DOI:10.2214/AJR.05.0245
AJR 2006; 187:W67-W76
© American Roentgen Ray Society
Calcific Myonecrosis: Keys to Recognition and Management
Helena M. O'Dwyer1,
Nizar A. Al-Nakshabandi1,
Khamis Al-Muzahmi1,
Anthony Ryan1,
John X. O'Connell2 and
Peter L. Munk1
1 Department of Radiology, Vancouver General Hospital, 855 West 12th Ave.,
Vancouver, BC, Canada, V5Z 1M9.
2 Department of Pathology, Surrey Memorial Hospital, Surrey, BC, Canada.
Received February 12, 2005;
accepted after revision April 20, 2005.
Address correspondence to P. L. Munk,
(plmunk{at}interchange.ubc.ca).
WEB
This is a Web exclusive article.
Abstract
OBJECTIVE. Calcific myonecrosis masses can become quite large and
worrisome for malignancy. The key to recognition is a combination of
radiologic imaging features and remote clinical history of injury associated
with compartment syndrome or vascular or neurologic compromise.
CONCLUSION. This article will highlight importance of correct
diagnosis by indentifying the severe and devastating complications following
inappropriate management.
Keywords: calcific myonecrosis • compartment syndrome • musculoskeletal imaging • soft-tissue neoplasms
Introduction
Calcific myonecrosis is a rare post-traumatic entity characterized by
latent formation of a dystrophic calcified mass occurring almost exclusively
in the lower limb. The condition was initially described by Gallie and
Thompson in 1960 [1]. This rare
disorder is characterized by a slowly enlarging, usually painful soft-tissue
mass in the anterior compartment of the lower limb. Although not well
understood, it is postulated that these lesions most likely result from
posttraumatic ischemia and cystic degeneration of the muscle. Of 36 cases
currently reported in the English language literature, all patients could
recall an injury with either compartment syndrome or neurovascular sequelae,
particularly peroneal nerve injury, occurring 10-64 years before in the
affected limb
[1-12].
Pathophysiology
Ischemic contractures and sensory deficits are known complications of
compartment syndrome. Calcific myonecrosis, however, is a rare sequel. The
current hypothesis is that an initial compartment syndrome decreases the
circulation within a limited space resulting in necrosis and fibrosis
[2]. Over time, repeated
intralesional hemorrhage causes the mass to enlarge and calcify
[3]. Late focal enlargement of
the mass may be caused by herniation through the muscle fascia.
The most common site of compartment syndrome is the lower leg, with the
anterior compartment the most frequently affected, followed by the lateral
compartment and the deep posterior compartment
[13]. This entity can also
occur in either of the two compartments of the forearm and any of the three
compartments of the thigh. A diagrammatic illustration of compartment syndrome
involving the lower limb is provided in Figures
1A,
1B,
1C,
1D, and
1E.
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Fig. 1C —Compartment syndrome Cross-sectional diagram through lower
limb shows inflammatory response after injury (fibular fracture), with
increased capillary permeability, leading to swelling, edema, pain, erythema,
and heat. It is illustrated here as swelling of anterolateral muscle
compartments of lower limb (arrowheads).
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Fig. 1E —Compartment syndrome When acute compartment syndrome goes
unrecognized or is poorly managed, increased intracompartmental pressure
results in decreased tissue perfusion, indicated by darkening and volume loss
of anterolateral musculature. Blood vessels collapse as interstitial pressure
overcomes intravascular pressure and hypoxic injury ensues with local tissue
ischemia, intracellular edema, anaerobic metabolism, and irreversible cell
damage.
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Imaging Features
Radiographs typically show a fusiform mass with peripherally oriented
plaquelike amorphous calcifications (Figs.
2A and
2B). The calcifications are
usually linear in orientation and sheetlike, and they present within the
entire muscle or compartment
[2] (Figs.
3A,
3B,
4A,
4B, and
4C), with mixed areas of
radiolucency (Fig. 5A). Smooth
bony erosions may be present with minimal periosteal reaction
[3,
5-7].
Occasionally, the erosions may be extensive and worrisome for a soft-tissue
tumor, in which case MRI may aid in differentiating this entity from a
sarcoma.
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Fig. 2A —68-year-old man with leg mass of gradual onset and history of
tibial fracture and compartment syndrome 30 years previously. Anteroposterior
(A) and lateral (B) radiographs show calcific myonecrosis
involving lateral midcalf compartment, with large, well-defined ovoid
peripherally calcified component; note old tibia fracture line (A)
(arrow).
