Document 62579

Hematogenous Osteomyelitis of the
Calcaneus in Children: Surgical Treatment
and Use of Implanted Antibiotic Beads
Hematogenous osteomyelitis is a relatively uncommon disorder that may prove elusive to early
diagnosis and treatment. Metaphyseal long bones are commonly involved and the calcaneus is rarely
affected. A high index of suspicion should be maintained regarding the pediatric patient with pain out
of proportion to a minor injury. Delay in the diagnosis of hematogenous osteomyelitis in the pediatric
patient can result in irreversible growth disturbances and devastating sequelae. The authors present a
typical case history with an unusual postoperative course and a review of the clinical aspects and
surgical treatment of hematogenous calcaneal osteomyelitis in a child.
Robert Kelsey, DPM, AACFAS1
Alex Kor, DPM, FACFAS2
Flavio Cordano, DPM, AACFAS
Osteomyelitis is a bacterial infection affecting the
skeletal system. Waldvogel et at. described three distinct
types of bone infection (1): osteomyelitis from hematogenous spread, osteomyelitis from direct extension of a
superficial infection, and osteomyelitis because of vascular insufficiency. Hematogenous osteomyelitis occurs
as a result of vascular dissemination of a distant bacterial
process and is always preceded by a period of bacteremia. Hematogenous osteomyelitis affects people of all
ages, but peak incidence occurs in childhood and in
adults older than 50 years of age (2-4). Children aged 8
to 12 have perhaps the highest incidence (4). The
metaphyses of long bones are the most common sites for
hematogenous osteomyelitis in children (3-5). Borris
and Helleland described osteomyelitis of the calcaneus
as a rare condition (6). Several reports identify the
calcaneus as involved in 5 to 8% of all cases of osteomyelitis (1, 7, 8). Misdiagnosis of hematogenous osteomyelitis in children is common because of nonspecific
signs and symptoms and variable presentation (1-5).
Delays in diagnosis may result in damage to growth
plates and long-term sequelae (6).
From the Department of Podiatric Surgery, Welborn Baptist Hospital, Evansville, Indiana.
1 Submitted while second-year resident. Address correspondence
to: Bini Hospital Medical Center, 855 Hospital Road, Suite 401, Silvis,
IL 61282.
2 Diplomate, American Board of Podiatric Surgery.
1067-2516/95/3406-0547$3.00/0
Copyright © 1995 by the American College of Foot and Ankle
Surgeons
Etiology
Hematogenous osteomyelitis occurs secondary to vascular spread of bacteria from a distant primary focus. In
children, the metaphyseal area of bone is the most
common site for hematogenous osteomyelitis (3-5).
Most likely, this is because of the vascular supply to this
area and the immaturity of tissues near the epiphyseal
growth plates. These immature tissues may be more
susceptible to infection because of an inherent lack of
immune mechanisms (4).
With respect to the calcaneus, the arterial blood
supply to the apophyseal growth plate is through a small
metaphyseal network of capillaries fed by branches of
nutrient arteries. These capillaries drain into a venous
sinusoidal network and ultimately to larger venules and
veins (4). Because of changes in the diameter of these
blood vessels, the flow of blood may be turbulent,
allowing transient bacteria to colonize. Also, a lack of
active phagocytic lining cells within both the afferent and
efferent metaphyseal blood vessels has been implicated
in the development of hematogenous osteomyelitis (4).
Embolization or trauma to this tiny vascular network can
result in thrombosis, which provides a nidus for infection. Transient bacteremia can result in the seeding of
bacteria that may proliferate in this relatively avascular
area, often unnoticed by the immune mechanisms of the
body. Common areas implicated in disseminated infection include the gastrointestinal tract, the genitourinary
tract, and the upper respiratory tract (2, 4).
It is uncommon to see joint involvement in children
between the ages 1 and 12 (4). This is because the
growth plate is not penetrated by capillary loops and the
VOLUME 34, NUMBER 6, 1995
547
infection can only spread laterally to the cortex. In
infants, some vessels enter the growth plate, and in
adults, there is no growth plate to serve as a barrier, thus
joint involvement is more common in these ages (1, 9).
