PERIOSTITIS. Delivered at the College of Physicians and Surgeons* Chicago, Illinois, % BY / N. SENN, M.D. (Milwaukee, Wisconsin), Professor of the Principles and Practice of Surgery and Clinical Surgery. Reported by William Whitford. [REPRINTED FROM THE PHILADELPHIA MEDICAL TIMES FOR JUL Y 24, 1886.] PERIOSTITIS. GENTLEMEN: We commence, this morning, the subject of the inflam- matory diseases of bone; second only in importance to the subject of fractures. It is well, before calling your attention to the pathological questions involved in this class of diseases, to refer very briefly to the pe- culiarities of bone-structure as compared with those of the soft parts. The periosteum is a fibrous membrane surrounding bone, all the bones being covered by this struc- ture, with the exception of the internal surface of the cranium and the articular surfaces of bone. Fibrous and unyielding in character, it is divided histologically and anatomically, as well as from a patho- logical stand-point, into two distinct and well-marked layers,—namely, the external layer, consisting of a stroma or nidus of con- nective tissue, with its fibres arranged both parallel and reticular, and the internal or osleogenelic layer,—the so-called cambium of Billroth,—composed of a layer of cells which we term osteoblasts, and which are attached to a fine reticulum of connective tissue between the external and the internal layer, which also constitutes the portion of the periosteum destined to furnish ma- terial for the growth and regeneration of bone. If we consider the denseness of the structure, its firm attachment to the subja- cent bone, and more particularly the ana- tomical relations existing between the vas- cular supply of the periosteum and the bone proper, we can readily imagine that any disease affecting primarily the periosteum or the bone is destined to affect the remain- ing structure by extension of the disease along the fibrous tissue and blood-vessels, from the periosteum to the bone or from bone to periosteum. The older patholo- gists taught that whenever bone was de- nuded of its periosteum it was invariably destined to become necrosed, believing that the essential vascular supply was fur- nished by the periosteum. Clinical obser- vation and experimental research, how- ever, have shown that the vascular supply derived from the periosteum is not essen- tial to the nutrition and growth of the subjacent bone. It has been demonstrated by experiments on animals, taking the case of the shaft of a long bone for instance, that if a ring of periosteum is removed under proper antiseptic precautions, if the bone is fractured at this particular point, after the healing of the external wound, the formation of callus progresses the same as though the periosteum had not been injured or removed, showing con- clusively that the callus which is destined to unite the fractured ends of the bone is not derived exclusively from the cam- bium, but its formation may take place entirely from the fractured surfaces of the bone itself, without participation of the periosteum or surrounding tissues. Great confusion has existed in classify- ing inflammatory diseases of bone. At one time pathologists believed that nearly all of the inflammatory diseases originated in the periosteum. It is well to state that, as a primary disease, periostitis is an exceed- ingly rare affection ; as a secondary lesion, it occurs during the course of almost every form of inflammation of the subjacent bone-tissue. Again, it was assumed that inflammation had its starting-point in the bone-substance proper: hence we read and hear so much of osteitis. Later re- search, however, and the results of experi- mentation have shown conclusively that ninety-five out of every hundred cases of inflammatory affections of bone originate primarily in the medulla,—that the so- called cases of primary periostitis and os- teitis are, in fact, in the majority of cases, only secondary lesions following osteo- myelitis. It has been observed in patho- logical specimens in all stages of inflam- mation and degeneration that the primary seat is almost invariably found in the med- ullary tissue; that the bone-tissue proper —the bone-cells—simply occupy a passive role in the inflammatory process. This is easily understood, if we consider, by anal- ogy, inflammation as it affects the soft tis- sues in other organs. You will remember that the blood-vessels and connective tissue 4 are usually the seat of primary changes in all forms of inflammation,—that they con- stitute the primary seat of degenerative changes and of transformation of mature tissue into inflammatory, embryonal, or granulation tissue. The more essential structures usually are passive in the inflam- matory process. The same holds true in cases of inflammation of bone. We can readily conceive, if the periosteum is the primary seat of inflammation in cases of periostitis, that by extension of the pro- cess along the blood-vessels and Sharpey’s fibres of