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Fig. 2B —68-year-old man with leg mass of gradual onset and history of
tibial fracture and compartment syndrome 30 years previously. Anteroposterior
(A) and lateral (B) radiographs show calcific myonecrosis
involving lateral midcalf compartment, with large, well-defined ovoid
peripherally calcified component; note old tibia fracture line (A)
(arrow).
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Fig. 3A —49-year-old man with ankle pain. Anteroposterior (A)
and lateral (B) radiographs of ankle show moderate amounts of
calcification oriented in thick sheetlike or linear pattern, especially at
periphery in both anterior and posterior muscular compartments.
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Fig. 3B —49-year-old man with ankle pain. Anteroposterior (A)
and lateral (B) radiographs of ankle show moderate amounts of
calcification oriented in thick sheetlike or linear pattern, especially at
periphery in both anterior and posterior muscular compartments.
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Fig. 4A —38 year-old-cyclist who suffered vascular injuries to
anterior tibial artery and subsequent compartment syndrome when hit by truck
as teenager, now presenting with painless enlarging mass. Anteroposterior
(A) and lateral (B) radiographs show sheetlike calcification in
anterior and lateral compartments of lower limb consistent with calcific
myonecrosis. C, Axial CT (width, 2000 H; level, 250 H) defines
peripheral nature of lobular calcification.
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Fig. 4B —38 year-old-cyclist who suffered vascular injuries to
anterior tibial artery and subsequent compartment syndrome when hit by truck
as teenager, now presenting with painless enlarging mass. Anteroposterior
(A) and lateral (B) radiographs show sheetlike calcification in
anterior and lateral compartments of lower limb consistent with calcific
myonecrosis. C, Axial CT (width, 2000 H; level, 250 H) defines
peripheral nature of lobular calcification.
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Fig. 4C —38 year-old-cyclist who suffered vascular injuries to
anterior tibial artery and subsequent compartment syndrome when hit by truck
as teenager, now presenting with painless enlarging mass. Axial CT (width,
2000 H; level, 250 H) defines peripheral nature of lobular calcification.
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Fig. 5A —75-year-old man with remote history of tibia fracture in his
teenage years. Patient was referred to rule out soft-tissue sarcoma.
Anteroposterior view of tibia and fibula shows peripheral fusiform mass with
sheetlike calcification mixed with areas of radiolucency, which is
characteristic of calcific myonecrosis (biopsy-proven), causing erosion of
adjacent tibia (arrow). Note old healed mid-tibia fracture
(arrowhead).
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CT more readily shows compartmental involvement. The fusiform mass often
has a cystic lobulated component that sometimes erodes into bone, presumably
because of a chronic pressure effect (Figs.
2D and
5B). Fluid calcium levels may
be seen representing communication between the necrotic muscle and the tendon
sheath [7,
8]. Associated reactive
periostitis of the underlying bone may be present; however, bone marrow
involvement has not been reported.
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Fig. 2D —68-year-old man with leg mass of gradual onset and history of
tibial fracture and compartment syndrome 30 years previously. Axial CT image
(bone window setting: width, 2000 H; level, 250 H) shows peripheral pattern of
calcification clearly. Mass is abutting lateral aspect of fibula and causing
thinning (C) and complete erosion (D) of adjacent cortex. Healed
mid-diaphyseal tibial fracture is again noted.
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Fig. 5B —75-year-old man with remote history of tibia fracture in his
teenage years. Patient was referred to rule out soft-tissue sarcoma.
Unenhanced CT of lower limb (width, 2000 H; level, 500 H) shows cystic mass
with plaquelike calcification replacing anterior muscular compartment of leg
and causing pressure erosion of tibia (arrowheads) indicating chronic
nature of this mass.
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MRI shows a well-circumscribed mass with heterogeneous signal on
T2-weighted sequences (Fig.
5E) and a homogeneous intermediate signal throughout the central
fluid region on T1-weighted images (Fig.
5C). The liquid center has a high signal on T2-weighted sequences
(Fig. 5D). These features are
present along the expected course of a muscle or compartment group. The mass
does not show enhancement after gadolinium administration, presumably
secondary to extensive necrosis
[7,
14]. Subtle feathery
periosteal bone reaction is better appreciated on STIR sequences compared with
CT (Fig. 5F). Because of the
calcium content, a susceptibility artifact represented by blooming can be
appreciated on the gradient echo images
(Fig. 5G).
