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A Passage to Injury
The American Journal of Medicine (2006) 119, 491-493
IMAGES IN RADIOLOGY Michael Bettmann, MD, Section Editor
A Passage to Injury Memduh Dursun, MD, Sabri Yilmaz, MD, Ensar Yekeler, MD Istanbul University, Istanbul Faculty of Medicine, Department of Radiology, Istanbul, Turkey
PRESENTATION An 18-year-old boy had redness, swelling, pain, and warmth on the anterior of his right lower leg for 8 weeks. Laboratory tests revealed leukocytosis with increased sedimentation and C-reactive protein levels. His history was unremarkable and included untreated pharyngitis 3 weeks prior to onset of his leg symptoms.
aging. Radiographs are important for initial patient screening and are helpful when cortical bone abnormalities are present; however, they have low sensitivity. When aggressive bone destruction occurs with periostitis and soft tissue swelling, the changes can simulate those characteristic of malignant neoplasms, especially Ewing’s sarcoma or osteo-
DIAGNOSIS The initial differential diagnosis included cellulitis, septic arthritis, and osteomyelitis. An x-ray of the patient’s right leg demonstrated a lytic lesion with mild peripheral sclerosis involving the distal metaphysis of his tibia (Figure 1). Further evaluation with magnetic resonance (MR) imaging was performed to determine whether the finding was caused by osteomyelitis or was the result of a tumor. A T1-weighted image uncovered a diffuse hypo-intense lesion in the distal tibia with an opening— or cloaca—in the periosteum; the lesion extended to the anterior soft tissue of the tibia (Figure 2). Inflammatory changes, which were not visible on the x-ray, were evident within the soft tissue. Post-contrast images further enhanced the lesion and also disclosed a fragment of dead bone surrounded by granulation tissue, a finding known as a sequestrum (Figure 3). MR images like these are typically associated with a diagnosis of osteomyelitis. Our patient’s infection reached from the distal metaphysis to the cortex of the tibia, causing the cloaca. Osteomyelitis, a destructive pyogenic infection of the bone, can directly reach the bone by hematogenous spread or from an open sore. It usually affects the metaphysial parts of long bones.1,2 The tibia (34%) and femur (33%) are the most frequent foci of chronic osteomyelitis, followed by the fibula (8%), the iliac crest (7%), a vertebra (3%), the humerus (3%), and other medullary bones (12%).3 Beyond the neonatal period, the most common organisms causing osteomyelitis are Staphylococcus aureus, Streptococcus pyogenes, and Haemophilus influenzae type b.4 Clinical findings combined with imaging results usually ensure a correct diagnosis of osteomyelitis. Imaging options include radiography, nuclear medicine studies, and MR im0002-9343/$ -see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.amjmed.2006.04.008
Figure 1 An x-ray of the right leg showed a lytic lesion with mild peripheral sclerosis on the distal metaphysis of the patient’s tibia, a finding denoted by the arrows. Neither periosteal reaction nor cortical thickening was observed at the lesion site.
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The American Journal of Medicine, Vol 119, No 6, June 2006
Figure 2 A diffuse hypo-intense lesion can be seen on the distal tibia in this T1-weighted magnetic resonance image. Arrows highlight a cloaca or channel in the periosteum. The lesion reached the inflamed soft tissue anterior to the tibia.
