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. 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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. 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