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THE THREE TYPES OF ACUTE A Clinical and Vascular J. TRUETA, OXFORD, the Nuffield Orthopaedic Fronz clinical It has been known characteristics child and from adult for many according constitute the generalised, Fraser (1924), HAEMATOGENOUS years to the three that age separate or septicaemic, Paschlau (1932) OSTEOMYELITIS Study ENGLAND (‘entre, Oxford acute haematogenous of the patient; thus clinical entities with osteomyelitis osteomyelitis few features phase of the disease from which and Green and Shannon (1936) varies in its of the infant, in common apart they all suffer. were among the first to isolate the infantile type from that of the child and to describe its main characteristics during early life, including its high mortality-up to 45 per cent in the series of Green and Shannon. Since the inception of antibiotic treatment, Greengard (1946), Thomson and Lewis (1950) and Dennison (1955) have further contributed to the study newborn and have insisted on the existence of two forms, the severe nevertheless. be pointed out that the so-called mild type refers only of this form of the disease, for even the milder to bone and joint in the infant. The separate nature of acute osteomyelitis years. years but the first full description ago (Zadek 1938). In a systematic study of treated 202 patients. This of acute experience of these three types of osteomyelitis. the disease in childhood, which sixteen in the years adult. inclusively. This the form in the condition be used I will begin in osteomyelitis is followed OF majority of contributing factors vary, has including and been adult was to summarise by mentioning covers the by a summary ACUTE severe the many twenty-one since 1944 main clinical disease damage for only the main clinical span of life between of the in the It must, figures lasting recognised given osteomyelitis here in the we have features features one of and infant and OSTEOMYELITIS This study of the severity of acute osteomyelitis inception of antibiotics (Table I). It is well recognised that acute haematogenous the cause adult in the haematogenous will SEVERITY may of osteomyelitis and the mild. to the mortality is based on osteomyelitis the nature experience is a disease and pathogenesis collected since in which of the the causal germ. Thus, whereas the prevalent bacteria in the older age groups-the child and the adultis the coagulase-positive staphylococcus pyogenes aureus, the streptococcus pyogenes appear responsible for most acute bone infections in infants (63 per cent in the series of Green and Shannon; 53 per cent in this series). The almost present on the severity and clinical characteristics of the three by an equal consensus of opinion regarding the causes responsible In the present paper I shall attempt to offer an explanation characteristics of acute osteomyelitis far been unable to find any similar As it is not my purpose here osteomyelitis, of the 41 B, VOL. B I have three variants, NO. 4, presented without NOVEMBER 1959 the any general age agreement existing at types is not accompanied for the three different types. for the diversity of clinical in the three ages in which they are grouped. I have so explanation in the medical literature at my disposal. to study the clinical aspect of the three types of acute table aim on the at statistical severity of the disease as a simple reminder accuracy. 671 672 J. TRUETA LOCALISATION Since the early experiments OF of Lexer PATHOGENIC (1896) BACTERIA it has been generally accepted that artery is the main route for bacteria causing osteomyelitis, even if other be excluded as a route for the infecting organisms. From the experiments know that an intravenous injection of bacteria localises in the metaphysial only two hours Hobo metaphysial children. in that after (1921) His region. inoculation showed and the side of the growth diagram (Fig. part that a focus played plate in causing 1) is based of infection the vascular by the on observations TABLE THE SEVERITY OF ACUTE may develop arrangement localisation of the of the normal OSTEOMYELITIS (per General severity before . and pathogenic structure AT to the bacteria of the in vessels Adults (under cent) one year) (per cent) Aors DIFFERENT Infants of all patients there. adjacent I HAEMATOGENOUS Children Frequency the nutrient bone vessels cannot of Koch (191 1) we veins in the bone (over sixteen years) (per cent) . 80 7 13 during early treatment Very severe. . . . 10 15 5 Severe . . . 25 20 10 . 65 65 85 5 23 20 . 15 20 25 . 