connective tissue which enter the subjacent bone, forming an uninterrupted vascular net-work and a continuous con- nective-tissue reticulum between the bone and the periosteum, inflammation can ex- tend from the periosteum into bone with- out primarily originating in the medullary tissue. It would be more proper to desig- nate such cases as interstitial inflammation of bone, for the same reason that we speak of interstitial inflammation of the kidney, liver, and lungs. The primary patholog- ical changes take place in the blood-vessels and in the connective tissue around the vessels, while the essential histological ele- ments occupy a passive position, suffering secondarily from nutritive changes due to pressure, from the inflammation in exuda- tion, which causes degeneration and ab- sorption of the tissue-elements when the process is slow, and death or necrosis when the exudation takes place rapidly. Consequently, in our classification of in- 5 flammatory diseases of bone, I will call your attention (a) to periostitis as a pri- mary disease, premising that as such it is an exceedingly rare affection. I will first discuss its aetiology. In cases of severe contusion, of compound and subcutaneous fractures, affecting primarily and directly the periosteum, the injury being followed by a certain degree of in- flammation, of a productive character, results in the exudation of formative ma- terial underneath the periosteum, the in- flammatory process results in infiltration of the connective tissue by migration of white corpuscles underneath and into the interstitial meshes of the periosteum. We have, then, a condition of subperiosteal in- filtration ; in fact, all changes of a histo- logical character destined to form tissue of its own kind, which serve as a basis for the production and reparation of the broken ends of the bone. Consequently, trau- matic periostitis is invariably of a produc- tive character, provided, however, that no infection has taken place. The pro- cess is one of restoration of the lost rela- tions of the injured parts. For instance, if the periosteum has become separated over a considerable surface of bone, as we find it frequently in cases of fractured rib, one side of the periosteum being lacerated, the other by a displacement be- tween the ends of the fractured bone be- coming separated or detached, with certain spaces between it and the bone, the result is a direct adhesion between the denuded 6 bone and the separated periosteum through the medium of an exudation which takes place under the cambium from the lacer- ated vessels and the stable tissue-cells at the site of injury. This form of periostitis you will recognize, clinically, by a slight degree of pain, a moderate amount of swelling, subsiding as the process of or- ganization proceeds and as reconstruction takes place. This is the so-called produc- tive periostitis, as we observe it in cases of injury and disease, uncomplicated by infec- tion. Its infective forms, on the other hand, more particularly that form which is the result of invasion of the specific microbes of suppuration at the seat of con- tusion, or fracture, or the indirect localiza- tion of the microbes through the medium of the circulation, invariably results in a process of destruction (suppuration). From your lectures on “Suppuration” you will remember that we made the positive asser- tion, “no microbes, no suppuration.” This assertion holds true in cases of peri- ostitis. Periostitis not resulting in sup- puration is produced by entirely different causes. As a primary disease, suppurative periostitis in its acute form is almost un- known. Secondary suppurative periostitis occurs in the majority of cases as an almost constant result of osteomyelitis, infection taking place by the specific pus microbes, the staphylococcus pyogenes aureus and albus. The extent of the periostitis is in- dicated by the area of the subjacent pri- mary bone-disease, the periostitis corre- sponding with the extent of microbic invasion. This form is characterized by a detachment of the periosteum from the subjacent bone, by the subperiosteal sup- puration ; consequently, in cases of this kind, on exposing the bone you will find the periosteum detached over the same area that marks the extent of the primary bone- disease. We must not necessarily conclude from the existence of periosteal separa- tion that the bone underneath is necrosed. The same reason which explains the in- tegrity of reproduction of bone when de- prived of the vascular supply from the periosteum will tend to show that, in pathological conditions, vitality of bone need not be impaired, from the fact that the periosteal blood-supply has been sacri- ficed by the inflammatory process. The bone may still receive an adequate blood- supply from the nutrient artery and the vessels entering the epiphyseal extremities of the long bones. Extension of the process takes place along the vessels, the microbic invasion being carried on through the medium of the