AJR 2003; 181:1559-1563
© American Roentgen Ray Society
Partial Hawkins Sign in Fractures of the Talus: A Report of Three Cases
Jamshid Tehranzadeh1,
Eric Stuffman2 and
Steven D. K. Ross3
1 Department of Radiological Sciences, University of California, Irvine College
of Medicine, 101 The City Dr., S, Rte. 140, Orange, CA 92868-3298.
2 University of California, Irvine College of Medicine, Orange, CA
92868-3298.
3 Department of Orthopedic Surgery, University of California, Irvine, Orange, CA
92868-3298.
Received May 5, 2003;
accepted after revision June 19, 2003.
Address correspondence to J. Tehranzadeh.
Abstract
OBJECTIVE. We introduce the concept of the partial Hawkins sign in
three cases of talar neck fracture that are associated with incomplete
avascular necrosis. Our objective is to call attention to the intraosseous
blood supply of the talar body, which can be interrupted by fractures to
produce patterns of incomplete avascular necrosis.
CONCLUSION. We conclude that the Hawkins sign does not always have
to be complete. Fractures of the talus occasionally can lead to partial
avascular necrosis because of the disruption of end arteries within the body
of the talus, even without subluxation or dislocation. Early recognition of
the partial Hawkins sign should lead to MRI evaluation that can more readily
define the involvement of the talar body and assist the treating physician in
recommending when the patient can bear weight.
Introduction
The Hawkins sign [1]
indicates subchondral talar dome osteopenia and signifies intact vascularity.
The presence of this sign after a talar fracture implies that avascular
necrosis (AVN) of the talus has not occurred. The Hawkins sign appears as a
line of subchondral lucency, first visible between 6 and 8 weeks after the
injury and reflecting disuse osteopenia in vascularized bone. To the best of
our knowledge, this sign has primarily been described as an all-or-none
phenomenon in radiographs. Incomplete avascular necrosis associated with talar
fracture has been previously described
[2–4].
In an article classifying avascular necrosis in 21 patients with talar neck
fracture, Thordarson et al. [4]
observed two patients who had correlation between the abnormalities on MRI and
radiographs with an incomplete Hawkins sign. A partial Hawkins sign, however,
was not previously described as a distinct entity. We introduce the concept of
a partial Hawkins sign in three cases of talar fractures. The follow-up of
these cases with regard to the ensuing avascular necrosis will be discussed. A
hypothesis as to why these cases turned out as they did, based on what is
known about the blood supply of the talus, will be presented.
Materials and Methods
Our study consisted of three men 19–46 years old (mean, 29.6 years),
all of whom suffered a fracture of the talus. The first patient injured
himself while jumping on a trampoline; the other two patients injured
themselves while falling from heights. All were originally evaluated on
radiographs (Figs. 1A,
1B,
1C,
1D,
1E,
1F,
1G,
1H,
2A,
2B,
2C,
2D,
3). The first patient also had
a repeated radiograph 1 week after the initial radiograph (Figs.
1B,
1C). All three patients
ultimately required surgery, and we obtained a followup radiograph at
6–8 weeks to assess healing and the possibility of avascular necrosis.
The first patient was further evaluated on MRI (Figs.
1F,
1G,
1H). The ankle was examined
using an extremity surface coil while the patient was lying in a supine
position. MRI was performed with a 1.5-T superconductive magnet (Eclipse
model, Picker International, Cleveland, OH). T1-weighted images (TR/TE,
680/10.5) were obtained in coronal, sagittal, and axial planes. T2-weighted
images (3,700/100) were acquired in the axial plane, and T2-weighted images
with fat saturation (3,900/100) were obtained in coronal, sagittal, and axial
planes. The field of view was 14 cm; matrix, 192 x 256; thickness, 3 mm;
interval, 1 mm; and number of excitations, 2. Follow-up radiographs were
obtained.
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Fig. 1A. —19-year-old man who sustained nondisplaced talar fracture
while jumping on trampoline. Initial oblique lateral radiograph of left ankle
obtained after injury shows oblique fracture at neck of talus
(arrows).
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Fig. 1B. —19-year-old man who sustained nondisplaced talar fracture
while jumping on trampoline. Lateral radiograph of left ankle obtained 1 week
after injury shows bone resorption at fracture site (arrows).
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Fig. 1C. —19-year-old man who sustained nondisplaced talar fracture
while jumping on trampoline. Anteroposterior radiograph of left ankle obtained
1 week after injury shows bone resorption at fracture site
(arrows).
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Fig. 1D. —19-year-old man who sustained nondisplaced talar fracture
while jumping on trampoline. Anteroposterior radiograph obtained 6 weeks after
injury shows partial Hawkins sign (arrowheads) on lateral dome and
ischemic changes and cancellous screws on medial talar dome.
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Fig. 1E. —19-year-old man who sustained nondisplaced talar fracture
while jumping on trampoline. Lateral radiograph shows oblique fracture of
talar waist with avascular necrosis and cancellous screws in proximal
segment.