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Fig. 5E —75-year-old man with remote history of tibia fracture in his
teenage years. Patient was referred to rule out soft-tissue sarcoma. Axial
T2-weighted fast spin-echo sequence (7,000/92) more inferiorly shows lobulated
mass with number of cystic components abutting tibia and thinning cortex.
Focal curvilinear areas of low-signal-intensity within mass correspond to
dense fibrosis and areas of calcification (arrows).
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Fig. 5C —75-year-old man with remote history of tibia fracture in his
teenage years. Patient was referred to rule out soft-tissue sarcoma. Axial
T1-weighted image of leg (TR/TE, 450/11) shows well-circumscribed mass of low
signal intensity replacing muscle in anterior compartment between tibia and
fibula. Note central low-signal-intensity dots (arrows) and
peripheral low-signal-intensity rim representing calcification
(arrowheads).
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Fig. 5D —75-year-old man with remote history of tibia fracture in his
teenage years. Patient was referred to rule out soft-tissue sarcoma. Axial
T2-weighted image (4,460/107) at proximal diaphyseal level shows
well-circumscribed mass (arrow) of high T2 signal-intensity because
of cystic necrosis centrally and liquefaction of muscle in anterior
compartment.
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Fig. 5F —75-year-old man with remote history of tibia fracture in his
teenage years. Patient was referred to rule out soft-tissue sarcoma. Coronal
STIR (4,500/45) of leg shows subtle bone marrow edema in tibia
(arrow), which is likely pressure effect from masslike calcific
myonecrosis.
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Fig. 5G —75-year-old man with remote history of tibia fracture in his
teenage years. Patient was referred to rule out soft-tissue sarcoma. Coronal
gradient echo (415/12; gradient/20) shows blooming from susceptibility
artifact and related to extensive calcification or hemosiderin in muscle
(arrows).
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Holobinko et al. [15]
reported increased uptake in the affected leg during the soft-tissue phase and
in the tibia and fibula throughout the bone phase during a triphasic
99mTc bone scan. Laboratory studies, including erythrocyte
sedimentation rate and alkaline phosphatase, are invariably normal.
Operative findings include necrosis of the muscle and replacement with
cysts of yellow-brown pasty material (Fig.
6). The neurovascular bundle (peroneal nerve) is usually not
identifiable. There may be erosion of the adjacent bone. The cyst wall
consists of elongated calcific shards of debris, which correspond to the
platelike calcification on imaging
[2]. Microscopically the wall
of the cyst is composed of hypocellular fibrous tissue with focal aggregates
of hemosiderinladen macrophages. Histopathologic examination reveals
cholesterol clefts, fibrin, and organizing thrombus comprising the cyst wall.
The cystic contents are an admixture of necrotic muscle and debris composed of
cholesterol, fibrin, and recent hemorrhage with embedded fragments of calcific
material (Fig. 7)
[3,
8-10].
Differential Diagnosis
The radiologic features described should allow proper differentiation of
calcific myonecrosis from neoplastic or inflammatory lesions based on the
characteristic peripheral calcification and central liquefaction. The
differential diagnosis of calcific myonecrosis is a calcified soft-tissue
mass. This includes hematoma, synovial sarcoma, epithelioid sarcoma,
soft-tissue osteosarcoma, and parosteal osteosarcoma
[4,
6,
9]. The differential diagnosis
for calcification in soft tissue includes myositis ossificans, posttraumatic
pseudoaneurysms, dermatomyositis/polymyositis, tumoral calcinosis, and
diabetic myonecrosis [9,
10].
A hematoma usually involves a history of recent trauma. Sarcomas tend to
affect young adults, are very aggressive in nature, enhance with contrast, are
not confined to a single muscle group, and do not usually have peripheral
calcification [2]. The
ossification pattern in parosteal osteosarcoma is different from that of
calcific myonecrosis, proceeding from the base of the lesion to its periphery.
The mass is usually attached in a sessile pattern to the external cortex,
which itself may be thickened. Bone erosion is rare and usually only seen in
recurrent tumors. Lique-faction of the center of a calcified soft-tissue
neoplasm is unusual.