vessels connecting the periosteum and the bone. Under favor- able circumstances, after an early evacua- tion of the products of inflammation, the bone not having become necrosed, the ab- scess cavity assuming a healthy granulating process, the detached periosteum may again become adherent to the apparently-dead bone, and the process of restoration ad integrum is completed. If the vessels within the bone become obliterated by 7 8 embolism or thrombo-phlebitis, necrosis is an inevitable occurrence, as these patho- logical conditions, from the very nature of their causation, are necessarily attended or followed by suppuration. You will recognize this form clinically from the in- tensity of the local and general symptoms and the rapidity with which the process extends. The entire shaft of a long bone may become denuded within forty-eight or seventy-two hours. It can be recog- nized again by paying proper attention to the clinical history of the case, by tracing the disease to the primary cause, suppu- rative osteomyelitis. Clinically, this form is important to remember from the fact that the suppuration is prone to extend to proximate joints. The periosteal separa- tion continuing along the epiphyseal line may produce a separation of the ligaments attached to the epiphysis, which may open a direct entrance of the pus microbes into the adjacent joint, thus producing direct invasion of the adjacent joint. The joint may also become affected by the infection gaining access through a perforation of the epiphysis, or by a secondary infective inflammation of the synovial membrane. Another distinct form (and one that we recognize as usually commencing primarily in the periosteal structure) is the so-called syphilitic periostitis, due to the action of the syphilitic virus directly upon the perios- teum. This form usually assumes a pro- ductive character; it seldom results in suppuration; it constitutes one of the 9 various and multiple manifestations of ter- tiary syphilis. It is one of the more con- stant and later clinical features of this dis- ease, affecting most frequently the cranium or the anterior surface of the tibia; the swelling usually assumes a circumscribed form, with well-marked margins, the ex- udation taking place into and underneath the periosteum,—the result of tissue-pro- liferation from the internal layer or cam- bium of the periosteum. Instead of the products of proliferation giving rise to the formation of pus, they form embryonal tissue from the mature histological ele- ments of the periosteum, and the process ultimately will terminate in the transfor- mation of granulation-tissue (i) into carti- lage and (2) into bone in the formation of so-called syphilitic exostosis. You have learned that in fractures of the skull union takes place by a minimum amount of pro- visional callus; consequently the product of tissue-proliferation in syphilitic perios- titis of the skull is more likely to be a granulation-tissue, and this granulation- tissue, on account of its failure or absence of the osteogenetic influence from the sub- jacent bone, is destined to undergo degen- eration, softening, removal by absorption, or suppuration. Another and exceedingly important form of periostitis is the so-called tubercular periostitis,—a periostitis due to the pres- ence of a different form of microbes—the bacillus of tuberculosis ; consequently, the products of inflammation are varied. It is a well-recognized fact that this form may exist as a local disease, independently of primary disease, in the lungs, although more frequently it occurs as a secondary lesion. The product of exudation takes place between the vessels and into the con- nective-tissue spaces, which produces a local anaemia at the site of the exudation ; consequently the product does not go on transforming itself into tissue of a higher type, but terminates in fungous granula- tions and caseation, a conversion of the products of a low type of tissue-prolifera- tion into a cheesy material; this cheesy material acting as an irritant favors inva- sion of the tissues by the bacillus of tu- berculosis, the area of anaemia increases, and we have added to the tubercular de- generation an additional element consist- ing of inflammation of the underlying bone, attended usually by a secondary form of infection by pus microbes, which determine suppuration. It is recognized clinically by the peculiar form of caries or destruction of bone underneath the peri- osteum, the granulations permeating and destroying the bone at different points, so that the surface of the bone presents a honeycombed appearance. If you examine an abscess-cavity the result of tubercular periostitis, you will be impressed with the fact that the internal lining of the abscess- walls consists of a deep layer of granula- tions, which usually have invaded the ad- jacent tissues. If the abscess has opened spontaneously, you will recognize the char- 11 acter of the disease by an extensive under- mining of the skin and the