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Fig. 1F. —19-year-old man who sustained nondisplaced talar fracture
while jumping on trampoline. Coronal spin-echo T1-weighted image (TR/TE,
680/10.5) of ankle shows focal area of low signal with obliteration of cortex
on medial dome of talus, corresponding to ischemic area on radiograph. Note
magnetization artifact from cancellous screws.
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Fig. 1G. —19-year-old man who sustained nondisplaced talar fracture
while jumping on trampoline. Sagittal section on medial talar dome of
T1-weighted image (518/10.5) shows characteristic ischemic changes and
avascular necrosis on medial anterior talar dome. Note magnetization artifact
from cancellous screws.
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Fig. 1H. —19-year-old man who sustained nondisplaced talar fracture
while jumping on trampoline. Coronal fat-saturated T2-weighted image
(3,990/100) of ankle shows early phase of ischemia as bone marrow edema in
medial dome of the talus. Note magnetization artifact from cancellous
screws.
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Fig. 2A. —46-year-old man who fell 15 ft (4.5 m) and sustained
nondisplaced talar fracture. Initial anteroposterior radiograph of left ankle
after injury shows mildly comminuted intraarticular talar body fracture
(arrows).
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Fig. 2B. —46-year-old man who fell 15 ft (4.5 m) and sustained
nondisplaced talar fracture. Initial lateral radiograph of left ankle after
injury shows mildly comminuted intraarticular talar body fracture
(arrows).
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Fig. 2C. —46-year-old man who fell 15 ft (4.5 m) and sustained
nondisplaced talar fracture. Anteroposterior radiograph obtained 7 weeks after
injury shows partial Hawkins sign (arrowheads) on lateral dome and
ischemic changes and cancellous screws on medial side.
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Fig. 2D. —46-year-old man who fell 15 ft (4.5 m) and sustained
nondisplaced talar fracture. Lateral radiograph shows fracture of talar waist
with avascular necrosis and two cancellous screws on proximal talus.
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Fig. 3. —24-year-old man who fell and sustained eversion injury of
ankle with displaced vertical talar dome fracture. Anteroposterior radiograph
obtained 6 weeks after open reduction and internal fixation shows transverse
fracture of medial malleolus transfixed with cancellous screw. Note oblique
distal fibular fracture with plate-and-screw fixation. Note impaction fracture
of lateral tibial plafond and lateral talar dome. Vertical fracture of dome of
talus is transfixed with cancellous screw. Note partial Hawkins sign
(arrowheads) on medial and ischemic changes of talus on lateral talar
dome with osteochondral injury of tibial plafond and talar dome on same side.
Note mild osseous resorption around screw tip.
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Results
A fracture of the talus was noted on the initial radiograph of all three
patients. There was one case of talar neck fracture with no displacement; one
case of mildly comminuted intraarticular talar body fracture; and one case of
displaced vertical fracture of the talar body that was associated with
osteochondral impaction of the lateral talar dome, lateral tibial plafond, and
fracture of the distal fibula. All of our patients underwent surgery for open
reduction and internal fixation.
Follow-up radiographs obtained after 6–8 weeks revealed a partial
Hawkins sign in all three patients, which indicated incomplete avascular
necrosis of the talus. MRI in the patient with a talar neck fracture revealed
a focal area of low signal with obliteration of the cortex on the medial dome
of the talus on T1-weighted images and mixed bright signal and edema on
fat-saturated T2-weighted images corresponding to an ischemic area on the
radiograph. All of the original fractures eventually healed.
Discussion
Fractures of the talus are difficult injuries with guarded prognoses.
Leland Hawkins [1] classified
talar neck fractures in three categories based on the displacement and
resulting degree of subluxation or dislocation in the subtalar and tibiotalar
joints. A Hawkins class I fracture is a nondisplaced fracture, without
subluxation or dislocation, and has a 0–15% risk of developing AVN. A
Hawkins class II fracture is a displaced vertical talar neck fracture with a
subluxation or dislocation of the subtalar joint and a 20–50% risk of
AVN. A Hawkins class III fracture is a displaced fracture extending through
the talar neck with dislocation at both the subtalar and tibiotalar joints and
a 69–100% risk of AVN. The degree of displacement and dislocation is
thought to be the primary means of the interruption of blood supply and
therefore the risk for the development of AVN. Canale and Kelly
[5] added a rare class IV
category in which the talar neck fracture was associated with a dislocation of
the ankle and subtalar joint, with an additional dislocation or subluxation of
the head of the talus at the talonavicular joint. Class IV fractures had a
reported AVN rate of 100%. Hawkins described a radiographic sign at 6 weeks
after injury in which there was disuse osteopenia in the subchondral bone of
the talus as seen on radiographs of the ankle. This disuse osteopenia could
only occur if the bone in this area had adequate blood supply. In clinical
practice, the Hawkins sign is used not only in fractures on the talar neck but
also in fractures of the talar body because these injuries also have the
potential to interrupt the blood supply to portions of the talus.
