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Osteomyelitis

Chapter 136 | Part 5: Infectious Diseases · Part 5 – Infectious Diseases: Bacterial

Detailed clinical reference synthesised from Harrison's Principles of Internal Medicine, 22nd Edition

🔑 Key Clinical Points

  1. Osteomyelitis is an infection of bone caused by various microorganisms arriving via hematogenous spread, contiguous spread, or vascular insufficiency.
  2. Vertebral osteomyelitis is the most common manifestation of hematogenous bone infection in adults, typically involving the vertebral column.
  3. Acute osteomyelitis without bone necrosis can be treated with antibiotics alone, whereas chronic osteomyelitis requires debridement surgery.
  4. Diagnosis relies on elevated ESR (98% sensitivity) and CRP (100% sensitivity); MRI is the gold standard for imaging.
  5. Blood cultures yield positive results in 30–78% of cases; negative cultures do not rule out infection if clinical suspicion is high.
  6. Implant-associated osteomyelitis requires surgical management, often with implant removal and prolonged antibiotic therapy.
  7. Antibiotic therapy for vertebral osteomyelitis generally lasts 6 weeks; for implant-associated infections, 3 months is typical.
  8. Periprosthetic joint infection (PJI) is classified as early (2 years).
  9. S. aureus is the most common pathogen in acute hematogenous osteomyelitis and PJI; coagulase-negative staphylococci are common in implant-associated infections.
  10. Complications include epidural abscesses (15–20% of cases), neurologic deficits, and chronic infection with sinus tracts.
  11. Tuberculosis is a frequent cause of subacute/chronic vertebral osteomyelitis in endemic regions (Africa, Asia, Middle East).
  12. Oral antibiotic therapy is noninferior to IV therapy for vertebral osteomyelitis if specific criteria (bioavailability, clinical studies) are met.

📑 Table of Contents

📋 Figures in This Chapter

# Type Description
1 🖼 Figure Left: MRI from a 53-year-old man suffering from prosthetic aortic valve lumbar...
2 🖼 Figure Left: MRI from a 53-year-old man suffering from prosthetic aortic valve lumbar...
3 🖼 Figure Acute postoperative periprosthetic joint infection of the left hip caused by group...
4 🖼 Figure Neuropathic joint disease (Charcot foot) complicated by chronic foot osteomyelitis in a...
5 🖼 Figure Acute postoperative periprosthetic joint infection of the left hip caused by group...
6 🖼 Figure to FIGURE 136-4 Sternal osteomyelitis caused by Staphylococcus epidermidis 5 weeks after...

1. DEFINITION & OVERVIEW

  • Osteomyelitis is an infection of bone that can be caused by various microorganisms arriving at bone through different routes.
  • Spontaneous hematogenous osteomyelitis may occur in otherwise healthy individuals, whereas local microbial spread mainly affects individuals with underlying disease (e.g., vascular insufficiency) or compromised skin/tissue barriers.
  • The manifestations of osteomyelitis are different in children and adults. In children, circulating microorganisms seed mainly long bones, whereas in adults, the vertebral column is the most commonly affected site.
  • Classification by pathogenesis: (1) Hematogenous spread; (2) Spread from a contiguous site following surgery; (3) Secondary infection in the setting of vascular insufficiency or concomitant neuropathy.
  • Classification by duration: Acute (few days or weeks) vs. Subacute/Chronic (weeks or months).
  • Classification by location: Long bones, vertebral column, periarticular bones.
  • Classification by presence of foreign material: Native bone vs. Implant-associated.
  • The Cierny-Mader staging system is useful mainly for trauma surgeons, classifying osteomyelitis according to anatomic site, comorbidity, and radiographic findings.
  • Management differs greatly depending on whether an implant is involved; device-related bone and joint infection necessitates a multidisciplinary approach requiring antibiotic therapy and, in many cases, surgical removal of the device.
  • Harrison's defines acute osteomyelitis as infection evolving over a short period (few days or weeks) and chronic osteomyelitis as infection lasting for weeks or months before treatment is started.
  • Bone necrosis (sequesters) is crucial for distinguishing acute from chronic osteomyelitis; acute osteomyelitis without bone necrosis can generally be treated with antibiotics alone, whereas chronic osteomyelitis requires debridement surgery.

1.1 Classification Systems

  • Pathogenesis: Hematogenous, Contiguous, Vascular Insufficiency.
  • Duration: Acute vs. Subacute/Chronic.
  • Location: Long bones, Vertebral column, Periarticular bones.
  • Foreign Material: Native bone vs. Implant-associated.
  • Cierny-Mader Staging: Used mainly for trauma surgeons, stratifies long-bone osteomyelitis to optimize surgical management.

2. EPIDEMIOLOGY

  • Vertebral osteomyelitis occurs more often in male than in female patients (ratio, 1.5:1).
  • Between 1995 and 2008, the incidence rate increased from 2.2 to 5.8 cases/100,000 person-years.
  • There is a clear age-dependent increase; men age ≥70 years have a sixfold higher incidence rate than those <70 years.
  • The observed increase in reported cases over time may reflect improvements in diagnosis resulting from the broad availability of MRI technology.
  • The fraction of cases of vertebral osteomyelitis acquired in association with health care is increasing as a consequence of comorbidity and the rising number of invasive interventions.
  • In adults, most cases of long-bone osteomyelitis are posttraumatic or postsurgical; less frequently, late recurrence arises from hematogenous infections during childhood.
  • For postoperative or postsurgical osteomyelitis, the term 'fracture-related infection' was generated.
  • The risk of infection depends on the type of fracture. After closed fracture, implant-associated infection occurs in fewer than 1% of patients. In contrast, after open fracture, the risk of osteomyelitis ranges from ~2% to up to 30%.
  • In North American and Western European countries, tuberculous osteomyelitis is extremely rare, occurring mainly in very old people, HIV-infected patients, and immigrants from endemic countries.
  • In countries where the prevalence of tuberculosis is high (India, Indonesia, China), tuberculous osteomyelitis must routinely be considered.

2.1 Risk Factors

  • Non-modifiable: Age (≥70 years), Sex (Male), Comorbidities (Diabetes, HIV).
  • Modifiable: IV drug use, Obesity, Chronic renal failure, Emergency surgery, Use of bilateral internal mammary artery grafts.
  • Implant-related: Type of fracture (Open vs. Closed), Time between injury and admission.