absence of symptoms indicative of acute inflamma- tion ; you will determine the nature of an ulcer thus formed by the characteristic pathological features presented,—the un- dermined’margins, the flabby granulations invading the subcutaneous tissues as well as the superficial portion of bone, the pro- cess of destruction advancing as infiltration proceeds. In making your differential diagnosis between the preceding forms of periostitis and the tubercular variety, you will en- deavor to elicit evidence of tuberculosis in other parts of the body by carefully inquiring into the clinical history of the case, and by subjecting the various organs which are the most frequent seat of the tubercular process to a scrutinizing exami- nation. Usually the epiphyseal extremi- ties of long bones and the short bones are anatomically predisposed to localization of tubercular processes. Some forms of periostitis are diffuse from the very beginning, as the primary cause invades the tissues in rapid succes- sion ; for instance, infection by the specific microbes of suppuration, in cases of acute suppurative osteomyelitis, attacks simul- taneously an extensive surface of bone and periosteum. On the other hand, the pres- ence of both the syphilitic and tubercular virus usually produces, primarily, a perios- titis of a circumscribed character. The acute form of diffuse periostitis being usu- ally a secondary affection, the primary form, on the other hand, is noted for its tendency to remain local and for its chro- nicity. From a pathological stand-point we rec- ognize three distinct and well-marked va- rieties of primary periostitis,—the osteo- plastic, the suppurative, and the fungous. The osteoplastic periostitis usually follows traumatism when no infection has taken place. The suppurative or destructive form is due to the invasion of pus microbes, the presence of which invariably produces suppuration, when the local conditions are favorable, whatever tissues may be in- volved j the tubercular variety terminates in caseation, suppuration following as a secondary sequence only after the tuber- cular deposit has become the seat of a sec- ondary infection caused by the presence of pus microbes. The so-called periostitis granulosa, or granuloma of Friedmann, is that form which is destined to remain sta- tionary, which shows no tendency to trans- formation of the granulations into tissue of a higher type. This form, primary or sec- ondary, as the case may be, either origi- nating in the periosteum itself or as the result of extension of the fungous process in bone, is noted clinically for its chronic character. Instead of an intense pain marking its onset, it comes slowly and insidiously; the tissues not being infil- trated rapidly by the products of inflam- mation, we have a process which, instead of making painful tension underneath the 12 periosteum or within the bone, is accom- panied pari passu with disintegration of pre-existing tissue, consequently the space occupied by the granulations is created at the expense of pre-existing tissues. • Periostitis granulosa is noted for its obstinacy to all kinds of treatment short of a thorough removal and for the latency with which the symptoms appear; conse- quently its clinical feature is best expressed by the word “progressive.” This form is always caused by invasion of tissues by the specific germs of tuberculosis. When sup- puration has taken place in the interior of such a swelling, the abscess-cavity contains flocculent pus and the various products of degeneration, while its walls are lined with granulation tissue. While the interior of the abscess contains but few, if any, of the bacilli, the germs are always found present in its walls, as has been observed by Koch and others who have made this subject a special study. In considering the symptoms and diag- nosis of periostitis, I call your attention first to the most conspicuous and impor- tant symptom, pain. Periostitis as it af- fects the distal phalanx—the so-called par- onychia (felon)—in the majority of cases is the result of infection due to traumatism; the injury may have been insignificant and .on that account may have been lost sight of when the disease manifests itself. In this particular locality, on account of the un- yielding structure of the tissues around the periosteum, but more particularly on ac- count of the rapidity with which the pro- cess of exudation takes place, we have pre- sented to us in a well-marked form that important pathological factor in the causa- tion of pain,—tension. As an early diag- nostic evidence in periostitis, pain is an important symptom, and is relieved only by removing tension. Tenderness is even a more important diagnostic element than pain itself. While pain may be present in some forms,—by this I mean a spon- taneous or idiopathic pain,—you occa- sionally will find, by testing the effect of pressure, evidences of tenderness before the patient complains of pain, as, for in- stance, in cases where the