Microbiology
Hematogenous osteomyelitis is usually caused by a
single organism that may or may not be detected in
blood cultures (10-12). Gram-positive cocci, especially
Staphylococcus aureus, are the most common pathogens,
and have been cultured in 59% and 74% of case studies
of hematogenous osteomyelitis (2-4, 10, 13). Age is a
factor in the consideration of common pathogens. Betahemolytic streptococcus is most common in infants (2,
13). Haemophilus injluenzae is common in children
younger than two (1, 3, 13). Staphylococcus aureus is
most common in children older than two and in adults
(2,14). Streptococcus species and Gram-negative organisms such as Escherichia coli may be present when a
urinary tract infection is implicated (13). Gram-negative
organisms, including Pseudomonas aeruginosa, are commonly noted in intravenous drug abusers or immunocompromised patients (13), and Salmonella typhi is a
common pathogen noted in patients with sickle cell
anemia (4, 13).
Clinical Presentation
Presentation is variable, depending upon the age of
the patient, the stage of the disease, and the virulence of
the infecting organism. Often there are no systemic signs
(4, 7). Hematogenous osteomyelitis is usually associated
with the abrupt onset of severe localized pain, tenderness, erythema, and edema. Most patients have difficulty
bearing weight. Patients mayor may not recall a definite
history of trauma to the area. Even minor trauma is
thought to cause thrombosis within small capillaries.
With concomitant transient bacteremia, pathogens may
colonize the area (2). Often there may be a recent
history of upper respiratory, urinary, or gastrointestinal
tract infection. Wang et al. reported that patients will
have a characteristic posture, which they called the
"Heel up sign," in which the patients did not allow the
heel to contact the bed, even while they were asleep (7).
Diagnosis
Early diagnosis is of utmost importance when osteomyelitis is suspected. However, early signs and symptoms are
nonspecific, and clinical diagnosis is especially difficult in
children. Delays in diagnosis and initiation of appropriate
treatment can result in long-term morbidity (3).
The foundation for the diagnosis of osteomyelitis
remains the isolation of bacteria from biopsy or direct
548
culture of bone. Mackowiak et al. proved that cultures
obtained from sinus tracts or affected soft tissues often
fail to identify the actual infecting organism (15). Conclusive diagnosis of osteomyelitis is determined by the
isolation of organisms from direct cultures.
Recent reports have demonstrated that laboratory
studies are often of limited use (7). Acute-phase reactants (erythrocyte sedimentation rate (ESR), and C-reactive protein) are usually elevated in patients with
osteomyelitis (3). The ESR is a nonspecific test measuring generalized inflammation, and may be elevated with
many diseases (2, 4). White blood cell counts (WBCs)
are rarely elevated early in disease, but polymorphonuclear leukocytosis with immature cells may exist (4).
Alkaline phosphatase serum levels may be slightly elevated; however, they are usually normal (2). Serum
alkaline phosphatase levels are typically elevated in
actively growing children and with osteoblastic bone
diseases such as neoplasms and Paget's disease. Blood
cultures are positive in only about 50% of confirmed
cases (3).
Hematogenous osteomyelitis originates in cancellous
bone and results in radiographic findings that demonstrate internal infection which progresses outward to the
cortex and periosteum. Radiographic changes lag 1 to 2
weeks behind clinical findings and occur in stages (2, 4,
5). Stage one occurs 3 days after the onset of symptoms
and involves local soft tissue swelling and loss of fascial
planes. Stage two occurs at days 3 to 7 and involves the
continued spread of soft tissue swelling and superficial
edema. Stage three involves actual changes to the structure of bone and does not occur until 10 to 21 days after
the onset of symptoms (5). Changes in bone density
cannot be detected radiographically until approximately
30 to 50% of the bone minerals are lost (4, 5). Because
of this lag in visible changes, radiographs taken at initial
presentation are often normal (3-5).
Later, radiographic changes may show periosteal elevation and formation of active pockets of infection
within the bone, known as involucra. Further progression may demonstrate cloacae or openings of the involucra through the periosteum into the soft tissue and areas
of dead bone or sequestra. Involucra and sequestra are
characteristic of chronic osteomyelitis and may take up
to 4 weeks to appear radiographically.