Myositis ossificans is a benign condition of heterotopic nonneoplastic bone
formation in soft tissue, which doesn't manifest clinically as a chronic
expanding mass [3]. It is
usually self-limiting, and spontaneous resolution can occur. The pattern of
calcification varies with maturation of the lesion. Initially a soft-tissue
mass is present, with faint periosteal reaction in adjacent bone. At 1 month,
floccular calcification occurs predominately in the periphery of the lesion,
with the center remaining relatively radiolucent, similar to calcific
myonecrosis. At approximately 8 weeks, a lacy pattern of new bone with a sharp
peripheral cortex is formed and a more prominent periosteal reaction is seen.
The mass continues to enlarge, with a zonal pattern of maturation, resulting
in an eggshell appearance abutting adjacent bone. From 6 months onward, the
mass usually shrinks away from the cortex, resulting in a dense ossified mass
[15]. Posttraumatic
pseudoaneurysms are rarely as extensive and heavily calcified as calcific
myonecrosis and enhance avidly after IV contrast, and calcification is usually
in an eggshell pattern.
Dermatomyositis and polymyositis have typical clinical and systemic
manifestations. Calcification in dermatomyositis doesn't often occur in adults
with the disease, but children with dermatomyositis may develop calcium
deposits years after the disease starts. The deposits generally develop in the
shoulder, pelvis, hip, calf, and thigh and may severely limit motion. The
masses that develop under the skin can rupture, and the calcium salts may
drain. These disease entities can be differentiated from calcific myonecrosis
by the widespread pattern of calcification. Tumoral calcinosis most frequently
involves large joints in young adults, especially men and the black
population. Radiographs reveal circular or oval well-demarcated masses of
calcium at articulations, especially the hips and shoulders, but also the
elbows, knees, and ankles. A lobulated inhomogeneous appearance is
characteristic, and subadjacent bone erosion may be evident. Radiolucent
linear bands separate the calcific foci, and the resulting appearance has been
likened to chicken wire. Fluid levels are occasionally seen. The periarticular
location and different calcification pattern should allow radiologic
differentiation from calcific myonecrosis. Long-term diabetic myonecrosis can
develop calcifications, so a history of diabetes mellitus must be excluded
[2,
3,
4,
10].
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Fig. 2C —68-year-old man with leg mass of gradual onset and history of
tibial fracture and compartment syndrome 30 years previously. Axial CT image
(bone window setting: width, 2000 H; level, 250 H) shows peripheral pattern of
calcification clearly. Mass is abutting lateral aspect of fibula and causing
thinning (C) and complete erosion (D) of adjacent cortex. Healed
mid-diaphyseal tibial fracture is again noted.
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Fig. 2E —68-year-old man with leg mass of gradual onset and history of
tibial fracture and compartment syndrome 30 years previously. Coronal gradient
MR sequences (TR/TE, 600/200 msec; gradient/20) show oval mass (D)
abutting anterolateral aspect of mid-fibular diaphysis, paralleling radiograph
findings. Peripheral rim of low signal intensity shows minimal blooming
artifact (arrowheads, E) consistent with peripheral
calcification. Mass is causing swelling of overlying skin. A coronal image
more anteriorly (F) shows old tibial fracture and inferior aspect of
peripherally calcified mass.
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Fig. 2F —68-year-old man with leg mass of gradual onset and history of
tibial fracture and compartment syndrome 30 years previously. Coronal gradient
MR sequences (TR/TE, 600/200 msec; gradient/20) show oval mass (D)
abutting anterolateral aspect of mid-fibular diaphysis, paralleling radiograph
findings. Peripheral rim of low signal intensity shows minimal blooming
artifact (arrowheads, E) consistent with peripheral
calcification. Mass is causing swelling of overlying skin. A coronal image
more anteriorly (F) shows old tibial fracture and inferior aspect of
peripherally calcified mass.
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Hemophilic pseudotumor and synovial cysts in rheumatoid arthritis may also
present on MRI as cystic masses with rim susceptibility artifacts. Although
accurate diagnosis often depends on knowledge of the patient's underlying
condition, the more classical appearances of hemophilia with periarticular
osteoporosis, multiple subchondral cysts, overgrowth of the epiphyses, and
widening of the intercondylar notch can aid differentiation. MRI is useful to
document whether the cyst communicates with an adjacent joint in rheumatoid
arthritis. The rim susceptibility artifact is caused by the presence of
fibrous tissue, hemosiderin, or both in the wall of the pseudotumor and dense
collagen composing the wall of a synovial cyst. The soft-tissue masses in
hemophilic pseudotumor and synovial cysts in rheumatoid arthritis rarely
calcify [16].