disease is deeply located,—where, upon examination, you are not able to recognize the presence of swelling, and where, from the absence of more reliable symptoms, you may have to rely almost exclusively upon this clinical evidence in arriving at a correct diag- nosis. Again, we have repeatedly stated that periostitis manifests a decided predi- lection for the neighborhood of joints; and when the disease is deeply situated,— as, for instance, near the hip-joint,—cir- cumscribed and long-continued tenderness may indicate to you the existence of local- ized periostitis, in the absence of more decisive symptoms. If the symptoms in such a case remain circumscribed, local, you may properly suspect the existence of periostitis, secondary or primary, as the case may be. The swelling in periostitis is the result of exudation and tissue-prolif- 14 eration, within and underneath the perios- teum, and when the disease has extended beyond its limits in a peripheral direction, the paraosteal tissues are also affected. As long as the exudation remains limited to the space beneath the periosteum, the swell- ing is slight, as the subperiosteal space is limited; but as soon as the external layer of the periosteum participates in the pro- cess, a paraosteal exudation is added, and the rapidity with which the swelling forms increases. You can readily imagine, from the firmness with which the periosteum is attached to bone, that if the product of inflammation is of a plastic character the space for the exudation is circumscribed, consequently the swelling is slight. In chronic cases, therefore, with a tendency to the formation of productive material, the swelling is moderate and increases slowly, while, on the other hand, in acute cases the swelling is slight as long as the products of inflammation and infection are limited to the periosteum, but as soon as the inflammation has extended to the tissues around the periosteum the swelling increases more rapidly in size as the neces- sary consequence of an increased area of tissue-proliferation. If the periosteum is incised at this stage of the disease, we have the means of direct inspection of the subjacent bone. In cases of acute perios- titis you may find the bone denuded over a considerable area, and presenting all the superficial evidences of necrosis; in chronic periostitis we have either the honeycombed 16 appearance of carious bone characteristic of tuberculosis, or the floor of the abscess is lined by a continuous uninterrupted layer of granulation-tissue. Inspection alone will give you a true picture of the condition of the bone underneath. In this part of the examination you may com- bine inspection with exploration, to satisfy yourselves of the condition of the bone. Where periostitis or superficial osteomye- litis has resulted in circumscribed necrosis, we have presented the condition known as caries necrotica ; but if you wish to exam- ine and ascertain the true condition of the bone without making an incision, you will resort to acupuncture with a disinfected straight needle. If the point of the needle comes in contact with firm, unyielding bone, with a smooth surface, you may satisfy yourselves that the bone is either intact or that separation of the periosteum has taken place without necrobiosis. If, however, on introducing the needle you feel a rough, uneven surface, and you can pene- trate the bone, you may rest assured that the periostitis has resulted in caries. Im- pairment of function may be an important element in diagnosis, and you may have to rely upon this evidence almost exclu- sively if the disease is located so remotely as to preclude the possibility of eliciting more positive symptoms. The effect of the diseased periosteum upon the function of the part will not only satisfy you that you are dealing with an inflammatory con- dition either in the periosteum or the superficial portion of the bone, but it will aid you materially in locating the disease, and to a certain degree indicate its extent. If, for instance, we have a periostitis in close proximity to the hip-joint,—if after eliminating all the elements which we gen- erally expect in cases of intra-articular dis- ease as evidenced by a careful examina- tion as to the effect of pressure and motion upon the joint, we have evidences pointing towards a chronic inflammation of the hip- joint; in such a case, impairment of func- tion limited to the area of motion, with loss of functional capacity of the joint, would indicate its existence. Infiltration is the first point in consider- ing the morbid anatomy of periostitis. In examining post-mortem specimens, you will have in acute cases, before suppura- tion has taken place, infiltration of white corpuscles into the connective-tissue spaces and underneath the periosteum. If, on the other hand, you examine the patho- logical conditions later, at a time when the results of a detrimental action of the pus microbes upon the products of exuda- tion and tissue-proliferation have