Bone scans with technetium-99-methylene diphosphate C9mTc-mdp) can provide early information for the
diagnosis of osteomyelitis prior to the appearance of
radiographic changes (3, 5, 11). 99ffiTc_mdp undergoes
chemiadsorption and attaches to the surface of active
osteoblasts in hydroxyapatite crystal. The 99mTc_mdp
bone scan is dependent upon adequate circulation of the
imaged area. 99mTc_mdp bone scans are very sensitive to
the detection of changes in bone but are nonspecific,
THE JOURNAL OF FOOT AND ANKLE SURGERY
since many conditions are known to increase bone
activity (5, 11). Increased radionuclide uptake is seen at
areas of tendon insertion, reactive periostitis, constant
stress, osteoarthritis, bone remodeling, tumor formation,
osteotomy sites, fracture sites, epiphyseal plates in children, and osteomyelitis (5, 18). Osteomyelitis is characterized by increased focal uptake of 99mTc_mdp on the
delayed image or third phase of the bone scan.
Sequential scans of 99mTc_mdp followed by scanning
with the radioisotope gallium-67-citrate (67Ga-citrate)
can help delineate bone and soft tissue involvement.
67Ga-citrate attaches to the lactoferrin found in neutrophils and the transferrin found in extracellular fluid in
the areas of inflammation, whether it involves bone or
soft tissue. 99mTc_mdp is concentrated in bone, thus the
use of two agents can often allow for delineation of bone
and soft tissue involvement (5, 11).
Eisenberg et al. advocated the use of indium-Ill
Cl1In)- labeled leukocyte scans when a definitive diagnosis could not be made on the basis of bone scan alone
(12). They noted that the 111In-WBC scan was sensitive
and specific in the diagnosis of osteomyelitis of the foot.
Disadvantages of ll1In-WBC scans include the expense,
high radiation dose, long procedure time, and poor
image resolution.
New imaging modalities recently introduced include
technetium-99 hexamethylpropyleneamine oxime 9mTcHMPAO)-labeled leukocyte scans and 99mTc-labeled
albumin scans. 99mTc-HMPAO-labeled leukocytes localize only in areas of infection, and these techniques are
excellent for diagnosing acute osteomyelitis in children
or in bone affected by trauma, surgery, or neuroarthropathy (18). These techniques follow the same principles as 67Ga-citrate and ll1In-labeled leukocyte scans
but utilize 99mTc to achieve lower radiation, a sharper
image, and a shorter procedure time (18).
Computed tomography (CT) is often useful in the
diagnosis and evaluation of osteomyelitis. CT scans
demonstrate increased attenuation of bone marrow
early in the disease prior to changes that can be noted on
plain films. This attenuation occurs because of the
edema or purulence that replaces fat in normal bone
marrow. CT is sensitive to early changes in cortical bone,
as well as soft tissue changes (16).
Magnetic resonance imaging (MRI) has also proven
to be more sensitive than plain films or bone scan in the
early evaluation of osteomyelitis (16, 17). MRI demonstrates bone marrow changes early in the disease process
and may be more sensitive than 99mTc_mdp bone scans
in the early detection of osteomyelitis. Osteomyelitis is
seen as a reduced (darker) signal from bone marrow fat
on the Trweighted image. Tz-weighted images typically
show an increased (brighter) signal than that of normal
e
bone marrow fat. Soft tissue involvement is easily visualized on MRI as well (16, 17).
Treatment
Treatment of acute hematogenous osteomyelitis remains controversial. Some evidence suggests that osteomyelitis can be treated by antibiotics alone (3). However,
in certain cases, surgery is obviously indicated. Surgical
debridement should always be considered when the
patient is not responding to antibiotics or a symptomatic
abscess is apparent (3).
Generally, 3 to 6 weeks of parenteral antibiotics are
indicated if nonsurgical treatment is pursued (2-4).
Most authors feel that initial drug therapy should be
given intravenously (13). Intravenous therapy may be
maintained or converted to oral therapy, which has
recently been shown to be efficacious (13). Empiric
antibiotics should be directed against the most common
infecting agents and adjusted according to culture and
sensitivity results (3). It should be remembered that
serum antibiotic levels are often inconsistent with the
actual levels reaching the wound site (24). Also, systemic
side effects become more likely with the administration
of higher levels of antibiotics (24).
Recently the use of antibiotic-impregnated polymethyl methacrylate (PMMA) beads placed within the
surgical wound has been advocated in the treatment of
infections, including osteomyelitis (19-26). Buckholtz
and Englebrecht were the first to report the use of
antibiotic-impregnated PMMA beads (19). Since then,
many uses for antibiotic beads have been studied, including the treatment of osteomyelitis (19-26).