Literature Review
There are currently 36 cases of calcific myonecrosis discussed in the
literature, 25 of which involve the lower limb. More recently, Larson et al.
[11] described a case
involving the forearm. All patients reported a previous injury in the affected
limb occurring 10-64 years before diagnosis of the mass, predominately
fractures, but blunt trauma, crush injury, knee ligament injury, and gunshot
wounds have also been implicated. Compartment syndrome and nerve injury,
particularly peroneal, appear to be prerequisites for development of calcific
myonecrosis.
Review of the available literature suggests that approximately 40% of
patients complain of pain but wait between 6 weeks and 15 years before seeking
medical attention. The anterolateral compartment of the calf was predominately
affected. More recent reports reveal other locations and associations with
calcific myonecrosis. Ryu et al.
[7] presented an unusual case
of calcific tenosynovitis of the extensor hallucis longus muscle associated
with calcific myonecrosis of the tibialis anterior muscle 47 years after a
right fibula and tibial condyle fracture. Holobinko et al.
[12] reported previously an
undescribed extension of calcific myonecrosis involving the muscle
compartments of the foot in a 37-year-old man after a right tibia fracture.
Larson et al. [11] reported
previously undescribed calcific myonecrosis in the left forearm of a
60-year-old man, 55 years after a crush injury, who presented with a painless
expansive left forearm mass.
Ten cases in the literature reported infectious complications after biopsy,
manifested by a chronic discharging sinus; nine required serial
débridements, with two of the nine requiring muscle flap grafts, and
one patient required an above-knee amputation
[2,
4-6,
9,
17,
18]. De novo infection before
any intervention or surgical procedures has also occurred. Snyder et al.
[19] reported culture-positive
Staphylococcus aureus from a draining sinus adjacent to the fibula
before surgical intervention. Holobinko et al.
[12] also described de novo
superinfection associated with preexisting calcific myonecrosis in two
patients. Presence of infection should not deter the appropriate treatment
plan, but it does necessitate consideration of IV antibiotic treatment.
Prognosis and Management
Calcific myonecrosis is a benign entity, although often uncomfortable and
disfiguring. Failure to recognize this lesion at imaging and with traditional
practice prompts a biopsy, occasionally with devastating results. We propose
calcific myonecrosis should be considered as a don't-touch lesion. If a
patient's request or discomfort demands intervention, biopsy should only be
done when complete surgical excision is contemplated. Several reports in the
literature describe chronic draining sinus formation, which requires extensive
surgery and secondary infection as after-biopsy sequelae. One case
necessitated below-knee amputation
[18]. There are also more
recent reports of de novo infection arising in these masses
[12].
Conclusion
Calcific myonecrosis can be confidently diagnosed when a mass in a single
muscle or muscle compartment with characteristic distinct peripheral,
plaquelike calcifications is present. Biopsy should be avoided because of the
high risk of complications and the possibility for conversion of sterile
necrotic tissue into an abscess. Conservative management is advocated, but, if
necessary for esthetics or symptom relief, complete surgical excision and flap
coverage is appropriate.
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Fig. 5H —75-year-old man with remote history of tibia fracture in his
teenage years. Patient was referred to rule out soft-tissue sarcoma.
Diagrammatic illustration of ischemia after poorly managed compartment
syndrome leads to extensive necrosis, fibrosis, and loss of function indicated
by atrophy of musculature. In rare cases, dystrophic calcification
(arrowhead) and liquefaction, which comprise entity called calcific
myonecrosis, occur as late sequelae. Cystic lobulated component
(asterisk) may cause chronic pressure erosion (arrow) of
adjacent bone (tibia).
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Fig. 5I —75-year-old man with remote history of tibia fracture in his
teenage years. Patient was referred to rule out soft-tissue sarcoma.
Anteroposterior diagram shows cystic degeneration and fibrosis of muscle
(arrow). Repeated intralesional hemorrhage causes mass to enlarge and
become herniated through muscle fascia, often prompting patient's clinical
presentation with enlarging mass.
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Acknowledgments
We would like to acknowledge Mike Mudri for his assistance preparing images
for this manuscript and Lorie Marchinkow for his illustrative diagrams of
compartment syndrome and calcific myonecrosis.
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Abstract
Introduction
