location of the epiphyseal bridge (4). (Fig.3) Bright suggests the following criteria for surgical intervention: (1) partial growth arrest proven by tomography; (2) at least 50% of the normal remaining open growth plate; (3) at least two years of expected longitudinal growth; (4) adequate and good quality skin covering the lesion, and (5) free of drainage at least one year of previously infected. (2)
On occasion, early radiographic growth plate fusion may appear, only to resolve with a resumption of normal growth (Fig. 4) In these circumstances, one must weigh all clinical and radiological parameters before embarking on aggressive surgical treatment.
II APOPHYSEAL INJURIES
Apophyseal represent promontories of bone which generally serve as attachments for a muscle or muscle group. As much, their shape and configuration are usually determined by their loading requirements. Apophyseal growth plates of physes, while similar histologically to epiphyseal physes have significantly increased numbers of collagen fibers crossing the growth plates and considerably less proliferating cartilage cells. This morphologic alteration help withstand tension forces that result from contractions. Muscle attachments to apophyses are very strong by virtue of interosseous fibers that are extensions of the tendinous portion of the muscle. As a result, avulsion of portions of bone or fractures through apophyseal growth plates occur more regularly than torn tendons in the pediatric age group.
While injuries to apophyses may occur from a direct blow, most are caused by muscular effort. Often quite disabling, these injuries produce few important sequelae. On rare occasions, they may be confused with other, more significant lesion, i.e. infection, neoplasm, etc.
Avulsion injuries tend to be less acute in their onset; patients often present with a history of aching pain, usually of several weeks or months duration. In most instances, however, the patient experiences a sharp, intense pain associated with running, jumping or quick movements and changes of direction.
A Elbow:
Medial Epicondyle. This is the second center of the distal humerus to ossify; usually appearing between five and seven years. Fusion to the adjacent metaphysic does not occur until 17 or 18 years. As a result, the physics remains open during a protracted period of childhood and adolescence rending it susceptible to avulsion type injuries. (5, 6)
The medial Epicondyle serves as the attachment for flexors and pronators of the forearm and the ulnar collateral ligament. Serves valgus stress at the elbow is the mechanism that leads to avulsion of the medial Epicondyle. (Fig. 5) The medial Epicondyle also shares a physis with the trochlea which does not ossify until about 10 years of age. Hence, fractures extending through the medial Epicondyle may continue through the trochlea and into the elbow joint. This complication, though rare, must be recognized since external fixation is necessary to ensure proper healing and maintenance of function. (7)
The radiographic appearance of medial Epicondyle avulsion is usually characterized by considerable soft tissue swelling along the medial elbow and distal humerus and distal displacement of the ossific nucleus and loss of the normal parallel position in relation to the metaphysis, are additional findings. Not uncommonly, a “flake†of the adjacent metaphysic, pulled off along with the Epicondyle, serves as a confirmatory finding.
Extension of a medial Epicondyle avulsion fracture through the trochlea and into the elbow joint is difficult and often impossible to determine radiographically. The presence of a large metaphyseal fragment suggests extension through the trochlea but is most a definitive finding. Since the medial Epicondyle is often extra-articular, the absence of a joint effusion supports the diagnosis of isolated epicondylar avulsion; the presence of joint effusion, however, is of little help. Post reduction clinical and radiographic evaluations are probably as important as anything in determining the presence of an intraarticular fracture. Range of motion examination and radiographic appearance of the reduced fracture will usually suffice, (7) Arthrography should be reserved for those cases where definitive determination cannot be made.
The act of throwing, especially the use of a twisting movement when trying to throw a “curve-ballâ€, may also contribute to medial Epicondyle injuries. “Little League†elbow, a condition is seen in adolescent baseball pitchers and other players results in part from this action and the associated valgus stress applied to the elbow. (8) Repeated injury of the tendonous attachments to the medial Epicondyle may cause fragmentation of the ossification centers. (Fig. 6) On occasion, the medial Epicondyle may develop as several separate centers normally so that careful clinical and historical correlation is necessary if the diagnosis of “Little League†elbow is to be based on this finding alone. Comparison with the opposite elbow may be helpful.