80 57 55 . Moderately Local damage during early Permanent severe . sustained before and treatment . . Transient . None Disability Very severe. In his studies . #{149} , 15 5 15 15 6 12 18 94 58 62 Severe #{149} . . Moderate . . . None . of experimental . . infection, Starr (1922) showed that the organisms responsible for the bone infection were carried by the blood stream until they reached what is referred to as “the finer capillaries of the juxta-epiphysial region of a long bone,” but he attributed the infection to the lowering of an undetermined general resistance” of the patient. Wilensky (1934) pointed out the importance of what he called the fixation points of the disease and supported the views of Hobo on the vascular responsibility in the onset of infection. Finally, Leveuf (1947) denied that the disease in the child was initially Iocalised in the metaphysis, as suggested by Lnnnelongue in 1879, and favoured the hypothesis of thrombosis of the main trunk of the nutrient artery from the onset of infection, as had been suggested by l-Iartmann as early as 1855, I cannot trace that proper mention has been made by any author of the fact that the vascular pattern of the long bones occurring during the first year of life, during childhood, THE JOURNAL. OF BONE AND JOINT .SUR(4ERV THE THREE Epiphysial Primary marrow TYPES OF ACUTE HAEMATOGENOUS 673 OSTEOMYELITIS marrow outgrowths Epiphysial cartilage point Descending limb- artery Venous network in Nutrient artery Nutrient vein Transition FIG. Diagram of marrow the course of a young I blood vessels in the rabbit. (After Hobo) of the ‘,L 2 1oops FIG. Figure sinusoids VOL. 41 B, NO. 4, 2-Vascular where the venous NOVEMBER 1959 FIG. under the growth limb of the vascular plate. Figure 3 3-Large loops under the growth venous plate end. 674 and J. at puberty, purpose is responsible here to suggest for that each of ACUTE by referring the it is precisely limit which explains the diverse clinical groups in which it presents itself. I begin TRUETA to this both its clinical and vascular osteomyelitis “par excellence.” three the types picture of acute OSTEOMYELITIS IN age group aspects, for apart of changing one which has been studies age of the age the and b, We from as the out the growth Morgan in to both (Trueta Trueta able adjacent this plate, 1959, been acute vascular microradiography have capillaries studied shown underlying and best carried repeatedly photography 1958a Morgan). one by all authors vascular have arrangement the in every considered The by It is my at each CHILDREN being centre osteomyelitis. arrangement osteomyelitis it is the from acute vascular and to confIrm the growth that plate in its metaphysial side are, apart from a narrow fringe at the periphery of the plate, the last ramifications of the nutrient artery; these. after turning system down in acute of large sinusoidal others for the loops (Fig. 2), reach a veins responsible with haemopoietic activity of the marrow (Fig. 3). It is here that slows down and that the pathogenic particularly :. the #{182}: end 4 FIG. supply of the from that of the specimen of eighteen epiphysis metaphysis. months. is periosteal and venous sinusoids In a study growth cartilage eighteenth largely Human metaphysis “child” The causes where vessels because none has distributed at the periphery changes 1957). is first obvious month, except a capillary of the staphy- of eight peripheral (Fig. 4). Thus. from the point the age of one year. lakes, beginning spreads for at through in a pattern labelled exactly end-arteries, of the occur loops. initially of vascular loops growth cartilage. of the vascular are Eventually along the proximal to upper femoral epiphysis represented by the growth months and is definitely vascular connections of view medium loop, side not of the vascular pattern of the human it was found that the vascular barrier at the age for some blood ideal that of the distribution of early stages of osteomyelitis. branches of the nutrient erroneously a system of the its metaphysis by spreading infection from the venous is thus occluded. Bone infection does metaphysial like those of the (Trueta of the corresponding to bone sepsis in the The peripheral artery, thrombosed artery itself finds system of the whole __________ secondarily the nutrient aureus, development. This the during coagulase-positive * lococcus The arterial disconnected bone blood flow bacteria, established before between epiphysis anatomy, the infant the and becomes at extensive early oedema. it is thinnest, involvement of the Transudates over the distal metaphysial veins in acute expand towards the surface part of the metaphysis, and from the cortex, disrupting all vascular connections between oedema and the periosteum lays down a new layer of bone-the from the cortex, visible after a few days on a radiograph (Fig. THE osteomyelitis of the of the bone across here the periosteum them. Soon involucrum-at 5). In another JOURNAL OF BONE child the cortex is raised pus follows the some distance work we have ANt) JOINT SURGERY THE found evidence of blood soon to the after by accompanies that are THREE typical OF ACUTE HAEMATOGENOUS of the mechanism of involucrum inner half cortex the the TYPES of the interruption of lifting of the of osteomyelitis the formation by the blood periosteum, in the child (Fig. thrombosis supply of the is responsible (Fig. 7). On the other hand, the isolation of the epiphysis epiphysial plate provides protection both for the epiphysis the rarity of joint infections and epiphysitis with growth treatment is defective (Fig. 8). 