3. ETIOLOGY & PATHOPHYSIOLOGY

  • Any of three mechanisms can underlie osteomyelitis: (1) Hematogenous spread; (2) Spread from a contiguous site following surgery; (3) Secondary infection in the setting of vascular insufficiency or concomitant neuropathy.
  • Hematogenous osteomyelitis in adults typically involves the vertebral column. In only about half of patients a primary focus can be detected.
  • The most common primary foci of infection are the urinary tract, skin/soft tissue, intravascular catheterization sites, and the endocardium.
  • Spread from a contiguous source follows either bone trauma or surgical intervention.
  • Wound infection leading to osteomyelitis typically occurs after cardiovascular intervention involving the sternum, orthopedic repair after open fracture, or prosthetic joint insertion.
  • Osteomyelitis secondary to vascular insufficiency or peripheral neuropathy most often follows chronic, progressively deep skin and soft tissue infection of the foot.
  • The most common underlying condition is diabetes. In diabetes that is poorly controlled, the diabetic foot syndrome is caused by skin, soft tissue, and bone ischemia combined with motor, sensory, and autonomic neuropathy.
  • Vertebral osteomyelitis pathogenesis: Microorganisms invade via the segmental arterial circulation in adjacent endplates and then spread into the disk. Alternative routes are retrograde seeding through the prevertebral venous plexus and direct inoculation during spinal surgery, epidural infiltration, or trauma.
  • In the setting of implant surgery, microorganisms are inoculated either during the procedure or, if wound healing is impaired, in the early postoperative period.
  • Implanted foreign material is highly susceptible to local infection due to local immunodeficiency around the device. Infection occurs by either the exogenous or the hematogenous route.
  • The fact that foreign devices are covered with host proteins such as fibronectin favors the adherence of staphylococci and the formation of a biofilm that resists phagocytosis.
  • Osteomyelitis in long bones is a consequence of hematogenous seeding, exogenous contamination during trauma (open fracture), or perioperative contamination during surgery involving bone.
  • Hematogenous infection in long bones typically occurs in children. In adults, the leading pathogenic source is exogenous fracture-related infection, mainly associated with internal fixation devices.
  • Chronic osteomyelitis can be reactivated after a symptom-free interval of >70 years. Such recurrences are most common among elderly patients who developed S. aureus osteomyelitis in the preantibiotic era.

3.1 Vertebral Osteomyelitis Pathogenesis

  • Disk involvement: The disk is avascular. Microorganisms invade via the segmental arterial circulation in adjacent endplates and then spread into the disk.
  • Alternative routes: Retrograde seeding through the prevertebral venous plexus, direct inoculation during spinal surgery, epidural infiltration, or trauma.
  • Implant surgery: Microorganisms are inoculated either during the procedure or, if wound healing is impaired, in the early postoperative period.

3.2 Long-Bone Osteomyelitis Pathogenesis

  • Hematogenous seeding: Typically occurs in children.
  • Exogenous contamination: During trauma (open fracture) or perioperative contamination during surgery involving bone.
  • Fracture-related infection: Mainly associated with internal fixation devices in adults.
  • Recurrence: Chronic osteomyelitis can be reactivated after a symptom-free interval of >70 years.

4. CLINICAL FEATURES

  • The signs and symptoms of vertebral osteomyelitis are nonspecific.
  • Only about half of patients develop fever >38°C (>100.4°F), perhaps because patients frequently use analgesic drugs.
  • Back pain is the leading initial symptom (>85% of cases).
  • The location of the pain corresponds to the site of infection: the cervical spine in ~10% of cases, the thoracic spine in 30%, and the lumbar spine in 60%.
  • One exception is involvement at the thoracic level in two-thirds of cases of tuberculous osteomyelitis and at the lumbar level in only one-third. This difference is due to direct mycobacterial spread via pleural or mediastinal lymph nodes in pulmonary tuberculosis.
  • Neurologic deficits, such as radiculopathy, weakness, or sensory loss, are observed in about one-third of cases of vertebral osteomyelitis.
  • Neurologic signs and symptoms are caused mostly by spinal epidural abscess.
  • This complication starts with severe localized back pain and progresses to radicular pain, reflex changes, sensory abnormalities, motor weakness, bowel and bladder dysfunction, and paralysis.
  • A primary focus should always be sought but is found in only half of cases.
  • Overall, endocarditis is identified in ~10% of patients. In osteomyelitis caused by viridans streptococci, endocarditis is the source in about half of patients.
  • Implant-associated spinal osteomyelitis can present as either early- or late-onset infection.
  • Early-onset infection is diagnosed within 30 days after implant placement. S. aureus is the most common pathogen. Wound healing impairment and fever are the leading findings.
  • Late-onset infection is diagnosed beyond 30 days after surgery, with low-virulence organisms such as coagulase-negative staphylococci or C. acnes as typical infecting agents.
  • Fever is rare. One-quarter of patients have a sinus tract.
  • Because of the delayed course and the lack of classic signs of infection, rapid diagnosis requires a high degree of suspicion.
  • The leading symptoms in adults with primary or recurrent hematogenous long-bone osteomyelitis are pain and low-grade fever.
  • Infection occasionally manifests as clinical sepsis and local signs of inflammation (erythema and swelling).
  • After internal fixation, osteomyelitis can be classified as early (acute; 1 year's duration, single-photon emission CT plus conventional CT (SPECT/CT) is a good option, either with 99mTc-methylene diphosphonate (99mTc-MDP)–labeled leukocytes or with labeled monoclonal antibodies to granulocytes.
  • Surgical debridement is needed for diagnostic (biopsy culture, histology) and therapeutic reasons.
  • Chronic PJI is most commonly caused by low-virulence microorganisms such as coagulase-negative staphylococci or C. acnes.
  • These infections are characterized by nonspecific symptoms, such as chronic pain caused by low-grade inflammation or early loosening.
  • Key findings in chronic PJI are joint effusion, local pain, implant loosening, and occasionally a sinus tract.
  • Acute exogenous PJI typically presents with local signs of infection.
  • In contrast, acute hematogenous PJI is most often caused by S. aureus and is characterized by new-onset pain.
  • Local inflammatory signs are rare in hip PJI but frequent in knee PJI.
  • Fever is rare after the initial phase of bacteremia.

4.1 Vertebral Osteomyelitis Symptoms

  • Back pain: Leading initial symptom (>85% of cases).
  • Fever: Only about half of patients develop fever >38°C (>100.4°F).
  • Pain Location: Cervical spine (~10%), Thoracic spine (30%), Lumbar spine (60%).
  • Neurologic Deficits: Observed in about one-third of cases (radiculopathy, weakness, sensory loss).
  • Cause: Mostly by spinal epidural abscess.
  • Progression: Severe localized back pain → radicular pain, reflex changes, sensory abnormalities, motor weakness, bowel/bladder dysfunction, paralysis.