Antibiotic beads combine the advantages of high local
antibiotic levels with low systemic concentrations, decreased risk of toxic systemic antibiotic side effects, low
incidence of resistance, low incidence of allergic reactions, and primary wound closure. Disadvantages include necessary strict patient compliance, relative immobilization and required bed rest, and the need for a
second surgical procedure for bead removal.
PMMA has no antibacterial activity but carries and
allows the release (elution) of impregnated antibiotics
into the surrounding tissues rapidly for the first 24 hr.
and then gradually at an average rate of 400 f.1g. to 600
ug.rbead/day (20). Immediately postoperatively, diffusion rates and local concentrations are very high and
systemic levels are low (20).
Bead fabrication has been well studied (19-21).
PMMA is formed in a highly exothermic chemical
reaction by combining a powdered polymer and a liquid
monomer to form a high-density solid. Antibiotic powder can be mixed with the polymer and suspended with
the cement as it hardens. The ratio of PMMA powder to
VOLUME 34, NUMBER 6, 1995
549
antibiotic powder should be 5:1. A more concentrated
antibiotic may not allow the beads to harden. As the
antibiotic-to-PMMA ratio increases, the total amount of
antibiotic released increases. Smaller beads have a
greater surface area-to-total volume ratio. About 5% of
the antibiotic in the bead will elute in the first 24 hr. and
only about 0.12% to 0.07% will be absorbed systemically
(20).
Typically, gentamicin alone has been used in combination with PMMA beads, although many antibiotics,
including tobramycin (22-24), vancomycin (22), and
ceftazidime (25) have been investigated. The ideal antibiotic is heat-stable, broad-spectrum, and elutes well
from the PMMA beads. Gentamicin is an excellent
choice for combination with PMMA because of its high
water solubility and excellent thermal stability. Gentamicin is a broad-spectrum bactericidal aminoglycoside
antibiotic active against some Gram-positive and most
Gram-negative organisms, including Staphylococcus and
Pseudomonas species. The allergy rate with gentamicin is
low and few bacteria are resistant. Antibiotic choice
should always be tailored to each individual case
(20-22).
In cases when surgery is the treatment of choice, all
necrotic tissue must be radically debrided regardless of
whether antibiotic beads are used. All foreign materials,
including osteosynthesis material, should be removed
and the surgery site should be irrigated with sterile saline
or antibiotic solution. If antibiotic beads are used, they
should fill the entire cavity. Most often, the antibiotic
beads are preformed and cooled prior to insertion to
prevent thermal necrosis of viable bone and cartilage.
Primary closure over the beads is preferable. The beads
are typically removed in 10 to 14 days.
developed male in a moderate amount of discomfort. He
was afebrile and his vital signs were stable. The left heel
was noted to be mildly edematous and erythematous and
was significantly warmer to the touch than the right heel.
The popliteal and inguinal lymph nodes were not palpable and there was no lymphangitis. Severe tenderness
was noted on palpation of the entire left calcaneus and
the patient was unable to bear weight on the left foot.
Range of motion of the left ankle joint elicited pain in
plantarflexion and dorsiflexion. Neurological and vascular status to both feet was intact. Right lower-extremity
examination was completely normal.
Laboratory studies taken at the initial visit revealed an
ESR of 58 mm./hr. WBC of 6500, with 44% neutrophils,
44% lymphocytes, 8% eosinophils, 3% monocytes, and
1% bands. Hemoglobin was 12.8 g./dl., hematocrit was
35.6%, and alkaline phosphatase was 328 V.IL. (normal
value 117 to 390 V .IL.). Blood cultures were negative.
Radiographs of both feet were normal.
Case History
A 9Vz-year-old white male was referred to the Welborn Clinic Podiatry Department with a 6-day history of
left heel pain. He was seen initially by his primary care
physician and was referred after he experienced continuing symptoms. The patient's mother recalled a history of
a minor fall on the left foot with no complaints of pain
approximately 2 weeks previously. Over the previous 6
days, the pain had been severe. At times, he could not
bear weight on his left heel and placing the foot in a
dependent position elicited considerable pain. He also
had a recent history of upper respiratory tract infection
including congestion, cough, and a reported fever of up
to 105°F. The patient had no other significant medical
history and no known allergies. His only current medication was cefaclor 250 mg. twice daily for 10 days for
the upper respiratory tract infection.