675 OSTEOMYELITIS 6). The of the nutrient outer half for the of large early deprivation artery. the cortical 6 FIG. FIG. 6-Experimental involucrum in the radius periosteum the two sheath. S A large involucrum covering the dead girl of six years. Radiographs taken after the onset of the disease. Summary-The aim children should formation of cause of the be to protect an sequestration. In the child severe generalised It seldom causes 41 B, NO. surgeon involucrum the tends disease toxaemia permanent 4, NOVEMBER to be more early 1959 stimulated from each which abscess. a large by lifting the and keeping by a polythene other haematogenous it is 7 of 7-A large cortical the ischaemic bone Figure acute production of a rabbit, cortex aseptically sequestrum and separated by the marrow osteomyelitis to the outer side of the cortex to prevent the cortex separated from its periosteum dangerous by massive absorption damage to growth. On was 9). from the separated enclosed between the involucrum, from in treating the blood supply which would leave cases in children growth of the growth plate (Fig. VOL. cortex in a eight weeks which sequestra from the metaphysis caused by the itself and for the joint, and explains inhibition in children, even if early Figure FIG. followed cortex by the to life than to limb, for it may in the and cause of toxins from the whole of the shaft. the contrary, in over 30 per cent of our increased vascularity of the metaphysial side 676 J. TRUETA ACUTE Table I shows that the OSTEOMYELITIS important IN characteristic the local severity ofthe disease, even in many cases As stated before, a particularly severe group umbilicus. It is my conviction that the THE more of INFANT acute considered occurs in outstanding osteomyelitis the clinical in the infant is in some classifications. newborn, infected from benign “ “ features of the disease at this the age should be attributed to the foetal vascular arrangement that persists in some bones up to the age of one year. with local variations corresponding to the time of full development of the epiphysial bone nucleus. Some research, published in this Journal (Trueta 1957), and others in the course of publication, may help to clarify this point. From the time in the embryo when the ossification of the central part of the shaft FIG. Figure years caused feature of the long bones has started, the 8 FIG. perichondral vessels progress 9 8-Radiograph showing acute osteomyelitis of the left femur in a girl of four taken three months after the onset of the disease. That no damage was by the infection to either of the epiphyses or adjacent joints is a common in children. Figure 9-Marked overgrowth of the affected tibia in a child of seven years persisting three years after the inception of osteomyelitis. towards the two ends of the cartilaginous “anlage” in a tortuous way, turning back when reach the still unossified cartilaginous ends of the bone. From the last stages of intra-uterine up to not yet limited the first by bone the “anlage,” perforating expand. forming situated close six months, large to the in some epiphyses, on the epiphysial the venous surface side, pre-existing lakes of the when vessels growth resembling epiphysis. the from plate growth cartilage the metaphysis (Fig. 10). At their they life is established penetrate ends metaphysial sinusoids (Fig. This explains the frequency the those 11). of but end of vessels They are infections of the joint and of the epiphysial side of the preliminary growth cartilage in the infant. In experimental work in this centre (Trueta 1958) it was shown that any severe damage to the cells at the epiphysial side of the growth plate is irreparable (Fig. 12); thus, both joint damage and arrest or disorganisation of growth are the consequences of the spread of bacteria to the ends of the nutrient artery in very early life (Fig. 13). THE JOURNAL OF BONE AND JOINT SURGERY THE THREE TYPES FIG. 10 Figure 10-Vessels perforating epiphysis(in the infant). Figure from the metaphysis Permanent growth epiphysial Another sometimes characteristic monstrously the bulging will remain the periosteal side richness vessels (Fig. the of blood and the OSTEOMYELITIS True acute haematogenous bones in adults haematogenous HAEMATOGENOUS growth plate in the But, (in only the rapid spread is the involucrum fertility of a transient alteration ______________ of which NO. _______ the osteomyelitis On of occasions osteomyelitis along the All occurs in whole this leads r .. length to FIG. 1959 ___________ 13 Examples of permanent epiphysial damage and lower ends of the femur caused osteomyelitis in the infant. large extraperiosteal abscesses been proper treatment from the the typical features of the disease of the vascular arrangement penetration of the growth 4, NOVEMBER lesion. no trace ______ following cartilage to and