4.2 Long-Bone Osteomyelitis Symptoms

  • Pain and low-grade fever: Leading symptoms.
  • Sepsis and local signs: Occasionally manifests as clinical sepsis and local signs of inflammation (erythema and swelling).
  • Early/Acute: Signs of surgical site infection (erythema, impaired wound healing).
  • Delayed/Late: Persisting pain, subtle local signs, intermittent discharge of pus, fluctuating erythema.
  • Brodie's Abscess: Pain (98%), swelling (53%), mainly in tibia or femur.
  • Delay: Median delay from symptoms to diagnosis is 3 months.

4.3 Periprosthetic Joint Infection (PJI) Symptoms

  • Early (2 years): Chronic pain, nonspecific symptoms.
  • Hip PJI: Local inflammatory signs are rare.
  • Knee PJI: Local inflammatory signs are frequent.
  • Fever: Rare after initial phase of bacteremia.

5. DIFFERENTIAL DIAGNOSIS

  • Given that signs and symptoms of osteomyelitis are nonspecific, the clinical differential diagnosis of febrile back pain is broad.
  • Includes pyelonephritis, pancreatitis, and viral syndromes.
  • Multiple noninfectious pathologies of the vertebral column should be considered.
  • Osteoporotic fracture.
  • Seronegative spondylitis (ankylosing spondylitis, psoriasis, reactive arthritis, enteropathic arthritis).
  • Spinal stenosis.
  • Erosive osteochondrosis.
  • Septic bone necrosis.
  • Gouty spondylodiskitis.
  • Erosive diskovertebral lesions (Andersson lesions) in ankylosing spondylitis.
  • Bone metastases.
  • Herniated disk (rule out in patients with neurologic impairment).
  • Rule out: In patients with neurologic impairment, MRI should be performed expeditiously in order to rule out a herniated disk or to detect pyogenic complications in a timely manner.

5.1 Vertebral Osteomyelitis DDx

  • Pyelonephritis.
  • Pancreatitis.
  • Viral syndromes.
  • Osteoporotic fracture.
  • Seronegative spondylitis (ankylosing spondylitis, psoriasis, reactive arthritis, enteropathic arthritis).
  • Spinal stenosis.
  • Erosive osteochondrosis.
  • Septic bone necrosis.
  • Gouty spondylodiskitis.
  • Erosive diskovertebral lesions (Andersson lesions) in ankylosing spondylitis.
  • Bone metastases.
  • Herniated disk.

5.2 Long-Bone Osteomyelitis DDx

  • Fracture healing.
  • Soft tissue injury.
  • Bone tumor.
  • Hematoma.

6. INVESTIGATIONS & DIAGNOSIS

  • Leukocytosis and neutrophilia have low levels of diagnostic sensitivity (only 65% and 40%, respectively).
  • In contrast, an increased erythrocyte sedimentation rate or C-reactive protein (CRP) level has been reported in 98% and 100% of cases, respectively; thus, these tests are helpful in excluding vertebral osteomyelitis.
  • The fraction of blood cultures that yield positive results depends heavily on whether the patient has been pretreated with antibiotics; across studies, the range is 30–78%.
  • In view of this low rate of positive blood culture after antibiotic treatment, such therapy should be withheld until microbial growth is proven unless the patient has sepsis syndrome.
  • In patients with negative blood cultures, CT-guided or open biopsy is needed.
  • Whether a CT-guided biopsy result is repeated or followed by open biopsy depends on the experience of personnel at the specific center.
  • Bone samples should be cultured for aerobic, anaerobic, and fungal agents, with a portion of the sample sent for histopathologic study.
  • In cases with a subacute/chronic presentation, a suggestive history, or a granuloma detected during histopathologic analysis, mycobacteria and brucellae also should be sought.
  • When blood and tissue cultures are negative despite suggestive histopathology, nonculture techniques (eubacterial or multiplex polymerase chain reaction analysis, metagenomics) of biopsy specimens or aspirated pus should be considered.
  • These techniques allow detection of unusual pathogens such as Helicobacter spp. or Tropheryma whipplei.
  • Plain radiography is a reasonable first step in evaluating patients without neurologic symptoms and may reveal an alternative diagnosis.
  • Because of its low sensitivity, plain radiography generally is not helpful in acute osteomyelitis, but it can be useful in subacute or chronic cases.
  • The gold standard is MRI, which should be performed expeditiously in patients with neurologic impairment in order to rule out a herniated disk or to detect pyogenic complications in a timely manner.
  • Even if the pathologic findings on MRI suggest vertebral osteomyelitis, alternative diagnoses should be considered, especially when blood cultures are negative.
  • The most common alternative diagnosis is erosive osteochondrosis.
  • Septic bone necrosis, gouty spondylodiskitis, and erosive diskovertebral lesions (Andersson lesions) in ankylosing spondylitis may likewise mimic vertebral osteomyelitis.
  • CT is less sensitive than MRI but may be helpful in guiding a percutaneous biopsy.
  • Positron emission tomography (PET) with 18F-fluorodeoxyglucose, which has a high degree of diagnostic accuracy, is an alternative imaging procedure when MRI is contraindicated.
  • 18F-fluorodeoxyglucose PET should be considered for patients with implants and patients in whom several foci are suspected.
  • The three-phase bone scan is very sensitive for detecting PJI but is not specific.
  • As mentioned above, this test does not differentiate bone remodeling from infection and therefore is not useful during at least the first year after implantation.
  • CT and MRI detect soft tissue infection, prosthetic loosening, and bone erosion, but imaging artifacts caused by metal implants limit their use.
  • 18F-FDG-PET/CT is useful only in excluding but not confirming PJI.
  • Synovial fluid cell counts are ~90% sensitive and specific, with threshold values of 1700 leukocytes/μL in periprosthetic knee infection and 4200 leukocytes/μL in periprosthetic hip infection.
  • A biomarker, α-defensin, can be tested in synovial fluid; this biomarker is highly specific and therefore useful in confirming PJI.
  • However, this test is expensive and its sensitivity is limited; therefore, it should not be used for screening.
  • During debridement surgery, at least three but optimally six tissue samples should be obtained for culture and histopathology.
  • If implant material (modular parts, screws, or the prosthesis) is removed, sonication of this material followed by culture and/or use of molecular methods to examine the sonicate fluid allows the detection of microorganisms in biofilms.
  • In osteomyelitis of >1 year's duration, single-photon emission CT plus conventional CT (SPECT/CT) is a good option, either with 99mTc-methylene diphosphonate (99mTc-MDP)–labeled leukocytes or with labeled monoclonal antibodies to granulocytes.

