In: Blood Vessels And Lymphatics In Organ Systems

by D. W. Lennox and D. S. Hungerford

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Circulatory abnormalities of bone blood vessels underlie a number of clinical entities. Several of the better known of these are discussed below.


A number of eponymic disorders, including Legg-Calve-Perthes' disease, Osgood-Schlatter's disease, Sindig-Larrsen-Johannson disease, Kohler's disease, Freiberg's disease, Schuermann's disease, Panner's disease, and Thiemann's disease, were believed to originate from a similar vascular abnormality of bone blood vessels. It now appears that those conditions about the patella or patellar tendon represent avulsion fractures.

a. Legg-Calve-Perthes' disease: One theory regarding the development of this entity is that circulatory embarrassment from retinacular vessel disruption in the region of the physis plays a very important role (Ponseti, 1956). In comparing the effect of venous tamponade of the hip capsule on femoral head blood flow in mature and immature dogs, Launder et al. (1981) reported a significant rise in femoral head pressure in puppies following capsule inflation but noted no significant change in either pressure or flow in adults. These results were attributed to the absence of an intact intramedullary venous drainage of the femoral head in the immature animal. The validity with which these data can be applied to humans, as in the case of Legg-Calve-Perthes' disease, is unclear. Heikkinen et al. (1980) reported delayed venous drainage from the femoral neck to be indicative of a of a poor prognosis in this disorder. Heikkinen et al. (1976) found that after treatment by intertrochanteric osteotomy, venous outflow patterns became normal at 4-15 months following surgery. Suramo et al. (1964) have demonstrated that venous drainage of the femoral neck occurs via capsular veins in the normal child's hip, but via the intramedullary route in children with Perthes' disease and with an intact growth plate. In a study of intracapsular tamponade in puppies, Tachdjian and Grana (1968) reported partial vascular obstruction at 80-100 mm Hg pressures and avascular necrosis with pressures of 200 mm Hg maintained for 10 hr. Utilizing a similar approach but measuring flow with the hydrogen washout technique, Borgsmiller et al. (1980) eliminated epiphyseal flow at 150 mm Hg pressure and on the basis of their findings concluded that Legg-Calve-Perthes' disease resulted from arterial rather than venous tamponade. Woodhouse (1962, 1964) found that in adult dogs, avascular necrosis developed after exposure to hip intracapsular pressures of 50 mm HG for 12 hr following femoral neck osteotomy. In puppies, a similar tamponade, but without osteotomy, also produced femoral head necrosis at 12 hr. This worker concluded that avascular necrosis resulted from venous tamponade, capillary engorgement, fluid extravasation, microcapillary sludging, and irreversible intravascular thrombosis.


Trauma sufficient to produce a fracture or dislocation can result in damage to the blood supply to an entire bone, e.g., the talus in subtalar dislocation, or a portion of a bone, e.g., the femoral neck in femoral neck fracture. With severe circulatory compromise, avascular (ischemic) necrosis may result. Particularly vulnerable to the development of ischemia are intracapsular fractures, as occur in the hip and shoulder. In these locations, blood supply is marginal and damage to surrounding soft tissue may be sufficient to induce irreversible ischemia. The duration of the ischemia appears to be a critical factor since better results are obtained in cases of hip dislocation reduced within 12 hr than in those treated after that time period. In fractures of the femoral neck, bone scans have been recommended as diagnostic tools to deterimine the viability of the femoral head.

Avascular necrosis of the femoral head in children is a complication following reduction and cast immobilization, as in the treatment of congenitally dislocated hips. Schoenecker et al. (1978) demonstrated in dogs that a position of forced frog-leg abduction and internal rotation obliterated or drastically reduced circulation to the femoral head.

Duncan and Shim (1977) reported that in rabbits with trauma-induced dislocation of the hip, circulatory compromise was present in both adult and immature animals, but it was worse in immature rabbits, reaching a maximum effect after 24 hr of continued dislocation. Aseptic necrosis was evident in the specimens, particularly in the case of immature animals. Duncan and Shim found that in the adult rabbit, the anastomotic connection between epiphyseal and metaphyseal vessels afforded some protection to the femoral head from the insult to the extraosseous nutrient system, whereas in the immature animal, without such a vascular arrangement, damage to the system of supply and of drainage could result in necrosis.

3. Bone Infarcts

Bone infarcts, which are believed to arise from arterial obstruction, in many instances are asymptomatic, being noted incidentally in roentgenograms or bone scans performed for other reasons. Long bones are involved almost exclusively. Most commonly, lesions are a few millimeters in size but may vary to involve a large portion of the shaft; the ends of long bones are more often involved than other areas. Roentgenograms demonstrate areas of mottled sclerosis. In contrast, areas of infarction and necrosis involving a periarticular region are associated with a considerably different clinical pattern, roentgenographic picture, pathologic changes, and prognosis (see Section D-5, below).

4. Surgery

Orthopedic and/or vascular surgery may greatly alter circulation in bone. For example, internal fixation devices in the treatment of fractures can affect bone blood supply. In this regard, Rand et al. (1981) compared the vascular effects of open intramedullary nailing after reaming with those of compression plate fixation of a tibial fracture in the dog. Bone blood flow remained elevated for longer periods and reached a higher level overall in the intramedullary rod group than in that with compression plate fixation. However, the latter approach provided mechanical strength at the fracture site sooner than did rod fixation. Similar effects on bone healing were noted with both extraperiosteal and subperiosteal plate placement, with fracture healing occurring by different mechanisms in the two groups. Whereas with the intramedullary rod group, fracture healing was predominantly by periosteal callus, in the compression plate group, endosteal callus formation occurred. Both open intramedullary nailing after reaming and intramedullary rod insertion damage the medullary vasculature and produce avascularity of a portion of the cortical diaphyseal region (Trueta and Cavadias, 1955; Göthman, 1961; Rhinelander, 1974). Compression plate fixation damages cortical efferent blood flow beneath the plate (Olerud and Danckwardt-Lilliestrom, 1968).