the by upper acute chronic early stages. may be attributed the fusion of the growth cartilages. by metaphysial vessels, its height reduced until finally vascular connections are established between the epiphysial and system of vessels (Fig. 16). From then on, the blood in the nutrient artery reaches of the epiphysis through large anastomoses; thus bacteria penetrating the nutrient VOL. 41 B, formation. ADULT sinuses when there has not adult, as in the other types, to the peculiarities By the progressive involucrum of the epiphysial are responsible reactions and for that occurs in is rare. formation. profuse severity through of the bone, the frequency of joint infections, the lack of large sequestration, and instead the irregular atrophy of the cortex, and the limited discharging In the rabbit). a young to the the adult but is usually localised to the short bones, particularly the vertebrae, following infections of the pelvis (Trueta and Wiley 1959). The main features of the condition in adults are 677 OSTEOMYELITIS infant contrary represents flow IN THE long acute the 14). the shaft 15). cambium layer of the periosteum both for the early exuberant the extraordinary remodelling succeeding years. ACUTE of of osteomyelitis large new bone along in later life (Fig. The extreme ACUTE FIG. 11 FIG. 12 the preliminary growth plate and expanding throughout the cartilaginous 11-Note the vascular expansions at the most distal part of the vessels ascending the surface of the cartilaginous femoral head (in early infancy). Figure 12plate damage caused by experimentally interfering with the blood flow to the towards epiphysial OF is metaphysial the surface artery may 678 J. TRUETA FR’. 14 Figure 14-Enormous involucrum in an infant for which the elasticity of the periosteum and its osteogenic power are responsible. Figure I 5-The large involucrum has completely disappeared four and a half years afterwards but the permanent epiphysial damage is interfering severely with growth. 15 FIG. be brought spread to the the The detachment thus vascular infection into fibrosis of the by pus preserves the more blood loops under the joint. periosteum difficult; supply the articular in this to the the adult prevents outer cartilage half and the (Trueta its adhesion formation of the cortex. not to the and progressive (Fig. a fracture to occur The tendency to from joint infection responsible for make Instead, absorption if no chronic phlebitis protection infection within the its 18). after and seq uestra the rapid may allow is used. in the bone, are the two main the crippling severity in the adult (Fig. capacity apparent and abscesses large 17). cortical 1953) cortex Consequently, formed condition reparative Harrison of subperiosteal are marrow, and and factors of the The lack the fusion the epiphysis makes chronic infection frequent sequel of acute osteomyelitis of of the most in the adult. DISCUSSION FIG. 16 An example end of established anatomical of acute of the vascular arrangement growth. Ample anastomoses between the epiphysial and vessels. vascular osteomyelitis. research-the after the have been metaphysial object It is beyond enlarge on my purpose therapeutic in this considerations, paper but to it may not be out of place to suggest some lines of treatment which are supported as much by of this paper-as by fifteen years of clinical study Specific antibiotic treatment instituted as early and as radically as possible must be the main aim of any treatment of acute haematogenous osteomyelitis in any of its three age forms. If started soon enough, it may control the infection before severe vascular damage has been caused I) in the epiphysial anlage” and joint in the infant, 2) in the cortex of the shaft in “ THE JOURNAL OF BONE ANt) JOINT SURGERY THE TYPES THREE the child, and 3) in the joint and severely affected regions When some antibiotic vascular lavage adults, conservative what the still joint the occurs, the main effective, object radical 679 OSTEOMYELITIS frequently the most because commonly the of the treatment must aspiration, or preferably appropriate be to reduce incision and in the infants and periosteum. are the for of the and treatment known, Early, remain bone HAEMATOGENOUS joint. the preservation blood flow One thing in must be never forgotten, and this is that no will ever reach the foci of infection the preservation ofsome local blood flow. The vascular anatomy predominance of infancy early In antibiotic procedures may affected antibiotic without in in the of ACUTE and bone marrow of the adult, these being in the three age types of bone infection. available or to the utmost. of the affected and splitting most of delay is not damage OF may also to a cellulitis streptococcus activity, has and invades On the a in childhood. been rightly germ such with the other joint hand, the infection haemolyticus, easily epiphysis. explain streptococcal and the staphylococcal life bone infection compared the the and the as lytic its nearby