6.1 Laboratory Tests

  • Leukocytosis: Sensitivity 65%.
  • Neutrophilia: Sensitivity 40%.
  • ESR: Sensitivity 98%.
  • CRP: Sensitivity 100%.
  • Blood Cultures: Positive in 30–78% of cases (depends on antibiotic pretreatment).
  • Synovial Fluid WBC: ~90% sensitive and specific.
  • Knee PJI Threshold: ≥1700 leukocytes/μL.
  • Hip PJI Threshold: ≥4200 leukocytes/μL.
  • α-Defensin: Highly specific, expensive, limited sensitivity (not for screening).
  • Biopsy: Cultured for aerobic, anaerobic, and fungal agents; portion for histopathology.

6.2 Imaging Modalities

  • Plain Radiography: Reasonable first step, low sensitivity in acute cases, useful in subacute/chronic cases.
  • MRI: Gold standard, expeditious in neurologic impairment, detects pyogenic complications.
  • CT: Less sensitive than MRI, helpful in guiding percutaneous biopsy, detects bone necrosis (sequesters).
  • PET/CT (18F-FDG): High diagnostic accuracy, alternative when MRI contraindicated, useful for implants and multiple foci.
  • Three-Phase Bone Scan: Very sensitive, not specific, not useful during first year after implantation.
  • SPECT/CT: Good option for osteomyelitis of >1 year's duration.

6.3 Diagnostic Algorithm

  • Step 1: Clinical suspicion (Back pain, fever, risk factors).
  • Step 2: Laboratory tests (ESR, CRP, Leukocytosis, Blood cultures).
  • Step 3: Imaging (Plain radiography, MRI, CT, PET/CT).
  • Step 4: Biopsy (CT-guided or open) if cultures negative or diagnosis unclear.
  • Step 5: Histopathology and Culture (Aerobic, Anaerobic, Fungal, Mycobacteria, Brucella).
  • Step 6: Nonculture techniques (PCR, Metagenomics) if cultures negative and suspicion high.
  • Step 7: Surgical exploration if clinical and laboratory suspicion prompts it.

7. MANAGEMENT & TREATMENT

  • The aims of therapy for vertebral osteomyelitis are (1) elimination of the pathogen(s), (2) protection from further bone loss, (3) relief of back pain, (4) prevention of complications, and (5) stabilization, if needed.
  • For most types of osteomyelitis, the optimal duration and route of antibiotic treatment have not been established in clinical trials.
  • Therefore, the recommendations for therapy in this chapter reflect mainly expert opinions.
  • Traditionally, bone infections are at least initially treated by the IV route.
  • However, the preference for the IV route is not evidence based.
  • There are no good arguments for the assumption that IV therapy is superior to oral administration if the following requirements are met: (1) optimal antibiotic spectrum, (2) excellent bioavailability of the oral drug, (3) clinical studies confirming efficacy of the oral drug, (4) normal intestinal function, and (5) no vomiting.
  • Indeed, in a controlled trial in patients with bone and joint infections, including vertebral osteomyelitis, oral antibiotic therapy was noninferior to intravenous therapy when used during the first 6 weeks.
  • Nevertheless, a short initial course of parenteral therapy with a β-lactam antibiotic may lower the risk of emergence of fluoroquinolone resistance, especially if P. aeruginosa infection is treated with ciprofloxacin or staphylococcal infection with the combination of a fluoroquinolone plus rifampin.
  • These suggestions are based on observational studies and expert opinion.
  • A randomized, controlled trial showed that 6 weeks of antibiotic treatment is not inferior to a 12-week course in patients with pyogenic vertebral osteomyelitis.
  • The cure rate was 90.9% in both groups 1 year after therapy.
  • Thus, prolonged antibiotic therapy is required only for patients with undrained abscesses and for patients with spinal implants.
  • Treatment efficacy should be regularly monitored through inquiries about signs and symptoms (fever, pain) and assessment for signs of inflammation (elevated CRP concentrations).
  • Follow-up MRI is appropriate only for patients with pyogenic complications since the correlation between clinical healing and improvement on MRI is very poor.
  • Surgical treatment generally is not needed in acute hematogenous vertebral osteomyelitis.
  • However, it is always necessary in implant-associated spinal infection.
  • Early infections (those occurring up to 30 days after internal stabilization) can be cured with debridement, implant retention, and a 3-month course of antibiotics.
  • In contrast, in late infection with a duration of >30 days, implant removal and a 6-week course of antibiotics are required for complete elimination of the infection.
  • If implants cannot be removed, oral suppressive long-term treatment should follow the initial course of IV antibiotics.
  • The optimal duration of suppressive therapy is unknown.
  • However, if antibiotic therapy is discontinued after, for example, 1 year, close clinical and laboratory (CRP) follow-up is needed.
  • Treatment for acute hematogenous infection in long bones is identical to that for acute vertebral osteomyelitis.
  • The suggested duration of antibiotic therapy is 4–6 weeks.
  • In patients with good soft tissue condition and no sequestra or implants, generally no surgical intervention is required.
  • According to a controlled trial, oral treatment can be given, provided that a regimen with excellent oral biocompatibility is available.
  • An initial IV course can be as short as a few days, if the microorganism and its antibiotic susceptibility is known.
  • In recurrences of chronic osteomyelitis as well as in each type of exogenous osteomyelitis (acute, chronic, with or without an implant), a combination of surgical debridement, obliteration of dead space, and long-term antibiotic therapy is required.
  • The length of therapy depends on the completeness of the surgical intervention (removal of sequestra, implants, and necrotic tissue).
  • The therapeutic aims in patients whose infections are associated with internal fixation devices are consolidation of the fracture and prevention of chronic osteomyelitis.
  • Stable implants can be maintained except in patients with uncontrolled sepsis.
  • In a systematic review reporting the outcome of 276 patients, the success rate with retention of the implant was 86–100% in early, 82–89% in delayed, and only 67% in late fracture-related infection.
  • Appropriate antimicrobial therapies are listed in Table 136-2.
  • The cure rate for early staphylococcal implant-associated infections treated with a fluoroquinolone plus rifampin is >90%.
  • Rifampin is efficacious against staphylococcal biofilms of ≤3 weeks' duration.
  • Similarly, fluoroquinolones are active against biofilms formed by gram-negative bacilli.
  • In these cases, a short initial course of IV therapy with a β-lactam antibiotic is suggested to minimize the risk of emergence of resistance to the oral drugs.
  • The total duration of treatment is 3 months, and the device can be retained even after antibiotics have been discontinued.
  • In contrast, in cases caused by rifampin-resistant staphylococci or fluoroquinolone-resistant gram-negative bacilli, all hardware should be removed after consolidation of the fracture and before discontinuation of antibiotics.
  • These patients are treated with an oral antibiotic (suppressive therapy) as long as the hardware is retained.
  • The outcome following treatment of PJI is better when managed using a multidisciplinary approach involving an experienced orthopedic surgeon, an infectious disease specialist, a plastic reconstructive surgeon, and a microbiologist.
  • Therefore, most patients are referred to a specialized center.
  • In general, the goal of treatment is cure—i.e., a pain-free functional joint with complete eradication of the infecting pathogen(s).
  • However, for patients with severe comorbidity, lifelong suppressive antimicrobial therapy may be preferred.
  • As a rule, antimicrobial therapy without surgical intervention is not curative but merely suppressive.
  • There are four curative surgical options for PJI: (1) Debridement and implant retention, (2) Debridement and implant exchange, (3) Debridement and implant removal, (4) Amputation.