sarcoma in children, histiocytic lymphoma in young adults, and skeletal metastasis in older patients.5 Nuclear medicine studies have improved sensitivity when compared with radiographs, but they have low specificity and are less helpful than MR imaging in evaluating adjacent soft-tissue aberrations. MR imaging is capable of revealing primary marrow abnormalities and secondary bone and soft-tissue abnormalities with better specificity than scintigraphy in patients with clinically suspected osteomyelitis.6 Primary signs of osteomyelitis on MR images are decreased T1 signal, increased T2 signal, and postgadolinium enhancement. Supportive secondary findings include adjacent soft tissue ulcers, cellulitis, phlegmon, abscess, sinus tracts, and cortical bone destruction.7 Unfortunately, the responsible pathogen is not captured by blood culture in as many as 50% of osteomyelitis cases.8 Histopathologic and microbiologic examinations of bone are the gold standard for diagnosing osteomyelitis.9
MANAGEMENT After the initial evaluation, staging, and establishment of microbial etiology and susceptibilities, treatment in-
cludes antimicrobial therapy, debridement with management of resultant dead space, and stabilization of bone, if necessary.10 For staphylococcal infection, by far the most common cause of osteomyelitis, a penicillinase-resistant semisynthetic penicillin (for example, oxacillin or nafcillin) is the drug of choice. First- or second-generation cephalosporins are acceptable alternatives, as is clindamycin for children who are allergic to penicillin.11 Few studies have specifically tested the efficacy of oral agents in treating osteomyelitis caused by methicillin-resistant S. aureus. In a recent investigation, 11 adults with methicillin- or vancomycin-resistant osteomyelitis were treated with linezolid, 600 mg twice a day, for a mean of 10 weeks (range, 6 to 19), and all of them demonstrated clinical and radiographic remission at 27 months (range, 17 to 41).12 Our patient underwent surgery for debridement of the pus and dead bone fragments. Although the primary source of infection was not identifiable, it might have been the previous episode of pharyngitis. A culture taken from the infected site grew S. aureus. Parenteral nafcillin was administered for 6 weeks. The patient was dis-
Dursun et al
A Passage to Injury
493
Figure 3 In this post-contrast image, the extensive lesion is enhanced. Notice the hypo-intense area indicated by the arrows. This is a sequestrum—a fragment of dead bone surrounded by granulation tissue. It was identified within the lesion on all magnetic resonance sequences.
charged and had an uneventful recovery over the subsequent 3 months.
References 1. Cheon JE, Chung HW, Hong SH, et al. Sonography of acute osteomyelitis in rabbits with pathologic correlation. Acad Radiol. 2001;8: 243-249. 2. Mah ET, LeQuesne GW, Gent RJ, Paterson, DC. Ultrasonic features of acute osteomyelitis in children. J Bone Joint Surg. 1994;76-B:969974. 3. Zuluaga AF, Galvis W, Saldarriaga JG, Agudelo M, Salazar BE, Vesga O. Etiologic diagnosis of chronic osteomyelitis, Arch Intern Med. 2006;166:95-100. 4. Vazquez M. Osteomyelitis in Children. Curr Opin Pediatr. 2002;14: 112-115. 5. Resnick D. Osteomyelitis, Septic Arthritis, and Soft Tissue Infection: Mechanisms and Situations. In: Resnick, D, ed. Bone and Joint Imaging. Philadelphia:WB Saunders; 1996: 660.
6. Collins MS, Schaar MM, Wenger DE, Mandrekar, JN. T1-weighted MRI characteristics of pedal osteomyelitis. AJR Am J Roentgenol. 2005;185:386-393. 7. Unger E, Moldofsky P, Gatenby R, Hartz W, Broder G. Diagnosis of osteomyelitis by MR imaging. AJR Am J Roentgenol. 1988;150:605610. 8. Zvulunov A, Gal N, Segev Z. Acute hematogenous osteomyelitis of the pelvis in childhood: diagnostic clues and pitfalls. Pediatr Emerg Care. 2003;19:29-31. 9. Mackowiak PA, Jones SR, Smith JW. Diagnostic value of sinus-tract cultures in chronic osteomyelitis. JAMA. 1978;239:2772-2775. 10. Cierny G, Mader, JT. The surgical treatment of adult osteomyelitis. In: Evarts CM, ed. Surgery of the Musculoskeletal System. New York: Churchill Livingstone; 1983:15-35. 11. Stengel D, Bauwens K, Sehouli J, et al. Systematic review and metaanalysis of antibiotic therapy for bone and joint infections. Lancet Infect Dis. 2001;1:175-188. 12. Rao N, Ziran BH, Hall RA, Santa ER. Successful treatment of chronic bone and joint infections with oral linezolid. Clin Orthop Relat Res. 2004;427:67-71.