The lateral condyle also may undergo change when subjected to the stress of throwing. Subchondral reabsorption, “cystic†lesions, and demineralization are among the recognized lateral condyle changes of “Little League†elbow. (Fig. 7) B Pelvis: Avulsion injuries usually resulting from various athletic endeavors represent the most common chrondro-osseous injuries about the pelvis. (10, 11) The anterior superior and anterior inferior iliac spines are points of attachments for the Sartorius and rectus femoris muscle respectively These are powerful flexors of the hip and may cause metaphyseal avulsions during running, licking and similar stressful exercises. While they often result from sudden muscular efforts and frequently evoke acute local pain, chronic aching in the area usually brings the patient to medical attention.
An apophyseal avulsion is usually recognized by an area of bony density within the adjacent soft tissue. The appearance varies depending upon the time interval between the injury and examination. The location of the injury also contributes to the roentgen appearance; ischial avulsion may be associated with exuberant callus formation. The roentgen appearance is usually typical, and when combined with the clinical history and symptomatology, is often conclusive. (Figs. 8, 9, 10,) Differentiation from a neoplastic process, while a theoretical dilemma, has not been a problem in our experience. Careful observation with repeated radiographs will usually clarify suspicion cases. Biopsy should be avoided unless there is a strong clinical suspicion of malignancy since healing avulsion fracture may be indistinguishable histological from malignant bone neoplasm.
C Knee:
Tibial Tuberosity. The quadriceps tendon inserts in a fan-like manner into the apophysis of the tibial tubercle and adjacent tibia. Acute fracture or avulsion of the tibial Tuberosity, or a portion thereof, may occur from direct trauma or from a sudden muscular contraction of the quadriceps mechanism. Classification of these injuries is based upon several features: 1) the degree of separation of the fracture from the adjacent metaphysis, 2) the accompanying soft tissue injury and possible functional impairment, and 3) extension into the tibial epiphysis with or without actual knee joint involvement. (Fig. 11)
The radiographic evaluation of these injuries is usually straightforward when the ossified structures are involved despite considerable normal developmental variations of the tibial tubercle. Accompanying soft tissue injury invariably occurs but the extent may not always be determined radiographically. Soft tissue edema in the region of the tubercle and loss of normal patellar tendon definition is usually evident but may escape detection if the film is not viewed with a bright light.
The posterior edge of the normal patellar tendon should present a straight and well-defined interface with the infrapatellar fat pad. With soft tissue injury, this tendon may be widened and lose its distinct margin. Avulsed fragments of the tibial tubercle, (Fig. 12) The metaphyseal origins of these fragments is usually apparent since their borders are often irregular and a defect in adjacent tubercle metaphysis can frequently be identified. Dysplastic ossification within the patellar tendon may develop the following injury. (Fig. 13)
Attention must also be paid to the patellar-tubercle distance which frequently is increased when the tubercle is avulsed. This observation may be missed if the film is taken with the knee extended; flexion of the knee will accentuate this injury. Comparable films of the opposite extremity in the same degree of flexion may be necessary to confirm the diagnosis.
Type 3 injuries, with propagation into the tibial epiphysis and knee joint may disrupt the normal articular surface, (Fig. 14) In general, the radiographic detection of this injury is not usually difficult and when obscure, may be enhanced with conventional tomography. Replacement of an avulsed tibial tubercle to the normal anatomic position is necessary in order to restore complete function and avoid the complication of patella adults with possible secondary chondromalacia patellae.
Osgood-Schlatter’s “diseaseâ€, most commonly seen in adolescent males, was originally felt to be caused by aseptic necrosis of the tibial tubercle. In all probability, it results from partial traumatic fragmentation of the apophyseal ossification center, as a result of the strong tensile force applied to that area.