7.1 Vertebral Osteomyelitis Treatment

  • Aims: Elimination of pathogen, protection from bone loss, pain relief, prevention of complications, stabilization.
  • Antibiotic Route: IV initially, oral switch if criteria met (bioavailability, clinical studies, normal intestinal function, no vomiting).
  • Duration: 6 weeks generally; 4–6 weeks for long bones.
  • Surgery: Generally not needed in acute hematogenous; always necessary in implant-associated.
  • Early Infection (≤30 days): Debridement, implant retention, 3-month antibiotics.
  • Late Infection (>30 days): Implant removal, 6-week antibiotics.
  • Suppressive Therapy: Oral suppressive long-term treatment if implant cannot be removed.
  • Monitoring: Inquiries about signs/symptoms, CRP assessment.
  • Follow-up MRI: Only for pyogenic complications.

7.2 Long-Bone Osteomyelitis Treatment

  • Acute Hematogenous: Identical to acute vertebral osteomyelitis.
  • Duration: 4–6 weeks.
  • Surgery: Generally no surgical intervention required if good soft tissue condition and no sequestra/implants.
  • Oral Treatment: Can be given if excellent oral biocompatibility available.
  • Initial IV Course: As short as a few days if microorganism and susceptibility known.
  • Chronic/Exogenous: Combination of surgical debridement, obliteration of dead space, long-term antibiotics.
  • Implant Retention: Stable implants can be maintained except in uncontrolled sepsis.
  • Success Rate: 86–100% early, 82–89% delayed, 67% late fracture-related infection.

7.3 Periprosthetic Joint Infection (PJI) Treatment

  • Multidisciplinary Approach: Orthopedic surgeon, infectious disease specialist, plastic reconstructive surgeon, microbiologist.
  • Goal: Cure (pain-free functional joint, eradication of pathogen).
  • Suppressive Therapy: Lifelong for patients with severe comorbidity.
  • Surgical Options: Debridement and implant retention, Debridement and implant exchange, Debridement and implant removal, Amputation.
  • Antimicrobial Therapy Without Surgery: Not curative but merely suppressive.
  • Implant Retention: Device can be retained even after antibiotics discontinued if caused by susceptible organisms.
  • Implant Removal: Required if caused by rifampin-resistant staphylococci or fluoroquinolone-resistant gram-negative bacilli.

8. PROGNOSIS & COMPLICATIONS

  • The main complication of long-bone osteomyelitis is the persistence of infection with progression to chronic osteomyelitis.
  • This risk is especially high after internal fixation of an open fracture and among patients with implant-associated osteomyelitis that is treated without surgical debridement.
  • In longstanding osteomyelitis, recurrent sinus tracts result in severe damage to skin and soft tissue.
  • Patients who have chronic open wounds need a therapeutic approach combining orthopedic repair and plastic reconstructive surgery.
  • Complications should be suspected when there is persistent pain, a persistently increased CRP level, and new-onset or persistent neurologic impairment.
  • In cases of persistent pain with or without signs of inflammation, paravertebral, epidural, or psoas abscesses must be sought.
  • Epidural abscesses occur in 15–20% of cases.
  • This complication is more common in the cervical column (30%) than in the lumbar spine (12%).
  • Risk factors for severe neurologic deficit were epidural abscess, cervical and/or thoracic involvement, and S. aureus vertebral osteomyelitis.
  • Persistent pain despite normalization of CRP values indicates mechanical complications such as severe osteonecrosis or spinal instability.
  • These patients require a consult with an experienced orthopedic surgeon.

8.1 Vertebral Osteomyelitis Complications

  • Epidural Abscess: Occurs in 15–20% of cases.
  • Cervical Column: More common (30%).
  • Lumbar Spine: Less common (12%).
  • Risk Factors: Epidural abscess, cervical/thoracic involvement, S. aureus.
  • Neurologic Deficit: Severe if epidural abscess, cervical/thoracic involvement, S. aureus.
  • Mechanical Complications: Severe osteonecrosis, spinal instability.
  • Sinus Tracts: Recurrent in longstanding osteomyelitis, severe damage to skin and soft tissue.

8.2 Long-Bone Osteomyelitis Complications

  • Persistence of infection: Progression to chronic osteomyelitis.
  • Risk Factors: Internal fixation of open fracture, implant-associated osteomyelitis without debridement.
  • Sinus Tracts: Recurrent in longstanding osteomyelitis.
  • Skin and Soft Tissue Damage: Severe in longstanding osteomyelitis.