mani- fested themselves, you will find evidences of suppuration. If the exudation is of a productive type, you will find an increase in the thickness of the osteoplastic layer, a proliferation of osteoklasts in the sub- stance of the periosteum, and, as a direct result of this tissue-proliferation, a trans- formation of mature into granulation or embryonal tissue. If, on the other hand, the disease has been the result of infection with the bacillus of tuberculosis, you will have all the evidences distinctive of tuber- cular process, wherever found, granulations, or, after suppuration has taken place, an abscess-cavity lined with fungous granula- tions and miliary tubercles. A careful microscopical examination of the inflam- matory product will determine the primary cause in certain forms of periostitis. In cases of acute periostitis attended by sup- puration, the vascular supply to the peri- osteum and bone is diminished by the exudation producing compression ; in other cases the circulation is speedily arrested, as a result of the effect of the primary mi- crobic cause of the periostitis upon the vessels themselves, and may produce a thrombo-phlebitis and a successive venous thrombosis, which are important patholog- ical elements in considering the effects of the circulation upon the products of exu- dation and the vitality of the tissues im- mediately concerned in the inflammatory process. In the tubercular variety the gradual diminution of the vascularization of the products of inflammation constitutes a most important factor, the existence of local areas of anaemia determining the fate of the inflammatory product, which is gradually transformed into a caseous ma- terial. As the production of new bone depends upon the primary cause, this ter- mination can only be expected in produc- tive or osteoplastic periostitis. The primary formation of a bone always takes place first in the immediate vicinity of blood-vessels, just the same as in the 18 19 formation of a callus after fracture. The deposition of bone takes place after rare- fying osteitis or inflammatory osteo-porosis. The death of bone following destructive periostitis may either involve a consider- able surface of the bone, producing necro- sis, or it may be more circumscribed, resulting in caries necrotica, or it takes place by interstitial absorption, which ends in caries. In considering the treatment of peri- ostitis, I am happy to make an exception to my general rule in regard to the effects of drugs. It is a well-known fact that syphilitic periostitis will yield very readily to the administration of mercury or iodide of potassium. In cases of this kind never resort to operative measures before having thoroughly tested the effects of antisyphi- litic treatment. The proof of a syphilitic origin of the periostitis will become ap- parent in many instances if after the ad- ministration of large doses of iodide of potassium the symptoms promptly subside. But the salutary effect of iodide of potas- sium is not limited to syphilitic periostitis, as this drug exerts a special effect upon other forms of inflammation of fibrous tissue, aside from its antisyphilitic effects, as it constitutes one of the most reliable means to promote absorption if adminis- tered internally. By large doses I mean from ten to twenty grains three or four times a day. It is not only prompt in neutralizing the effect of the syphilitic virus, but, by hastening absorption, it diminishes tension, and thus relieves pain. Its administration always produces a salu- tary effect in cases of plastic periostitis when following other causes than syphilis. If a case prove obstinate, and iodide of potassium fails, put your patient under the influence of mercury by inunction, or give small doses of corrosive sublimate, combined with twenty or thirty grains of iodide of potassium, until you produce its physiological effect or until the active symptoms subside. Equable compression, by giving support to the circulation, by condensing the connective-tissue spaces, favors absorption, and should always be resorted to. Counter-irritation, by apply- ing tincture of iodine or by blistering, should be employed for the same purpose. If the pain is intense you may divide the dense periosteum by subcutaneous section or incision under antiseptic precautions, and these measures will prove the most reliable means of securing prompt relief. In all cases of purulent periostitis no time should be lost in evacuating the in- flammatory products by free incision, fol- lowed by thorough disinfection of the abscess-cavity, drainage, and antiseptic dressing. Tubercular periostitis calls for thorough removal of all infected tissues by evidement or the use of the actual cautery. All these operations upon bone must be done under the strictest antiseptic precau- tions. Asepsis in these cases is an essen- tial factor in treatment, as it affords the greatest immunity against further destruc- tive processes in the soft tissues and the subjacent bone.