Initial examination showed a well-nourished, well550
Figure 1. 99mTc-mdp three-phase bone scan. Note markedly increased uptake in left calcaneus, indicative of possible osteomyelitis.
THE JOURNAL OF FOOT AND ANKLE SURGERY
Figure 2. Lateral projection of left calcaneus. Note early
lytic area adjacent to apophysis.
At this time, the differential diagnosis included calcaneal apophysitis, stress fracture, hematogenous osteomyelitis, contusion, and neoplasm. A 99mTc_mdp bone
scan was performed and revealed intensely increased
activity in the left heel in both the blood pool and final
bone scan image (Fig. 1). Based on clinical history, age
of the patient, and lack of radiographic change, the
uptake was felt to be consistent with osteomyelitis of the
left calcaneus.
The patient was admitted to Welborn Baptist Hospital
2 days after initial presentation for administration of
intravenous nafcillin (25 mg./kg.) and local supportive
measures. Repeat radiographs, taken 7 days after the
original films, revealed a possible area of destruction of
bone adjacent to the left calcaneal apophysis (Figs. 2, 3).
Over the next 6 days, the patient noted a decrease in
symptoms and was afebrile. Sedimentation rate remained steady at 32 mm./hr., and blood values continued
to be normal.
A CT scan performed 4 days after admission demonstrated two prominent lytic lesions of the posterior
aspect of the left calcaneus adjacent to the apophysis
(Fig. 4). Laboratory values continued to be normal, and
clinically, the patient appeared to be improving.
Seven days later, the patient had a return of symptoms, and radiographs revealed the lytic lesions to be
more prominent (Fig. 5). Preoperative CT scans were
obtained, and suggested progression of the lytic process
(Fig. 6). At this point, surgical debridement was suggested because of the patient's continued disability and
the radiographic progression of the lesions. The patient's parents were apprised of potential risks, the
possibility of growth disturbance, and the possible need
for a bone-grafting procedure if the defect was large.
The patient was subsequently transported to the operating room for removal of the necrotic bone and implan-
Figure 3. Axial projection of left calcaneus. Note early lytic
area (arrow).
Figure 4. CT scan of both feet. Note two prominent lytic
lesions adjacent to left calcaneal apophysis.
tation of gentamicin and Claforarrt-impregnated PMMA
beads 2 weeks after initial presentation.
Operative Procedure
Under general anesthesia, with a pneumatic thigh
tourniquet set at 300 mm. Hg, a 7-cm. curvilinear
incision was made on the posterolateral aspect of the left
calcaneus. Neurovascular structures were retracted and
3
Hoechst-Roussel Pharmaceuticals, Inc., Somerville, NJ.
VOLUME 34, NUMBER 6, 1995
551
Figure 7. Surgical incision revealing necrotic bone.
Figure 5. Lateral projection of left calcaneus.
Figure 8. Postoperative lateral projection of left calcaneus
displaying PMMA beads within cavity.
Figure 6. CT scan of both feet. Note obvious progression of
lytic lesions.
dissection was carried deep to the calcaneus. The periosteum on the lateral aspect of the calcaneus was
reflected, exposing three prominent, gray, cystic lesions
containing soft necrotic bone and debris. All necrotic
bone was debrided, resulting in one large lateral cavity
(Fig. 7). Fragments of necrotic bone were submitted for
immediate Gram stain and aerobic, anaerobic, acid-fast,
and fungal cultures. Fluoroscopy was utilized to ensure
that all necrotic areas had been evacuated. The cavity
measured approximately 1.8 em. X 0.8 em. and was 2.0
em. deep. The area was then irrigated with vancomycin
antibiotic solution (1 gm. of vancomycin/WOO ml. of
sterile saline). The Gram stain revealed Gram-positive
cocci consistent with Staphylococcus aureus.
Five previously fabricated gentamicin-Claforan-impregnated beads formed on a 22-gauge wire were then
inserted into the cavity in the calcaneus. Skin was closed
552
over a drain and the remaining 22-gauge wire was left
protruding from the incision. A sterile dressing and
removable posterior splint were applied.