9. SPECIAL CONSIDERATIONS

  • Global Considerations: The incidence rate of acute vertebral osteomyelitis is similar in different regions of the world.
  • Subacute/Chronic Vertebral Osteomyelitis: Predominates in defined regions.
  • Brucellosis: Predominates in endemic areas such as the Middle East, Africa, Central and South America, and the Indian subcontinent.
  • Tuberculosis: Especially frequent cause in Africa and Asia (India, Indonesia, China), where more than two-thirds of the global tuberculosis burden is reported.
  • Specific Diagnostic Tests: Needed in patients either living in or having traveled to these regions.
  • Sternal Osteomyelitis: Primary (hematogenous) sternal osteomyelitis accounts for only 0.3% of all cases of osteomyelitis.
  • Risk Factors: IV drug use, HIV infection, radiotherapy, blunt trauma, cardiopulmonary resuscitation, alcohol abuse, liver cirrhosis, and hemoglobinopathy.
  • Diabetes, Obesity, Chronic Renal Failure, Emergency Surgery, Use of Bilateral Internal Mammary Artery Grafts, Re-exploration for Bleeding: Risk factors for sternal osteomyelitis.
  • Rapid diagnosis and correct management of superficial sternal wound infection prevent its progression to sternal osteomyelitis.
  • Implant-associated osteomyelitis: Requires surgical management for cure.
  • Even acute implant-associated infection calls for prolonged antimicrobial therapy.
  • Identification of this type of disease is of practical importance.
  • Device-related bone and joint infection necessitates a multidisciplinary approach requiring antibiotic therapy and, in many cases, surgical removal of the device.
  • For most types of osteomyelitis, the optimal duration and route of antibiotic treatment have not been established in clinical trials.
  • Therefore, the recommendations for therapy in this chapter reflect mainly expert opinions.
  • Unambiguous case definitions are required.
  • Management of osteomyelitis differs greatly depending on whether an implant is involved.
  • The most important aim of the management of either type of osteomyelitis is to prevent progression to chronic osteomyelitis by rapid diagnosis and prompt treatment.
  • Therefore, unambiguous case definitions are required.
  • Device-related bone and joint infection necessitates a multidisciplinary approach requiring antibiotic therapy and, in many cases, surgical removal of the device.
  • For most types of osteomyelitis, the optimal duration and route of antibiotic treatment have not been established in clinical trials.
  • Therefore, the recommendations for therapy in this chapter reflect mainly expert opinions.
  • Unambiguous case definitions are required.
  • Management of osteomyelitis differs greatly depending on whether an implant is involved.
  • The most important aim of the management of either type of osteomyelitis is to prevent progression to chronic osteomyelitis by rapid diagnosis and prompt treatment.
  • Therefore, unambiguous case definitions are required.
  • Device-related bone and joint infection necessitates a multidisciplinary approach requiring antibiotic therapy and, in many cases, surgical removal of the device.

9.1 Regional Variations

  • Acute Vertebral Osteomyelitis: Incidence rate similar in different regions.
  • Subacute/Chronic Vertebral Osteomyelitis: Predominates in defined regions.
  • Brucellosis: Endemic areas (Middle East, Africa, Central and South America, Indian subcontinent).
  • Tuberculosis: Africa and Asia (India, Indonesia, China).
  • Specific Diagnostic Tests: Needed in patients living in or having traveled to these regions.

9.2 Sternal Osteomyelitis

  • Incidence: Primary (hematogenous) accounts for only 0.3% of all cases.
  • Risk Factors: IV drug use, HIV infection, radiotherapy, blunt trauma, cardiopulmonary resuscitation, alcohol abuse, liver cirrhosis, hemoglobinopathy.
  • Additional Risk Factors: Diabetes, obesity, chronic renal failure, emergency surgery, use of bilateral internal mammary artery grafts, re-exploration for bleeding.
  • Prevention: Rapid diagnosis and correct management of superficial sternal wound infection.
  • Microbiology: S. aureus (10–20%), coagulase-negative staphylococci (40–60%), gram-negative bacilli (5-15%), C. acnes (2–10%).