Although Osgood-Schlatter’s disease is usually a well-defined and easily diagnosed entity, other bone and/or soft tissue lesions may occur in this region. Arteriovenous malformation, osteomyelitis, benign and malignant tumors of bone and soft tissue have been reported. (13)
D Ankle:
The juvenile counterpart of the “Tillaux fracture†in adults is a Salter type III injury of the distal tibial physis. Closure of this growth plate begins in the mid-portion, progresses medially and then laterally. (14, 15) For a period of up to 12 to 18 months, the lateral physis may remain unfused rending it particularly vulnerable to a fracture. Extreme lateral rotation of the foot causes a stretching of the anterior tibiofibular ligaments leading to an avulsion type injury of the lateral epiphysis (Fig. 15.)
The radiographic diagnosis of juvenile Tillaux fracture is usually straightforward. Best seen in the mortise view, it produces a vertical fracture line through the epiphysis. (Fig, 16A) The epiphysis growth plate medial to the fracture line is fused; the lateral unfused portion may widen.
The plain film findings are diagnostic in most cases, but the use of computed tomography may be helpful both in the pre- and post- reduction evaluation (16). (Fig. 16B) When two or three part tri-plane fracture is suspected, the use of CT often is of great benefit. Complications and sequelae of these fractures are not common if the fragments are maintained in good alignment. The potential for premature growth arrest is minimal since they usually occur near the time of physiologic closure. Injury to the articular cartilage and failure to restore continuity of the joint surface carries a risk of future arthritic change.
FRACTURES THROUGH PATHOLOGIC BONE
Localized lesions and generalized conditions which weaken normal bone may result in fractures that occur with relatively minor trauma. Non-ossifying fibromas or benign cortical defects are common benign lesions usually discovered incidentally. On rare occasion, they present clinically as fractures with relatively minor trauma. (Fig. 17, 18) Because of the frequency of these lesions and the fact that they are so often discovered as films are taken for other reasons (trauma, pain, etc.), they may present problems in both diagnosis and management.
After the gross fracture has occurred, one has little choice but conservative treatment until healing occurs. The need to treat with current and packing before a fracture has occurred, and indeed after a healed fracture may present a dilemma for the patient and physician.
A high degree of individuality must be exercised in the approach to these conditions and must take into account the age of the child and the physical activity that is contemplated. While the latter can rarely be predicted, a more aggressive approach should naturally be considered in those patients who contemplate physically demanding sports.
The following roentgen criteria have been suggested as guidelines for the prophylactic surgical treatment of these lesions:
1. Non fibular location
2. Greater than 33mm long
3. Greater than 50% of bone width
4. Anticipation of physical contact or stressful
Sports or other activity (17)
Fractures through simple cysts or other benign lesions of bone must be handled on an individual basis. Most bone cyst fractures will heal spontaneously, but there are no data to support the hypothesis that the cyst is more (or less) likely to heal as a result of a fracture. We have seen one case of malignant degeneration (osteosarcoma) in what was felt to be a six-year period.
COMPLICATIONS OF FRACTURES
A complete review of fracture complications is beyond the scope of this presentation. Nevertheless, I would like to illustrate a few unique situations where prompt recognition and proper treatment may prevent considerable morbidity and disability.
Pinckney, Currarino, and Kennedy have called attention to the damage of what might otherwise be considered a relatively benign injury, a stubbed toe. (18) They emphasize the risk of secondary osteomyelitis when Salter type I or II fracture of the epiphyseal growth plate of the distal phalanx of the great toe are associated with bleeding from the base of the nail bed or skin laceration in the immediate area. Prompt antibiotic therapy prevented this complication in two of their patients. We have seen a similar case in which osteomyelitis complicated a fracture of distal phalanx of the toe and a break in the overlying skin. (Fig. 19) The close relation of the skin to the periosteum, at the root of the nail with no intervening soft tissue, is the explanation given by these authors for the high incidence of complicating osteomyelitis.