There were no complications and postoperative radiographs revealed the PMMA beads to be intact and filling
the entire cavity created from the debridement of necrotic bone (Figs. 8, 9). Operative cultures grew Staphylococcus aureus and the patient was maintained on
intravenous nafcillin, with daily dressing changes and
strict bed rest. His symptoms improved and ESR decreased to 26 mm./hr. after surgical intervention.
Thirteen days after implantation, the patient was
brought back to the operating room for removal of
implanted beads. Under general anesthesia, with a pneumatic thigh tourniquet set at 300 mm. Hg, the same
incisional approach was utilized and tissues were again
dissected to the level of the calcaneus. The PMMA
beads were found to be intact and all were removed. An
THE JOURNAL OF FOOT AND ANKLE SURGERY
Figure 11. Lateral radiograph of left calcaneus 1 year after
surgery. Note filling of previous lytic areas.
Figure 9. Postoperative left axial calcaneal projection.
Figure 12. Lateral radiograph of left calcaneus 3 years after
surgery. Complete healing of bony defect is noted.
Figure 10. Lateral radiograph of left calcaneus after removal of PMMA beads. Note the lytic areas of bone.
immediate Gram stain from the cavity was negative for
organisms. The cavity was cultured and the beads themselves were sent for culture and sensitivity. The surgical
site was irrigated with vancomycin solution, the wound
was inspected, and no further necrotic debris was noted.
Tissues were closed in layers, and a dry sterile dressing
and posterior splint were applied.
The patient tolerated the procedure and anesthesia
with no sequelae. All cultures were negative and the
ESR decreased to 18 mm./hr. After removal of the
PMMA beads, postoperative lateral radiographs revealed lytic areas (Fig. 10). The patient developed a mild
erythematous rash with urticaria and pruritus on postoperative day 2 and was switched to Ancef" 750 mg.
every 6 hr. He progressed well and was discharged
4
Smith Kline & French Labs, Philadelphia, PA.
without symptoms to home care with a bivalved cast and
crutches, strict instructions to remain nonweightbearing,
and intravenous Ancef" (1 gm. every 6 hr. for 6 weeks).
When seen 40 days after the removal of the PMMA
beads, radiographs revealed early filling of the lytic
lesions , and the patient had no recurrence of symptoms .
Th e patient was returned to protected weightbearing at
that time, and returned to normal activities with full
unprotected weightbearing at 12 weeks. At 1 year postsurgery, the patient was asymptomatic and radiographs
revealed complete filling of the lytic lesions (Fig. 11). At
3 years post-surgery, the patient remained completely
asymptomatic and had recently returned to playing
sports without discomfort. Radiographs were normal
(Fig. 12), and there was no obvious deformity of the heel
(Fig. 13). The patient reported that the affected foot was
actually slightly larger than the unaffected foot . Radiographic measurements of both feet showed an anteriorto-posterior length of 7 ern. on the left calcaneus and 6V2
em. on the right calcaneus. From superior to inferior, the
VOLUME 34, NUMBER 6, 1995
553
Figure 13. Photograph of left foot with no obvious deformities 3 years after surgery .
left calcaneus measured 4 em. and the right calcaneus
measured 3 1/ 2 em.
Discussion
With respect to the diagnosis of suspected osteomyelitis, the authors recommend ordering plain radiographs first. If changes are seen on plain films, then at
least 30% to 50% of bone mineral has been lost and the
diagnosis can be suspected without further imaging. If
radiographs are equivocal, the authors recommend doing a 99ffiTc_mdp bone scan. If the 99ffiTc_mdp bone scan
is positive , bone infection may be suspected; however,
there are many noninfectious processes that can cause
radionuclide uptake. A 99ffiTc-H MPAO- labeled leukocyte scan is excellent for diagnosing acute osteomyelitis
and ruling out noninfectious causes because it localizes
only in areas of infection. At the time this case presented, the option of 99ffiTc-HMPAO leukocyte scans
was not available.
A serious complication of hematogenous osteomyelitis in children is growth disturbance. Damage to the cells
on the epiphyseal side of the growth plate is irreversible
and results in disorganized bone growth. Growth abnormalities may be seen if there is damage to the calcaneal
apophysis. Borris and Helleland reported on growth
disturbances following calcaneal osteomyelitis in two
cases (6). They pointed out that the calcaneal apophysis
does not begin to ossify until the age of four. An
infection that occurs before the epiphyseal plates close
may result in damage to the growth potential of the
apophysis. The apophysis is complete by the age of 12 to
14, thus the extent of the deformity may not be seen until
then.