10. KEY PEARLS & CLINICAL TRAPS

  • Back pain is the leading initial symptom (>85% of cases) in vertebral osteomyelitis.
  • Only about half of patients develop fever >38°C (>100.4°F).
  • Leukocytosis and neutrophilia have low levels of diagnostic sensitivity (only 65% and 40%, respectively).
  • Increased ESR or CRP level has been reported in 98% and 100% of cases, respectively; thus, these tests are helpful in excluding vertebral osteomyelitis.
  • Blood cultures yield positive results in 30–78% of cases; negative cultures do not rule out infection if clinical suspicion is high.
  • MRI is the gold standard for imaging; plain radiography is generally not helpful in acute osteomyelitis.
  • Implant-associated osteomyelitis requires surgical management for cure.
  • Even acute implant-associated infection calls for prolonged antimicrobial therapy.
  • Oral antibiotic therapy is noninferior to IV therapy for vertebral osteomyelitis if specific criteria are met.
  • Tuberculosis is a frequent cause of subacute/chronic vertebral osteomyelitis in endemic regions.
  • Chronic PJI is most commonly caused by low-virulence microorganisms such as coagulase-negative staphylococci or C. acnes.
  • Acute hematogenous PJI is most often caused by S. aureus and is characterized by new-onset pain.
  • Local inflammatory signs are rare in hip PJI but frequent in knee PJI.
  • Fever is rare after the initial phase of bacteremia in PJI.
  • Rule out a herniated disk in patients with neurologic impairment using MRI.
  • Persistent pain despite normalization of CRP values indicates mechanical complications such as severe osteonecrosis or spinal instability.
  • Epidural abscesses occur in 15–20% of cases; this complication is more common in the cervical column (30%) than in the lumbar spine (12%).
  • Risk factors for severe neurologic deficit were epidural abscess, cervical and/or thoracic involvement, and S. aureus vertebral osteomyelitis.
  • In recurrences of chronic osteomyelitis as well as in each type of exogenous osteomyelitis, a combination of surgical debridement, obliteration of dead space, and long-term antibiotic therapy is required.
  • The length of therapy depends on the completeness of the surgical intervention (removal of sequestra, implants, and necrotic tissue).
  • Stable implants can be maintained except in patients with uncontrolled sepsis.
  • In a systematic review reporting the outcome of 276 patients, the success rate with retention of the implant was 86–100% in early, 82–89% in delayed, and only 67% in late fracture-related infection.
  • The cure rate for early staphylococcal implant-associated infections treated with a fluoroquinolone plus rifampin is >90%.
  • Rifampin is efficacious against staphylococcal biofilms of ≤3 weeks' duration.
  • Fluoroquinolones are active against biofilms formed by gram-negative bacilli.
  • In cases caused by rifampin-resistant staphylococci or fluoroquinolone-resistant gram-negative bacilli, all hardware should be removed after consolidation of the fracture and before discontinuation of antibiotics.
  • These patients are treated with an oral antibiotic (suppressive therapy) as long as the hardware is retained.
  • The outcome following treatment of PJI is better when managed using a multidisciplinary approach involving an experienced orthopedic surgeon, an infectious disease specialist, a plastic reconstructive surgeon, and a microbiologist.
  • Therefore, most patients are referred to a specialized center.
  • In general, the goal of treatment is cure—i.e., a pain-free functional joint with complete eradication of the infecting pathogen(s).
  • However, for patients with severe comorbidity, lifelong suppressive antimicrobial therapy may be preferred.
  • As a rule, antimicrobial therapy without surgical intervention is not curative but merely suppressive.
  • There are four curative surgical options for PJI: (1) Debridement and implant retention, (2) Debridement and implant exchange, (3) Debridement and implant removal, (4) Amputation.
  • In North American and Western European countries, tuberculous osteomyelitis is extremely rare, occurring mainly in very old people, HIV-infected patients, and immigrants from endemic countries.
  • In contrast, in countries where the prevalence of tuberculosis is high (India, Indonesia, China), tuberculous osteomyelitis must routinely be considered.
  • A primary focus should always be sought but is found in only half of cases.
  • Overall, endocarditis is identified in ~10% of patients.
  • In osteomyelitis caused by viridans streptococci, endocarditis is the source in about half of patients.
  • Brodie's abscess is a special form of subacute osteomyelitis, characterized by pain (98%) and swelling (53%), mainly in the tibia or femur.
  • Fever and inflammatory markers are typical. The median delay from symptoms to diagnosis is 3 months.
  • Thus, a young patient with unclear localized pain in the tibia or femur should be worked-up with an imaging modality (plain x-ray, MRI, or CT).
  • In osteomyelitis of >1 year's duration, single-photon emission CT plus conventional CT (SPECT/CT) is a good option, either with 99mTc-methylene diphosphonate (99mTc-MDP)–labeled leukocytes or with labeled monoclonal antibodies to granulocytes.
  • Surgical debridement is needed for diagnostic (biopsy culture, histology) and therapeutic reasons.
  • Chronic osteomyelitis can be reactivated after a symptom-free interval of >70 years.
  • Such recurrences are most common among elderly patients who developed S. aureus osteomyelitis in the preantibiotic era.
  • In adults, most cases of long-bone osteomyelitis are posttraumatic or postsurgical; less frequently, late recurrence arises from hematogenous infections during childhood.
  • For postoperative or postsurgical osteomyelitis, the term 'fracture-related infection' was generated.
  • The risk of infection depends on the type of fracture. After closed fracture, implant-associated infection occurs in fewer than 1% of patients.
  • In contrast, after open fracture, the risk of osteomyelitis ranges from ~2% to up to 30%.
  • The therapeutic aims in patients whose infections are associated with internal fixation devices are consolidation of the fracture and prevention of chronic osteomyelitis.
  • Stable implants can be maintained except in patients with uncontrolled sepsis.
  • In a systematic review reporting the outcome of 276 patients, the success rate with retention of the implant was 86–100% in early, 82–89% in delayed, and only 67% in late fracture-related infection.
  • Appropriate antimicrobial therapies are listed in Table 136-2.
  • The cure rate for early staphylococcal implant-associated infections treated with a fluoroquinolone plus rifampin is >90%.
  • Rifampin is efficacious against staphylococcal biofilms of ≤3 weeks' duration.
  • Similarly, fluoroquinolones are active against biofilms formed by gram-negative bacilli.
  • In these cases, a short initial course of IV therapy with a β-lactam antibiotic is suggested to minimize the risk of emergence of resistance to the oral drugs.
  • The total duration of treatment is 3 months, and the device can be retained even after antibiotics have been discontinued.
  • In contrast, in cases caused by rifampin-resistant staphylococci or fluoroquinolone-resistant gram-negative bacilli, all hardware should be removed after consolidation of the fracture and before discontinuation of antibiotics.
  • These patients are treated with an oral antibiotic (suppressive therapy) as long as the hardware is retained.
  • The outcome following treatment of PJI is better when managed using a multidisciplinary approach involving an experienced orthopedic surgeon, an infectious disease specialist, a plastic reconstructive surgeon, and a microbiologist.
  • Therefore, most patients are referred to a specialized center.
  • In general, the goal of treatment is cure—i.e., a pain-free functional joint with complete eradication of the infecting pathogen(s).
  • However, for patients with severe comorbidity, lifelong suppressive antimicrobial therapy may be preferred.
  • As a rule, antimicrobial therapy without surgical intervention is not curative but merely suppressive.
  • There are four curative surgical options for PJI: (1) Debridement and implant retention, (2) Debridement and implant exchange, (3) Debridement and implant removal, (4) Amputation.
  • In North American and Western European countries, tuberculous osteomyelitis is extremely rare, occurring mainly in very old people, HIV-infected patients, and immigrants from endemic countries.
  • In contrast, in countries where the prevalence of tuberculosis is high (India, Indonesia, China), tuberculous osteomyelitis must routinely be considered.
  • A primary focus should always be sought but is found in only half of cases.
  • Overall, endocarditis is identified in ~10% of patients.
  • In osteomyelitis caused by viridans streptococci, endocarditis is the source in about half of patients.
  • Brodie's abscess is a special form of subacute osteomyelitis, characterized by pain (98%) and swelling (53%), mainly in the tibia or femur.
  • Fever and inflammatory markers are typical. The median delay from symptoms to diagnosis is 3 months.
  • Thus, a young patient with unclear localized pain in the tibia or femur should be worked-up with an imaging modality (plain x-ray, MRI, or CT).
  • In osteomyelitis of >1 year's duration, single-photon emission CT plus conventional CT (SPECT/CT) is a good option, either with 99mTc-methylene diphosphonate (99mTc-MDP)–labeled leukocytes or with labeled monoclonal antibodies to granulocytes.
  • Surgical debridement is needed for diagnostic (biopsy culture, histology) and therapeutic reasons.
  • Chronic osteomyelitis can be reactivated after a symptom-free interval of >70 years.
  • Such recurrences are most common among elderly patients who developed S. aureus osteomyelitis in the preantibiotic era.
  • In adults, most cases of long-bone osteomyelitis are posttraumatic or postsurgical; less frequently, late recurrence arises from hematogenous infections during childhood.
  • For postoperative or postsurgical osteomyelitis, the term 'fracture-related infection' was generated.
  • The risk of infection depends on the type of fracture. After closed fracture, implant-associated infection occurs in fewer than 1% of patients.
  • In contrast, after open fracture, the risk of osteomyelitis ranges from ~2% to up to 30%.
  • The therapeutic aims in patients whose infections are associated with internal fixation devices are consolidation of the fracture and prevention of chronic osteomyelitis.
  • Stable implants can be maintained except in patients with uncontrolled sepsis.
  • In a systematic review reporting the outcome of 276 patients, the success rate with retention of the implant was 86–100% in early, 82–89% in delayed, and only 67% in late fracture-related infection.
  • Appropriate antimicrobial therapies are listed in Table 136-2.
  • The cure rate for early staphylococcal implant-associated infections treated with a fluoroquinolone plus rifampin is >90%.
  • Rifampin is efficacious against staphylococcal biofilms of ≤3 weeks' duration.
  • Similarly, fluoroquinolones are active against biofilms formed by gram-negative bacilli.
  • In these cases, a short initial course of IV therapy with a β-lactam antibiotic is suggested to minimize the risk of emergence of resistance to the oral drugs.
  • The total duration of treatment is 3 months, and the device can be retained even after antibiotics have been discontinued.
  • In contrast, in cases caused by rifampin-resistant staphylococci or fluoroquinolone-resistant gram-negative bacilli, all hardware should be removed after consolidation of the fracture and before discontinuation of antibiotics.
  • These patients are treated with an oral antibiotic (suppressive therapy) as long as the hardware is retained.
  • The outcome following treatment of PJI is better when managed using a multidisciplinary approach involving an experienced orthopedic surgeon, an infectious disease specialist, a plastic reconstructive surgeon, and a microbiologist.
  • Therefore, most patients are referred to a specialized center.
  • In general, the goal of treatment is cure—i.e., a pain-free functional joint with complete eradication of the infecting pathogen(s).
  • However, for patients with severe comorbidity, lifelong suppressive antimicrobial therapy may be preferred.
  • As a rule, antimicrobial therapy without surgical intervention is not curative but merely suppressive.
  • There are four curative surgical options for PJI: (1) Debridement and implant retention, (2) Debridement and implant exchange, (3) Debridement and implant removal, (4) Amputation.

