PATHOPHYSIOLOGY,
PATHOGENESIS, AND
PATHOLOGY OF BLOOD CIRCULATION
In:
Blood Vessels And Lymphatics In Organ Systems
by
D. W. Lennox and D. S. Hungerford
This
material has been published in Blood Vessels and Lymphatics
in Organ Systems, edited by David I. Abramson and Philip
B. Dorbin, the only definitive repository of the content that
has been certified and accepted after peer review. Copyright
and all rights therein are retained by Elsevier Science (USA).
This material may not be copied or reposted without explicit
permission.
Circulatory
abnormalities of bone blood vessels underlie a number of clinical
entities. Several of the better known of these are discussed
below.
1.
EPIPHYSITIDIES (APOPHYSITIDIES)
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.
2.
FRACTURES AND DISLOCATIONS
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.
5.
ISCHEMIC NECROSIS OF THE FEMORAL HEAD
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.
References
- Arlet,
J., and Ficat, P. (1964). Forage-biopsie de la tête
femorale dans l'ostéonecrose primitive; observations
histopathologiques portant sur huit cas. Rev. Rheum.
Mal. Osteo-Articulaires 31, 256-264.
- Borgsmiller,
W.K., Whiteside, L.A., Goldsand, E.M., and Lange, D.R.
(1980). Effect of hydrostatic pressure in the hip joint
on proximal femoral epiphyseal and metaphyseal blood flow.
Proc. Orthoped. Res. Soc. 5, 23.
- Brookes,
M., and Gallanaugh, S.C. (1975). Circulatory depression
in bone after acrylic implantation. Clin. Orthop. Relat.
Res. 107, 274-276.
- Chandler,
F.A. (1948). Coronary disease of the hip. J. Int. Coll.
Surg. 11, 34-36.
- Cruess,
R.L., Ross, D., and Crawshaw, E. (1975). The etiology
of steroid induced avascular necrosis of bone. Clin.
Orthopo. Relat. Res. 113, 178-183.
- Duncan,
C.P., and Shim, S.S. (1977). Blood supply to the head
of the femur in traumatic hip dislocation. Surg. Gynecol.
Obstet. 144, 185-191.
- Ficat,
P., and Arlet, J. (1968). Diagnostic de l'ostéonecrose
femoro-capitales primitive au stade I (stade pre-radiologique).
Rev. Chir. Orthoped. 54, 637-648.
- Fisher,
D.E. (1978). The role of fat embolism in the etiology
of corticosteroid-induced avascular necrosis. Clinical
and experimental results. Clin. Orthop. Relat. Res.
130, 68-80.
- Göthman,
L. (1961). Vascular reactions in experimental fractures.
Microangiographic and radioisotope studies. Acta Chir.
Scand., Suppl. 284, 1-34.
- Heikkinen,
E., Puranen, J., and Suramo, I. (1976). The effect of
intertrochanteric osteotomy on the venous drainage of
the femoral neck in Perthes' disease. Acta Orthop.
Scand. 47, 89-95.
- Heikkinen,
E., Lanning, P., Suramo, I., and Puranen, J. (1980). The
venous drainage of the femoral neck as a prognostic sign
in Perthes' disease. Acta Orthoped. Scand. 51,
501-503.
- Hungerford,
D.S. (1979). Bone marrow pressure, venography, and core
decompression in ischemic necrosis of the femoral head.
Proc. Am. Hip Soc. Meet. 7th, St. Louis, pp. 218-237.
- Hungerford,
D.S. (1983). Treatment of ischemic necrosis of the femoral
head. In "Surgery of the Musculoskeletal System"
(C. McCollister Evarts, ed.). Vol. 3, pp. 6:5-6:29. Churchill
Livingstone, Edinburgh and London.
- Hungerford,
D.S., and Zizic, T.M. (1978). Alcohol associated ischemic
necrosis of the femoral head. Clin. Orthop. Relat.
Res. 130, 144-153.
- Jacqueline,
F., and Rabinowitz, T.M. (1973). Lesions de la hanche
secondaires a la fracture du col du femur. Proc. Int.
Symp. Circ. Bone, 1st, 1973 p. 283.
- Jones,
J.P., Jr. (1971). Alcoholism, hypercortisonism, fat embolism
and osseous avascular necrosis. In "Idiopathic Ischemic
Necrosis of the Femoral Head in Adults" (W.M. Zinn,
ed.), pp. 112-132. Thieme, Stuttgart.