The second complication of muscular skeletal injury is the presence of radiopaque foreign material at the site of injury. Dr. Fisher first suggested to me that all glass is radiopaque. After radiographing a large number and variety of glass objects, I was convicted of the truth of her statement (19). I have yet to see a proven case where the embedded glass was not visualized radiographically.
CHILD ABUSE
There are many historical accounts of the syndrome of child abuse but Dr. Fredric Silverman’s Rigler Lecture of 1972 should be read by everyone interested in this problem. (20) Dr. Silverman gives credit to Dr. Ambroise Tardieu, Professor of Legal Medicine at the University of Paris from 1861 to 1879, for first describing the feature of this syndrome. Tardieu outlined the demographic, social, psychiatric, and medical features that were, except for the roentgenographic findings similar in all respects to those that we recognize today. Caffey, in 1946, was probably the first t publish examples of the radiographic features of child abuse, but it wasn’t until 1953 when Silverman, one of his former pupils, corrected the clinical pattern of intentional trauma and abuse with the development of these characteristic fractures, (21, 22) The term, “The Battered Child†was coined by Kempe in 196, 100 years after Tardieu, 15 years after Caffey, and 10 years after Silverman called attention to this problem. (23)
Without trying to cover this subject in any substantial manner, I would like to stress a few salient features that may be of help in the diagnosis of this potentially fatal condition. Radiologists are usually alerted to the possibility of child abuse when skeletal surveys in films are requested. On occasion, however, one may recognize the “tell-tale†signs on film studies obtained for other reasons. I would like to illustrate several examples of child abuse that were recognized from chest studies requested for other reasons.
Rib fractures occur rarely in children from normal activity. When present, they should raise one’s suspicion of child abuse, especially when located in the posterior, paraspinal location, and when they appear to be in different stages of healing. (Fig. 20A) One is occasionally faced with the argument that rib fractures were caused by a parent attempting to “resuscitate†a chocking or apneic child. The presence of fracture of other bones, often the humerus, can be used as confirmatory evidence of child abuse. (Fig. 20B)
In recent years, cranial computed tomography has identified cases of child abuse that might have been overlooked previously. (24) Skulled fractures have been the traditional roentgen markers of cranial injury prior to the advent of this improved imaging technique (Fig. 21A, B). A wide variety of severe intracranial changes are now recognized in abused children, however, in the absence of skull fractures (Fig. 22.). These changes include subdual hematomas and effusions, cerebral contusion, and atrophy, etc. Cerebral contusions are most frequently seen and may appear as high density, isodensity, or low-density areas depending upon the relative amount of hemorrhage and edema. These injuries are thought to result from direct blunt trauma, accounting for extensive intracranial abnormality in the absence of skull fractures.
I want to again express my thanks to this society for allowing me to share in the honor of this day. Mary Fisher remains a symbol of excellence to which we, her former students and colleagues aspire. As long as we have teachers like her in our training programs, we will exhaust our supply of great radiologists. (Fig. 23)
In his farewell address to the graduating medical school class at the University of Pennsylvania in 1889, Sir William Osler read a poem about his revered mentor and great teacher, Dr. Palmer Howard. I can think of no better words to reflect my sentiments and those f my colleagues and former students of Mary Fisher. (Fig, 24)
“WHATWAYMYDAYS DECLINE,
I FELT AND FEEL, THO LEFT ALONE,
HER BEING WORKING IN my OWN,
THE FOOTSTEPS OF HER LIFE IN MINEâ€
Sir William Osler
AQUANIMATAS, 1889
BIBLIOGRAPHY
1. Ogden J A: Skeletal growth mechanisms injury pattern. J Pediater Orthop 2:371 377, 1982.
2. Bright R W: Partial growth arrest: Identification, classification, and results of treatment. Orthop Trans 6:65, 1982.
3. Langenskod A: Surgical treatment of partical closure of the growth plate. J Pediatr Orthop 1:3 11, 1981.
4. Carlson W O, Wenger D R: A mapping method to prepare for surgical excision of a partial physical arrest. J Pediatr Orthop 4:232, 1984.