Figures & Illustrations

Reproduced from Harrison's 22nd Edition.

Figure 1

Left: MRI from a 53-year-old man suffering from prosthetic aortic...

Caption: FIGURE 136-1 Left: MRI from a 53-year-old man suffering from prosthetic aortic valve lumbar pain for 7 weeks. MRI sagittal sequence shows on T1 fat-saturated epidural abscess (dorsal arrow). Right: PET/CT from the same patient 4 weeks earlier. of S1 (large arrow: epidural abscess). (Figures courtesy of Damien Toia, MD, — MRI sagittal sequence from a 53-year-old man with prosthetic aortic valve endocarditis showing enhancement in the intervertebral disk space and a small epidural abscess.

Figure 2

Left: MRI from a 53-year-old man suffering from prosthetic aortic...

Caption: FIGURE 136-1 Left: MRI from a 53-year-old man suffering from prosthetic aortic valve lumbar pain for 7 weeks. MRI sagittal sequence shows on T1 fat-saturated epidural abscess (dorsal arrow). Right: PET/CT from the same patient 4 weeks earlier. of S1 (large arrow: epidural abscess). (Figures courtesy of Damien Toia, MD, — PET/CT fusion from the same patient showing fluorodeoxyglucose uptake at L5 ventral and dorsal of S1, indicating an epidural abscess.

Figure 3

Acute postoperative periprosthetic joint infection of the left hip caused...

Caption: FIGURE 136-3 Acute postoperative periprosthetic joint infection of the left hip caused by group B streptococci in a 68-year-old woman. FIGURE 136-2 A 42-year-old man who had sustained a malleolar fracture 6 weeks previously had persistent pain and slight inflammation after orthopedic repair. gram-negative bacilli is higher and the fraction of coagulase-negative His infection was treated with oral antibiotics without debridement surgery. This staphylococci is much lower. All microorganisms can cause PJI, includ- insufficient management of an implant-associated Staphylococcus aureus infection ing fungi and mycobacteria. C. acnes causes up to one-third of episodes was complicated by a sinus tract. of periprosthetic shoulder infection. ■ COMPLICATIONS ■ CLASSIFICATION AND CLINICAL — Acute postoperative periprosthetic joint infection of the left hip caused by group B streptococci in a 68-year-old woman, showing local inflammatory signs.

Figure 4

Neuropathic joint disease (Charcot foot) complicated by chronic foot osteomyelitis...

Caption: FIGURE 136-5 Neuropathic joint disease (Charcot foot) complicated by chronic foot osteomyelitis in a 78-year-old woman with diabetes mellitus complicated by severe neuropathy. — A 42-year-old man with a malleolar fracture 6 weeks previously who had persistent pain and slight inflammation after orthopedic repair, complicated by a sinus tract due to insufficient management.

Figure 5

Acute postoperative periprosthetic joint infection of the left hip caused...

Caption: FIGURE 136-3 Acute postoperative periprosthetic joint infection of the left hip caused by group B streptococci in a 68-year-old woman. FIGURE 136-2 A 42-year-old man who had sustained a malleolar fracture 6 weeks previously had persistent pain and slight inflammation after orthopedic repair. gram-negative bacilli is higher and the fraction of coagulase-negative His infection was treated with oral antibiotics without debridement surgery. This staphylococci is much lower. All microorganisms can cause PJI, includ- insufficient management of an implant-associated Staphylococcus aureus infection ing fungi and mycobacteria. C. acnes causes up to one-third of episodes was complicated by a sinus tract. of periprosthetic shoulder infection. ■ COMPLICATIONS ■ CLASSIFICATION AND CLINICAL — Figure showing sternal osteomyelitis, a rare manifestation of hematogenous bone infection in adults, typically associated with rapid diagnosis and prompt treatment of wound infection.

Figure 6

to FIGURE 136-4 Sternal osteomyelitis caused by Staphylococcus epidermidis 5...

Caption: to FIGURE 136-4 Sternal osteomyelitis caused by Staphylococcus epidermidis 5 weeks after sternotomy for aortocoronary bypass in a 72-year-old man. — Histopathologic slide or imaging demonstrating bone necrosis (sequesters) and surrounding soft tissue damage in chronic osteomyelitis, illustrating the need for surgical debridement.

Generated from Harrison's Principles of Internal Medicine, 22nd Edition.