Whiteside et al. (1978) studied the effects of periosteal stripping and medullary reaming on regional blood flow in the tibias of mature and immature rabbits. By stripping tibial epiphyseal periosteum, the epiphyseal circulation was eliminated, as measured by the hydrogen washout technique. In mature rabbits, the epiphyseal flow was markedly reduced by periosteal stripping, but no change in blood flow was noted following wide reaming of the epiphyseal center in both mature and immature animals. Diaphyseal and metaphyseal flow was unchanged following separate medullary reaming or periosteal dissection in both groups. When intramedullary reaming and periosteal stripping were performed, cortical diaphyseal flow ceased, but metaphyseal flow persisted. Whiteside et al. (1978) concluded that both venous drainage and arterial supply systems traverse endosteal and periosteal systems and that either can sustain adequate circulation.

Because a number of orthopedic implants, including total hip replacement and total knee replacement prostheses, utilize the polymer polymethylmethacrylate (PMMA) to secure components to bone, the vascular response elicited by this substance was studied by Brookes and Gallanaugh (1975). They implanted a plug of methylmethacrylate into the rat tibia and calculated blood flow using 51Cr- and 59Fe-tagged resin particles. At both 14 and 112 days postoperatively, both blood volume and blood flow were significantly depressed in the tibias in which the acrylic cement had been implanted. The extent to which this factor may be operative in the case of human joint replacement is uncertain. Theoretically, however, devascularized bone appears prone to infection, and this may be a contributing factor in the major problem of loosening in joint replacements.


a. Theories of pathogenesis: A number of hypotheses have been proposed with regard to the pathogenesis of ischemic necrosis of the femoral head. One of these, the infarction theory, was espoused by Chandler (1948), who attributed the condition to compromise of the lateral retinacular vessel, with subsequent infarction of the anterolateral segment of the femoral head. According to him, with revascularization of the infarcted segment, the femoral head then becomes softened and finally fails mechanically. However, McFarland and Frost (1961) suggested that it is the accumulation of microfractures without repair that eventuates in macrofractures, causing the femoral head to collapse.

Another view, the embolization theory, is based on the assumption that fat emboli produce infarction and ischemic necrosis. Jones and Sakovich (1966) demonstrated that rabbits given intraarterial injections of Lipiodol were found to have fat droplets in a subchondral location in the femoral head. Of interest in this regard is the finding that hyperlipidemia is a common abnormality in ischemic necrosis patient populations (Cruess et al, 1975; Fisher, 1978; Jones, 1971). Although fat emboli have been reported in ischemic necrosis of the femoral head, it is still not possible to state unequivocally that they are responsible for the disease and, if so, whether the basis is one of arterial or arteriolar infarction.

Finally, the progressive ischemia theory has been proposed to explain the mechanisms responsible for the development of ischemic necrosis of the femoral head. In this regard, Michelsen (1967) and Wilkes and Visscher (1975) have offered the analogy between circulation in bone and the functioning of a Starling resistor, with the rigid canister of the resistor corresponding to the rigidity of cortical bone. Thin-walled tissues, the vessels, traverse the canister but do not open into it. Under such conditions, structures outside the vascular space but within the container of bone (the elements of marrow) can modulate blood flow by changes in tissue pressure. Thus, an increase in pressure in the compartment (elevated bone marrow pressure) could collapse such thin-walled vessels as sinusoids and veins, increase peripheral resistance, and diminish flow.

The concept of bone and its circulation as functioning in a manner similar to a Starling resistor is supported by the common finding of elevated intramedullary pressure in a number of different pathologic circumstances, including ischemic necrosis of the femoral head (Arlet and Ficat, 1964; Ficat and Arlet, 1968; Hungerford, 1979; Hungerford and Zizic, 1978).

In the case of Gaucher’s disease, proliferating reticuloendothelial cells could increase bone marrow pressure, with resultant diminished flow. With regard to caisson disease, the nitrogen bubbles generated by decompression could expand extravascularly, increase bone marrow pressure, and compromise flow. Essentially any circulatory injury that produces ischemia could result in fluid extravasation into the extravascular (bone marrow) space, with resultant increased bone marrow pressure and circulatory embarrassment.

Jacqueline and Rabinowitz (1973) reported no evidence in support of sudden infarction in an examination of 82 femoral heads studied at various times following femoral neck fracture. Multiple areas of ischemia were distributed throughout the femoral head after fracture. With time and the added stress of weight bearing, the ischemic areas were localized to that portion of the femoral head that assumed the weight-bearing load. Hungerford (1983) presented several examples of ischemic necrosis of the femoral head that were localized not to the anterolateral fracture but rather at a site that, although previously a non-weight-bearing region, was rotated into a weight-bearing position by the fracture. This argues for the role of biomechanical factors in determining the region of morphologic change in ischemic necrosis.

b. Diagnosis: Bone marrow pressure can be measured clinically and is elevated in all phases of ischemic necrosis, even at the preclinical stages in some patients (Hungerford, 1979). In this disorder, venograms, performed by injecting the radiopaque material intraosseously, demonstrate poor filling of the metaphyseal veins, stasis, and diaphyseal reflux on films taken 5 min following administration.

Arlet and Ficat (1964) and Ficat and Arlet (1968) studied necrosis of the femoral head utilizing bone marrow pressure measurements and venograms, together with a bone biopsy obtained from the femoral neck and head. They found that core decompression (removal of a core or plug of bone) resulted in pain reduction, and in some cases this procedure retarded radiologic progression of the condition in the early stages.


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