Another important consideration is the possibility of a
pathologic fracture after surgical debridement of the
calcaneus. The authors recommend that strict non554
weightbearing be maintained to protect against calcaneal fracture and its devastating sequelae. Protected
weightbearing may be initiated when clinical symptoms
have subsided and there is radiographic evidence of
bone healing.
Large defects within the calcaneus often require autogenous or allogenic bone grafting to strengthen or
reconstruct the weakened bone. It may be unusual that
the patient in this case did not require a bone graft to fill
the large defect created by debridement of infected
bone. Prior to removal of the antibiotic beads, bone
grafting was considered but opted against. Because of
the patient's age and the fact that the growth plate was
not disturbed, the authors felt that the defect would fill
and an additional procedure could be avoided . In this
case there was no growth abnormality noted at the
3-year follow-up. Clinically the heel was normally
shaped and radiographs revealed no defects. The patient
actually reported that the affected foot was slightly
larger than the unaffected foot and that he had returned
to full activities without symptoms.
Summary
Acute hematogenous osteomyelitis of the calcaneus is
an uncommon but potentially devastating and deforming
disorder in children. Confusing laboratory studies and
slowly developing radiographic changes make early diagnosis difficult. Physicians must incorporate a high
index of suspicion along with a careful history and
physical examination to make an accurate early diagnosis. Laboratory studies and early radiographs are often
not diagnostic. Radionuclide scanning, CT scans, or
MRI may aid in the diagnosis , although a biopsy of the
infected bone is the definitive diagnostic tool. Untreated
osteomyelitis of the calcaneus can potentially damage
the growing epiphysis in children, resulting in severe
deformities and long-term sequelae. Prompt and effective treatment results in fewer sequelae and a good
prognosis. The authors have presented an unusual case
of hematogenous osteomyelitis of the calcaneus that did
not require a bone graft following extensive debridement. At 3 years post-surgery, the patient has returned
to a normal lifestyle.
Acknowledgments
The authors thank Robert Kaylor, DPM, Terence
Alvey, DPM, Karry Ann Shebetka, DPM, and Lori
Kelsey, MA, CCC-SLP, for their assistance in preparing
and reviewing the manuscript.
References
THE JOURNAL OF FOOT AND ANKLE SURGERY
1. Wald vogel, F. A., Medoff, G., Swarts , M. N. Ost eomyelitis: review
of the clinical features, therapeutic considerations and unusual
asp ects. N. Engl. J. Med. 282:198 - 206, 1970.
2. Fox,!. M., Aponte, J. M. Hematogenous osteomyelitis of the
calcaneus. J. A. P. M. A. 83:681-684, 1993.
3. Mustafa, M. M., Saez-Llorens, x., McCracken, G. H., Nelson, J.
Acute hematogenous pelvic osteomyelitis in infants and children.
Pediatr. Infect. Dis. J. 9:416-421, 1990.
4. Stone, R. A., Uhlman, R. A., Zeichner, A. M. Acute hematogenous osteomyelitis, a case report. J. A. P. M. A. 72:31-34, 1982.
5. Donohue, T. W., Kanat, I. O. Radionuclides: their use in osteomyelitis. J. A. P. M. A. 77:284-289, 1987.
6. Borris, L. c., Helleland, H. Growth disturbance of the hind part of
the foot following osteomyelitis of the calcaneus in the newborn.
J. Bone Joint Surg. 68A:302-305, 1986.
7. Wang, E. H. M., Simpson, S., Bennet, G. C. Osteomyelitis of the
calcaneum. J. Bone Joint Surg. 74B:906-909, 1992.
8. Feigin, R. D., McAlister, W. H., San Joaquin, V. H., Middelkamp,
J. N. Osteomyelitis of the calcaneus. Am. J. Dis. Child. 119:61-65,
1970.
9. Antoniou, D., Conner, A. N. Osteomyelitis of the calcaneus and
talus. J. Bone Joint Surg. 56A:338-345, 1974.
10. Dich, V. Q., Nelson, J. D., Haltalin, K. C. Osteomyelitis in infants
and children: a review of 163 cases. Am. J. Dis. Child. 129:
1273-1278, 1975.