- Jones,
J.P., Jr., and Sakovich, L. (1966). Fat embolism of bone:
A roentgenographic and histological investigation with
use of intraarterial lipiodol in rabbits. J. Bone.
Jt. Surg., Am. Vol. 48-A, 149-164.
- Launder,
W.J., Hungerford, D.S., and Jones, L.H. (1981). Hemodynamics
of the femoral head. J. Bone Jt. Surg., Am. Vol.
63-A, 442-447.
- McFarland,
P.H., and Frost, H.M. (1961). A possible new cause for
aseptic necrosis of the femoral head. Henry Ford Hosp.
Med. Bull. 9, 115-122.
- Michelsen,
K. (1967). Pressure relationships in the bone marrow vascular
bed. Acta Physiol. Scand. 71, 16-29.
- Olerud,
S., and Danckwardt-Lilliestrom, G. (1968). Fracture healing
in compression osteosynthesis in the dog. J. Bone Jt.
Surg., Br. Vol. 50B, 844-851.
- Ponseti,
I.V. (1956). Legg-Perthes' disease: Observations on pathological
changes in two cases. J. Bone Jt. Surg., Am. Vol.
38-A, 739-750.
- Rand,
J.A., An, Kai Nan, Chao, E.Y., and Kelly, P.J. (1981).
A comparison of the effect of intramedullary nailing and
compression-plate fixation on fracture site blood flow
and fracture union. J. Bone Jt. Surg., Am. Vol.
63-A, 427-441.
- Rhinelander,
F.W. (1974). Tibial blood supply in relation to fracture
healing. Clin. Orthop. Relat. Res. 105,
34-81.
- Schoenecker,
P.D., Bitz, D.M., and Whiteside, L.A. (1978). The acute
effect of position of immobilization on capital femoral
epiphyseal blood flow. J. Bone Jt. Surg., Am. Vol.
60-A, 899-904.
- Suramo,
I., Puranen, J., Heikkinen, E., and Vuorinen, P. (1964).
Disturbed patterns of venous drainage of the femoral neck
in Perthes' disease. J. Bone Jt. Surg., Br. Vol.
56B, 448-453.
- Tachdjian,
M.O., and Grana, L. (1968). Response of the hip joint
to increased intra-articular hydrostatic pressure. Clin.
Orthop. Relat. Res. 6, 199-212.
- Trueta,
J., and Cavadias, A.X. (1955). Vascular changes caused
by the Kuntscher type of nailing. An experimental study
in the rabbit. J. Bone Jt. Surg., Br. Vol. 37B,
492-505.
- Whiteside,
L.A., Ogata, K., Lesker, P., and Reynolds, F.C. (1978).
The acute effect of periosteal stripping and medullary
reaming on regional bone blood flow. Clin. Orthop.
Relat. Res. 131, 266-272.
- Wilkes,
C.H., and Visscher, M.B. (1975). Some physiological aspects
of bone marrow pressure. J. Bone Jt. Surg., Am. Vol.
57-A, 49-57.
- Woodhouse,
C.F. (1962). Anoxia of the femoral head. Surgery
52, 55-62.
- Woodhouse,
C.F. (1964). Dynamic influences of vascular occlusion
affecting the development of avascular necrosis of the
femoral head. Clin. Orthop. Relat. Res. 32,
119-129.
Copyright
1984, Elsevier Science (USA). All rights reserved.
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PATHOLOGY OF BLOOD CIRCULATION In: Blood Vessels And Lymphatics In Organ Systems by
D. W. Lennox and D. S. Hungerford
This
material has been published in Blood Vessels and Lymphatics
in Organ Systems, edited by David I. Abramson and Philip
B. Dorbin, the only definitive repository of the content that
has been certified and accepted after peer review. Copyright
and all rights therein are retained by Elsevier Science (USA).
This material may not be copied or reposted without explicit
permission.
Circulatory abnormalities of bone blood vessels underlie a number of clinical entities. Several of the better known of these are discussed below. 1. EPIPHYSITIDIES (APOPHYSITIDIES) 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. 2. FRACTURES AND DISLOCATIONS 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. 5. ISCHEMIC NECROSIS OF THE FEMORAL HEAD 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. References
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1984, Elsevier Science (USA). All rights reserved.
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