coagulase- positive staphylococcus aureus, the common aggressor of the bone in childhood, needs for its development a stagnant or moderately active circulation such as that in the venous sinusoids under the growth plate. It may well be that the rarity of streptococcal bone infections in children is not so much due bacteraemia at that this germ to localise this it is. as highly yet. to a lack of a streptococcal age as to the incapacity in metaphysial sinusoids; mere conjecture, but I. The clinical Figure 17-Acute osteomyelitis of the The infection extends from end to end No large cortical sequestra are formed. I consider Severe joint possible. CONCLUSIONS three age features types of acute by the differing AND haematogenous 2. In the infant the condition joint infection, a large involucrum FIG. 17 FIG. of damage infection of their causes but severe and only transient by phlebitis within the bone caused in acute osteomyelitis in an adult. and of the femur SUMMARY osteomyelitis nature 18 adult fibula. of the bone. Figure 18- vascular are conditioned bone in their respective pattern. often permanent damage to the epiphysial shaft and damage metaphysis. and 3. In the child the condition is responsible for extensive cortical damage with involucrum formation, but, except for some stimulation of growth, permanent damage to the growth cartilage and to joints is exceptional. Chronicity of the disease is rare if treatment has been effective. 4. In the infection; and 5. adult the frequently The 6. VOL. Some 41 B, leaves vascular of infection osteomyelitis is absorbed chronic general of the instead of the long bones is rare. of sequestrating. infection characteristics are NO. acute cortex in the bones The bone marrow. in each age group It causes whole and very of the their relation described. directives 4, NOVEMBER for 1959 management based on these facts are frequent bone suggested. joint is invaded to the onset 680 TRUETA . REFERENCES W. M. (1955): Haematogenous Osteitis in the Newborn. Lancet, ii, 474. J. ( 1924) : Acute Osteomyelitis. British Medical Journal, ii, 605. GREEN, W. T., and SHANNON, J. C. (1936): Osteomyelitis of Infants. A Disease Different of Older Children. Archives of Surgery, 32, 462. GREENGARD, J. (I 946) : Acute Hematogenous Osteomyelitis in Infancy. Medical Clinics 30, 135. DENNISON, FRASER, from of Osteomyelitis North America, HARTMANN, F. (1855): Nekrose, herbeigefuhrt durch Verstopfung des Foramen nutritium. Virchows Archiv f#{252}r pathologische Anatomie und Physiologie, 8, 114. HoBO, T. (1921): Zur Pathogenese der akuten haematogenen Osteomyelitis. Acta Scholae Medicinalis Universitatis Imperialis in Kioto, 4, 1. KOCH, J. (1911): Untersuchungen Uber die Lokalisation der Bakterien, das Verhalten des Knochenmarkes und die Ver#{228}nderungen der Knochen, insbesondere der Epiphysen, bei Infektionskrankheiten. Zeitschrift f#{252}r Hygiene und Infektionskrankheiten, 69, 436. LANNELONGUE, 0. (1879): De l’ost#{233}omy#{233}lite aigu#{235}pendant Ia croissance. Paris. LEVEUF, J. (1947): Les lesions initiales de l’ost#{233}omyelite aigue. Revue d’Orthop#{233}die, 33, 177. LEXER, E. (1896): Experimente #{252}ber Osteomyelitis. Langenbecks Archiv f#{252}r klinische Chirurgie, 53, 266. MORGAN, J. D. (1959): Blood Supply of Growing Rabbit’s Tibia. Journal of Bone and Joint Surgery, 41-B, 185. PASCHLAU, G. (1932): Die Besonderheiten der Osteomyelitis im frUhen Kindesalter. Monatsschrift f#{252}r Kinderheilkunde, 55, 280. STARR, C. L. (1922): Acute Hematogenous Osteomyelitis. Archives of Surgery, 4, 567. THOMSON, J., and LEWIS, I. C. (1950): Osteomyelitis in the Newborn. Archives of Disease in Childhood, 25, 273. TRUETA, J. (1957): The Normal Vascular Anatomy of the Human Femoral Head during Growth. Journal of Bone and Joint Surgery, 39-B, 358. TRUETA, J. (I 958a): Trauma and Bone Growth. SociCtC Internationale de Chirurgie OrthopCdique et de Traumatologie. Septi#{232}me Congr#{232}s International de Chirurgie Orthop#{233}dique Barcelone, 16-21 septembre 1957. Proc#{232}s-verbaux, rapports, discussions et communications particuliCres, p. 329. Bruxelles: Imprimerie des Sciences, s.a. TRUETA, J. (1958b): TRUETA, J., and Man. TRUETA, Journal J., La vascularisation M. HARRISON, of Bone and and MORGAN, Joint J. des H. M. Surgery, D.: The 35-B, The de Chirurgie os et l’ost#{233}og#{233}nCse.Revue (1953): Vascular Normal Vascular Anatomy Orthop#{233}dique, 44, 3. of the Femoral Head in Adult 442. Contribution to Osteogenesis; Studies Journal of Bone and Joint Surgery (in course of publication). TRUETA, J., and WILEY, A. M. (1959): The Vascular Anatomy of the Spine and its Relation to Osteomyelitis. Journal of Bone and Joint Surgery, 41-B, 796. WILENSKY, A. 0. (1934): Osteomyelitis. Its Pathogenesis, Symptomatology and Treatment. by the Injection Method. Macmillan ZADEK, Pyogenic Vertebral New York: The Company. I. (1938): Acute Osteomyelitis of the Long Bones of Adults. Archives THE JOURNAL of Surgery, OF BONE 37, 531. AND JOINT SURGERY