The blood supply of the talus (Fig.
4) has been well described in the literature
[1,
6–8].
Despite variations in individual anatomy, five major vessel sources enter the
talus in the area of the talar neck. The extraosseous blood supply comes from
three arteries: the posterior tibial artery, the anterior tibial artery, and
the perforating peroneal artery. The main artery supplying blood to the body
of the talus is the artery of the tarsal canal
[9]. An anastomotic ring around
the inferior neck of the talus is formed by the artery of the tarsal canal and
the artery of the tarsal sinus, but the body of the talus tends to have
limited intraosseous anastomosis so that interruption of any vessel may lead
to areas of bone necrosis in the distribution of that vessel. The medial body
of the talus is supplied by the artery of the tarsal canal, which is a branch
of the posterior tibial artery, and the deltoid branch, which originates from
the posterior tibial artery or the artery of the tarsal canal. The perforating
peroneal artery and the anterior tibial artery contribute branches to the
sinus tarsi region and the lateral portion of the talar body. The head of the
talus is supplied by branches of the anterior tibial artery; most blood
supplied to the head and neck of the talus arises from the dorsalis pedis
artery. The intraosseous blood supply is a network of three or four
anastomoses throughout the body of the talus. The branches of these
anastomoses originate mainly from the artery of the tarsal canal
[9].
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Fig. 4. —Schematic drawing showing arterial supply of talus.
Extraosseous blood supply comes from three arteries: posterior tibial artery,
anterior tibial artery, and perforating branch of peroneal artery. Main
arterial supply to talar body is from artery of tarsal canal, which is a
branch of posterior tibial artery and contains deltoid branch. It also
supplies portion of anastomotic ring around talus with help of artery of
tarsal sinus. Each of these arteries produces perforating vessels to supply
specific areas of talar body.
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In Hawkins class I fractures with no subluxation of the ankle and subtalar
joint, only the blood supply entering through the neck is disrupted. In
Hawkins class II fractures, with a subluxed or dislocated subtalar joint, the
artery of the tarsal canal and the dorsal blood supply from the neck are often
disrupted. The medial blood supply also can be disrupted. In Hawkins class III
vertical talar neck fractures with the body dislocated from the ankle or
subtalar joints, the three main sources of blood supply are often damaged. In
Hawkins class IV injuries with a displaced vertical talar neck fracture and an
associated dislocation of the ankle, subtalar joint, and talar head, all three
main sources of blood are disrupted
[9].
The Hawkins sign, which classically begins in the medial subchondral bone
of the talar dome and progresses laterally, appears between 6 and 8 weeks
after a fracture. Open anatomic reduction and internal fixation within
6–8 hours result in lower incidence of AVN
[2,
10]. Complete
revascularization after surgery takes 6 months to 3 years. The Hawkins sign is
highly sensitive but less specific; its absence cannot predict avascularity
[9].
Morris [3] indicates that
when partial AVN occurs, it preferentially involves the lateral portion of the
talus. This predilection is explained by the fact that most of the blood
supply comes from the medial side via the artery of the tarsal canal and by
the protection afforded to this vessel by its association with the deltoid
ligament. To further illustrate this point, Dunn et al.
[11] showed that feet
dislocated in an anterior direction experienced a high rate of AVN, whereas
medial dislocations resulted in preservation of the blood supply via the
medial vessels and a correspondingly low risk of AVN. Although there is more
circulation and better protection on the medial side of the talus, our
findings in two cases of medial avascular necrosis show that these vessels can
be interrupted and result in incomplete AVN.
The Hawkins sign has been helpful in assessing the talus for bone necrosis
after fractures of the talar neck; in clinical practice, this use has been
expanded to the fractures of the talar body. Talar neck fractures are
extraarticular, occurring in the anatomic neck of the talus and not involving
the articular surfaces. Talar body fractures involve the articular surfaces of
the ankle and the subtalar joints and may have a higher incidence of
interruptions of the interosseous arterial supply. When treating fractures of
the talus that have some avascular necrosis, there is no consensus in the
literature regarding the amount of time patients must not bear weight to
protect against segmental collapse as the bone is being revascularized. In an
attempt to stratify the risk of late collapse on the basis of the percentage
of the talar body involved, Thordarson et al.
[4] devised a classification of
MRI signal changes in fractures of the talar neck in which two of 21 patients
had incomplete Hawkins signs. They also gave recommendations regarding how
long patients should not bear weight on their injuries.
Our cases show that partial avascular necrosis occurs in talar body
fractures and that a partial Hawkins sign can be indicative of this process.
Even without joint dislocation or large amounts of displacement, these talar
body fractures can lead to segmental avascular necrosis because of the
location of the fracture lines that interrupt the intraosseous end arteries.
Our study also suggests that early visualization of a Hawkins sign can be an
indication for an MRI evaluation to assess the percentage of involvement and
help guide appropriate treatment.
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Abstract
Introduction