IMAGES IN RADIOLOGY Michael Bettmann, MD, Section Editor
A Passage to Injury Memduh Dursun, MD, Sabri Yilmaz, MD, Ensar Yekeler, MD Istanbul University, Istanbul Faculty of Medicine, Department of Radiology, Istanbul, Turkey
PRESENTATION An 18-year-old boy had redness, swelling, pain, and warmth on the anterior of his right lower leg for 8 weeks. Laboratory tests revealed leukocytosis with increased sedimentation and C-reactive protein levels. His history was unremarkable and included untreated pharyngitis 3 weeks prior to onset of his leg symptoms.
aging. Radiographs are important for initial patient screening and are helpful when cortical bone abnormalities are present; however, they have low sensitivity. When aggressive bone destruction occurs with periostitis and soft tissue swelling, the changes can simulate those characteristic of malignant neoplasms, especially Ewing’s sarcoma or osteo-
DIAGNOSIS The initial differential diagnosis included cellulitis, septic arthritis, and osteomyelitis. An x-ray of the patient’s right leg demonstrated a lytic lesion with mild peripheral sclerosis involving the distal metaphysis of his tibia (Figure 1). Further evaluation with magnetic resonance (MR) imaging was performed to determine whether the finding was caused by osteomyelitis or was the result of a tumor. A T1-weighted image uncovered a diffuse hypo-intense lesion in the distal tibia with an opening— or cloaca—in the periosteum; the lesion extended to the anterior soft tissue of the tibia (Figure 2). Inflammatory changes, which were not visible on the x-ray, were evident within the soft tissue. Post-contrast images further enhanced the lesion and also disclosed a fragment of dead bone surrounded by granulation tissue, a finding known as a sequestrum (Figure 3). MR images like these are typically associated with a diagnosis of osteomyelitis. Our patient’s infection reached from the distal metaphysis to the cortex of the tibia, causing the cloaca. Osteomyelitis, a destructive pyogenic infection of the bone, can directly reach the bone by hematogenous spread or from an open sore. It usually affects the metaphysial parts of long bones.1,2 The tibia (34%) and femur (33%) are the most frequent foci of chronic osteomyelitis, followed by the fibula (8%), the iliac crest (7%), a vertebra (3%), the humerus (3%), and other medullary bones (12%).3 Beyond the neonatal period, the most common organisms causing osteomyelitis are Staphylococcus aureus, Streptococcus pyogenes, and Haemophilus influenzae type b.4 Clinical findings combined with imaging results usually ensure a correct diagnosis of osteomyelitis. Imaging options include radiography, nuclear medicine studies, and MR im0002-9343/$ -see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.amjmed.2006.04.008
Figure 1 An x-ray of the right leg showed a lytic lesion with mild peripheral sclerosis on the distal metaphysis of the patient’s tibia, a finding denoted by the arrows. Neither periosteal reaction nor cortical thickening was observed at the lesion site.
492
The American Journal of Medicine, Vol 119, No 6, June 2006
Figure 2 A diffuse hypo-intense lesion can be seen on the distal tibia in this T1-weighted magnetic resonance image. Arrows highlight a cloaca or channel in the periosteum. The lesion reached the inflamed soft tissue anterior to the tibia.