11. Howie, D. W., Savage, J. P., Wilson, T. G., Paterson, D. The
technetium phosphate bone scan in the diagnosis of osteomyelitis
in childhood. J. Bone Joint Surg. 65A:431-437, 1983.
12. Eisenberg, B., Wrege, S. S., Altman, M. 1., Moore, J. W. Bone
scan: indium-WBC correlation in the diagnosis of osteomyelitis of
the foot. J. Foot Surg. 28:532-536, 1989.
13. Arnoff, S. c., Scoles, P. V. Treatment of childhood skeletal infections. Pediatr. Clin. North Am. 30:271-280, 1983.
14. Axler, D. A., Terleckyj, B., Abramson, C. The microbiologic
aspects of osteomyelitis. J. A. P. A. 67:691-694, 1977.
15. Mackowiak, P., Jones, S., Smith, J. Diagnostic value of sinus tract
cultures in chronic osteomyelitis. J. A. M. A. 239:2772-2775, 1978.
16. Rogers, L. F. Infections and inflammations of bones, ch. 1. In Paul
and Juhl's Essentials of Radiologic Imaging, 5th ed., pp. 178-204,
edited by J. H. Juhl, A. B. Crummy, J. B. Lippincott Co., Philadelphia, 1987.
17. Cohen, M. D., Cory, D. A., Kleiman, M., Smith, J. A., Broderick,
N. J. Magnetic resonance differentiation of acute and chronic
osteomyelitis in children. Clin. Radiol. 41:53-56, 1990.
18. Fox, I. M., Zeiger, L. Tc-99m-HMPAO leukocyte scintigraphy for
the diagnosis of osteomyelitis in diabetic foot infections. J. Foot
Surg. 32:591-596, 1993.
19. Buckholtz, H. W., Englebrecht, H. Uber die Depotwirkung einiger
Antibiotica bei Verrnischung mit dem Kunstharz Palacos.
Der Chirurg. 11:511-515, 1970.
20. Marcinko, D. E. Gentamicin-impregnated PMMA beads: an introduction and review. J. Foot Surg. 24:116-121, 1985.
21. Calhoun, J. H., Mader, J. T. Antibiotic beads in the management
of surgical infections. Am. J. Surg. 157:443-449, 1989.
22. Stabile, D. E., Jacobs, A. M. Development and application of
antibiotic-loaded bone cement beads. J. A. P. M. A. 80:354-359,
1990.
23. Scott, D. M., Rotschafer, J. C., Behrens, F. Use of vancomycin and
tobramycin polyrnethylmethacrylate impregnated beads in the
management of chronic osteomyelitis. Drug Intell. Clin. Pharm.
22:480-483, 1988.
24. Eckman, J. B., Henry, S. L., Mangino, P. D., Seligson, D. Wound
and serum levels of tobramycin with the prophylactic use of
tobramycin impregnated polymethylmethacrylate beads in compound fractures. Clin. Orthop. ReI. Res. 237:213-215, 1988.
25. Soto-Hall, R., Saenz, L., Tavernetti, R., Cabaud, H. E., Cochran,
T. P. Tobramycin in bone cement. Clin. Orthop. ReI. Res. 175:
60-64, 1983.
26. Tomczak, R. L., Dowdy, N., Storm, T., Caldarella, D. Use of
Ceftazidime-impregnated polymethylmethacrylate beads in the
treatment of pseudomonas osteomyelitis. J. Foot Surg. 28:
542-546, 1989.
Additional References
Baker, A. S., Greenham, L. W. Release of gentamicin from acrylic
bone cement. J. Bone Joint Surg. 70A:1551-1557, 1988.
Caprioli, R., Testa, J., Cournoyer, R. W., Esposito, F. J. Prompt
diagnosis of suspected osteomyelitis by utilizing percutaneous bone
culture. J. Foot Surg. 25:263-269, 1986.
Christian, E. P., Bosse, M. J., Robb, G. Reconstruction of large
diaphyseal defects without free fibular transfer, in grade-IIIB tibial
fractures. J. Bone Joint Surg. 71A:994-1003, 1989.
Stabile, D. E., Jacobs, A. M. Local antibiotic treatment of soft tissue
and bone infections of the foot. J. A. P. M. A. 80:345-353, 1990.
VOLUME 34, NUMBER 6, 1995
555