5. Chessare J W, et al: Injuries of medical Epicondyle. Ossification center of the humerus. Am J Roentgenol 129:49 55, 1977.
6. Silberstein M J, et al: Some vagaries of the medical Epicondyle. J Bone Joint Surg 6 A:524 528, 1981.
7. Cothay DM: Injury to the lower medial epiphysis of the humerus before the development of the ossific center, report of a case. J Bone Surg 49B: 766 767, 1967.
8. Brogdon BG, Crow N E: Little leaguer’s elbow. Am J Roentgenol 83:671 675, 1960.
9. Torg J S et al: The effect of competitive pitching on the shoulder and elbows of preadolescent baseball players. Pediatrics 49:267 271, 1972.
10. Fernbach S K, Wilkinson R H: Avulsion injuries of the pelvis and proximal femur. Am J Roentgenol 137:581, 1981.
11. Khoury M B et al: Bilateral avulsion fractures of the anterior superior iliac spines in sprinters. Skeletal Radiol 13:65 67, 1985.
12. Ogden J A, Southwick W O: Osgood-Schlatter’s disease and tibial Tuberosity development. Clin Orthop 116:180, 1976.
13. D’Ambrosia R D, MacDonald G L: Pitfalls in the diagnosis of Osgood-Schlatter’s disease. Clin Orthop 110:206 209 1975.
14. Kleiger B, Mankin H J: Fractures of lateral portion of the distal tibial epiphysis. J Bone Joint Surg 46A:25-32 1964.
15. MacNealy G A, et al: Injuries if the distal tibial epiphysis: systematic radiographic evaluation. Am J Roentgenol 138:683 689, 1982.
16. Cone R O, et al: Triplane fractures of the distal tibial epiphysis radiographic and CT studies. Radiology 153:763 767, 1984.
17. Arata M A, et al: Pathological fracture through non-ossifying fibromas: review of the Mayo Clinic experience. J Bone Joint Surg 63-A: 980 988, 1981.
18. Pinckney L E, et al: The stubbed great toe: a cause of occult compound fractures and infection. Radiology 138:375 377, 1981.
19. Felman A H, Fisher M S: Radiographic detection of glass in soft tissue. Radiology 92:524 526, 1966.
20. Silverman F N: Unrecognized trauma in infants, the battered child syndrome, and the syndrome of Ambroise Tardieu. Rigler lecture. Radiology 104: 337 353, 1972.
21. Caffey J: Multiple fractures in the long bones of infants suffering from chronic subdural hematoma. Am J Roentgenol 56:163 173, 1946.
22. Silverman F N: The roentgen manifestations of unrecognized skeletal trauma in infants. Am J Roentgenol 69:413 426, 1953.
23. Kempe C H, et al: The battered child syndrome. JAMA 181:17 24, 1962.
24. Tsai F Y, et al: Computed tomography in child abuse head trauma. CT, J Comp Tomo 4:277 286, 1980.
Originally the "lower counties" of Pennsylvania, and thus one of three Quaker colonies founded by William Penn, Delaware has developed its own set of traditions and history.
Start in Philadelphia, take two days to tour around Delaware Bay. Down the New Jersey side to Cape May, ferry over to Lewes, tour up to Dover and New Castle, visit Winterthur, Longwood Gardens, Brandywine Battlefield and art museum, then back to Philadelphia. Try it!
Millions of eye patients have been asked to read the passage from Franklin's autobiography, "I walked up Market Street, etc." which is commonly printed on eye-test cards. Here's your chance to do it.
Grievances provoking the American Revolutionary War left many Philadelphians unprovoked. Loyalists often fled to Canada, especially Kingston, Ontario. Decades later the flow of dissidents reversed, Canadian anti-royalists taking refuge south of the border.