sarcoma in children, histiocytic lymphoma in young adults, and skeletal metastasis in older patients.5 Nuclear medicine studies have improved sensitivity when compared with radiographs, but they have low specificity and are less helpful than MR imaging in evaluating adjacent soft-tissue aberrations. MR imaging is capable of revealing primary marrow abnormalities and secondary bone and soft-tissue abnormalities with better specificity than scintigraphy in patients with clinically suspected osteomyelitis.6 Primary signs of osteomyelitis on MR images are decreased T1 signal, increased T2 signal, and postgadolinium enhancement. Supportive secondary findings include adjacent soft tissue ulcers, cellulitis, phlegmon, abscess, sinus tracts, and cortical bone destruction.7 Unfortunately, the responsible pathogen is not captured by blood culture in as many as 50% of osteomyelitis cases.8 Histopathologic and microbiologic examinations of bone are the gold standard for diagnosing osteomyelitis.9
MANAGEMENT After the initial evaluation, staging, and establishment of microbial etiology and susceptibilities, treatment in-
cludes antimicrobial therapy, debridement with management of resultant dead space, and stabilization of bone, if necessary.10 For staphylococcal infection, by far the most common cause of osteomyelitis, a penicillinase-resistant semisynthetic penicillin (for example, oxacillin or nafcillin) is the drug of choice. First- or second-generation cephalosporins are acceptable alternatives, as is clindamycin for children who are allergic to penicillin.11 Few studies have specifically tested the efficacy of oral agents in treating osteomyelitis caused by methicillin-resistant S. aureus. In a recent investigation, 11 adults with methicillin- or vancomycin-resistant osteomyelitis were treated with linezolid, 600 mg twice a day, for a mean of 10 weeks (range, 6 to 19), and all of them demonstrated clinical and radiographic remission at 27 months (range, 17 to 41).12 Our patient underwent surgery for debridement of the pus and dead bone fragments. Although the primary source of infection was not identifiable, it might have been the previous episode of pharyngitis. A culture taken from the infected site grew S. aureus. Parenteral nafcillin was administered for 6 weeks. The patient was dis-
Dursun et al
A Passage to Injury
493
Figure 3 In this post-contrast image, the extensive lesion is enhanced. Notice the hypo-intense area indicated by the arrows. This is a sequestrum—a fragment of dead bone surrounded by granulation tissue. It was identified within the lesion on all magnetic resonance sequences.
charged and had an uneventful recovery over the subsequent 3 months.
References 1. Cheon JE, Chung HW, Hong SH, et al. Sonography of acute osteomyelitis in rabbits with pathologic correlation. Acad Radiol. 2001;8: 243-249. 2. Mah ET, LeQuesne GW, Gent RJ, Paterson, DC. Ultrasonic features of acute osteomyelitis in children. J Bone Joint Surg. 1994;76-B:969974. 3. Zuluaga AF, Galvis W, Saldarriaga JG, Agudelo M, Salazar BE, Vesga O. Etiologic diagnosis of chronic osteomyelitis, Arch Intern Med. 2006;166:95-100. 4. Vazquez M. Osteomyelitis in Children. Curr Opin Pediatr. 2002;14: 112-115. 5. Resnick D. Osteomyelitis, Septic Arthritis, and Soft Tissue Infection: Mechanisms and Situations. In: Resnick, D, ed. Bone and Joint Imaging. Philadelphia:WB Saunders; 1996: 660.
6. Collins MS, Schaar MM, Wenger DE, Mandrekar, JN. T1-weighted MRI characteristics of pedal osteomyelitis. AJR Am J Roentgenol. 2005;185:386-393. 7. Unger E, Moldofsky P, Gatenby R, Hartz W, Broder G. Diagnosis of osteomyelitis by MR imaging. AJR Am J Roentgenol. 1988;150:605610. 8. Zvulunov A, Gal N, Segev Z. Acute hematogenous osteomyelitis of the pelvis in childhood: diagnostic clues and pitfalls. Pediatr Emerg Care. 2003;19:29-31. 9. Mackowiak PA, Jones SR, Smith JW. Diagnostic value of sinus-tract cultures in chronic osteomyelitis. JAMA. 1978;239:2772-2775. 10. Cierny G, Mader, JT. The surgical treatment of adult osteomyelitis. In: Evarts CM, ed. Surgery of the Musculoskeletal System. New York: Churchill Livingstone; 1983:15-35. 11. Stengel D, Bauwens K, Sehouli J, et al. Systematic review and metaanalysis of antibiotic therapy for bone and joint infections. Lancet Infect Dis. 2001;1:175-188. 12. Rao N, Ziran BH, Hall RA, Santa ER. Successful treatment of chronic bone and joint infections with oral linezolid. Clin Orthop Relat Res. 2004;427:67-71.