# CIM Case: Brodie's Abscess ## Clinical Scenario **Patient:** 18-year-old Malaysian international student **Presentation:** 6-week history of left knee pain and swelling, initially attributed to soccer injury, worsening despite rest **Relevant history:** Previously healthy, no prior infections or surgery, no immunocompromise, no recent travel to endemic areas, no systemic symptoms (no fever, night sweats, weight loss) **Examination findings:** - Well-appearing young man, afebrile - Warm, tender swelling over medial aspect of proximal tibia - No overlying skin changes or sinus - Full range of motion at knee (limited by pain at extremes) - No effusion - No regional lymphadenopathy - Neurovascularly intact distally - Remainder of examination unremarkable --- ## Investigations Provided ### Laboratory Results | Test | Result | Normal Range | Interpretation | |------|--------|--------------|----------------| | Hb | 142 g/L | 130-170 g/L | Normal | | WCC | 8.5 ×10⁹/L | 4-11 ×10⁹/L | Normal | | Platelets | 285 ×10⁹/L | 150-400 ×10⁹/L | Normal | | CRP | 18 mg/L | <5 mg/L | ↑ Mildly elevated | | ESR | 25 mm/hr | <15 mm/hr | ↑ Mildly elevated | | Albumin | 42 g/L | 35-50 g/L | Normal | | Creatinine | 78 μmol/L | 60-110 μmol/L | Normal | | Blood cultures | Negative | - | No growth | ### Imaging **Image 1: AP and Lateral Radiographs of Left Knee/Proximal Tibia** **Radiological features:** - Well-defined lucent lesion in proximal tibial metaphysis - Eccentric location (medial) - Size approximately 3 x 2cm - **Dense sclerotic rim** (reactive bone) - No aggressive periosteal reaction - No cortical breakthrough - No soft tissue mass - Open physis (skeletally immature) **Image 2: MRI of Left Proximal Tibia** **Findings:** - Well-defined T2-hyperintense lesion in proximal tibial metaphysis - **Penumbra sign**: High T1 signal rim around abscess cavity (granulation tissue) - Surrounding marrow oedema - No cortical breach - No soft tissue abscess - Thin rim enhancement on post-contrast images --- ## Questions & Model Answers **Diagnosis: Brodie's Abscess (Subacute Osteomyelitis)** **Differential Diagnosis:** | Diagnosis | Supporting Features | Against | |-----------|---------------------|---------| | **Brodie's abscess** | Well-defined lytic lesion with sclerotic rim, penumbra sign, metaphyseal location, mild inflammatory markers | No systemic symptoms | | Eosinophilic granuloma (LCH) | Lytic lesion in young patient | Usually more aggressive appearance, no sclerotic rim | | Chondroblastoma | Epiphyseal/apophyseal lesion, young patient | This lesion is metaphyseal, no matrix | | Aneurysmal bone cyst | Young patient, expansile lesion | Fluid-fluid levels expected on MRI | | Giant cell tumour | Lytic lesion | Usually in closed physis, epiphyseal-metaphyseal | | Enchondroma | Lytic lesion | Usually in diaphysis, cartilage matrix expected | **Key Features of Brodie's Abscess:** - Subacute to chronic presentation (weeks to months) - Minimal or absent systemic symptoms - Normal or mildly elevated inflammatory markers - Well-defined lytic lesion with sclerotic rim - Metaphyseal location (most common) - **Penumbra sign** on MRI (pathognomonic) > **Consultant Tip:** The penumbra sign (T1-bright rim around the abscess) is highly specific for Brodie's abscess. It represents vascular granulation tissue and helps distinguish from tumours. **Pathophysiology:** | Stage | Description | |-------|-------------| | Initial infection | Haematogenous spread to metaphysis (slow vascular flow) | | Host containment | Balance between organism virulence and host immunity | | Abscess formation | Walled-off cavity with granulation tissue | | Chronic phase | Dense sclerotic bone forms around abscess | **Why Metaphyseal Location?** - Tortuous vascular loops in metaphysis - Slow blood flow facilitates bacterial seeding - Relative avascularity at metaphyseal side of physis - Lack of phagocytic cells in this zone **Microbiology:** | Organism | Frequency | Notes | |----------|-----------|-------| | **Staphylococcus aureus** | 50-60% | Most common at all ages | | Coagulase-negative staph | 10-15% | Consider in prosthetic joints | | Streptococci | 5-10% | Group A and B | | Kingella kingae | 5-10% | Common in children <5 years | | Culture negative | 30-50% | Due to prior antibiotics or low virulence | **Important Considerations:** - Prior antibiotics reduce culture yield significantly - Prolonged transport affects culture sensitivity - Histology confirms infection even if cultures negative - Consider TB in endemic regions (this patient from Malaysia) > **Consultant Tip:** Up to 50% of Brodie's abscesses are culture-negative. This doesn't change the need for surgical debridement - histology will confirm the diagnosis. **Roberts Classification of Brodie's Abscess (by Location):** | Type | Location | Description | |------|----------|-------------| | **Ia** | Metaphyseal | Centred in metaphysis, long axis parallel to bone | | **Ib** | Metaphyseal | Centred in metaphysis, extending to cortex | | **II** | Epiphyseal | Involving epiphysis (crosses physis) | | **III** | Diaphyseal | Within diaphysis | | **IV** | Cortical | Eccentric, cortical location | **This Patient: Type Ib** (metaphyseal, eccentric, approaching cortex) **Imaging Characteristics:** | Feature | Description | |---------|-------------| | Radiograph | Lucent lesion with sclerotic rim, ± sequestrum | | CT | Better defines cortical involvement, sequestra | | MRI (T1) | Low signal cavity, **high signal penumbra rim** | | MRI (T2) | High signal fluid in cavity, surrounding oedema | | MRI (contrast) | Rim enhancement | **Penumbra Sign Explained:** - T1-bright rim = vascular granulation tissue - Present in pyogenic infections - Absent in tuberculosis and tumours - Sensitivity ~75%, specificity ~95% for infection > **Consultant Tip:** The Roberts classification helps predict complexity of surgical access. Type II lesions crossing the physis may require careful technique to avoid growth disturbance. **Management Approach:** **Step 1: Confirm Diagnosis** - Biopsy essential before definitive treatment - CT-guided or open biopsy - Send for: Gram stain, culture (aerobic, anaerobic, TB, fungal), histology **Step 2: Surgical Management** | Approach | Description | |----------|-------------| | **Curettage and debridement** | Standard approach, create cortical window | | Fenestration | Curettage + leave wound open (larger cavities) | | Local antibiotic delivery | PMMA beads or calcium sulphate with antibiotics | | Bone grafting | Usually not required if cavity small | **Surgical Technique:** 1. Cortical window (large enough for visualisation) 2. Thorough curettage of cavity (send tissue for culture/histology) 3. High-pressure lavage 4. Local antibiotic delivery (optional but recommended) 5. Closure over drain or leave open (depends on size/contamination) **Step 3: Antibiotic Therapy** | Phase | Duration | Route | Agent | |-------|----------|-------|-------| | Initial | 2-4 weeks | IV | Flucloxacillin (or vancomycin if MRSA) | | Consolidation | 4-6 weeks | Oral | Clindamycin or fluoroquinolone | | Total | 6-12 weeks | - | Guided by clinical response | **Empirical Regimen (pending cultures):** - **Flucloxacillin** 2g IV Q6H (covers S. aureus) - Add **gentamicin** if Gram-negative cover needed - Consider **vancomycin** if MRSA risk factors > **Consultant Tip:** Surgical debridement is essential - antibiotics alone fail in up to 70% of cases. The cavity must be opened and debrided to allow healing. **Outcomes:** | Outcome | Percentage | |---------|------------| | Complete resolution | 85-95% | | Recurrence | 5-10% | | Progression to chronic osteomyelitis | 2-5% | | Growth disturbance (in children) | Rare if physis spared | **Factors Affecting Outcome:** | Factor | Impact | |--------|--------| | Adequacy of debridement | Most important factor | | Organism identification | Guides targeted therapy | | Compliance with antibiotics | Essential for cure | | Host factors (diabetes, immunocompromise) | Worse outcomes | | Delay in diagnosis | Larger cavity, more difficult treatment | **Complications:** | Complication | Prevention/Management | |--------------|----------------------| | **Recurrence** | Adequate debridement, full antibiotic course | | **Pathological fracture** | Protected weight-bearing, bone grafting if large defect | | **Growth disturbance** | Avoid iatrogenic physis damage | | **Chronic osteomyelitis** | Early diagnosis and adequate treatment | | **Secondary abscess** | Complete debridement | **Monitoring:** - Clinical review at 2, 6, and 12 weeks - Inflammatory markers (CRP) should normalise - Repeat imaging at 3 months to confirm healing - Long-term follow-up until skeletal maturity if physis at risk > **Consultant Tip:** CRP is the best marker for treatment response. Expect it to normalise within 2-3 weeks of adequate surgery and antibiotics. Persistently elevated CRP suggests inadequate debridement or resistant organism. **When to Suspect Tuberculous Osteomyelitis:** | Feature | Pyogenic | Tuberculous | |---------|----------|-------------| | Presentation | Weeks | Months to years | | Systemic symptoms | Usually absent | May have night sweats, weight loss | | Inflammatory markers | Mildly elevated | Variable | | X-ray | Sclerotic rim | **Less sclerosis**, soft tissue swelling | | MRI | Penumbra sign present | Penumbra sign **absent** | | Cultures | Usually positive | Often negative, need AFB/PCR | **This Patient's Risk Factors for TB:** - Malaysian origin (TB-endemic region) - International student (possible recent exposure) **Workup for TB if Suspected:** - QuantiFERON Gold or Mantoux test - Chest X-ray - Tissue for AFB smear, TB culture (takes 6-8 weeks) - TB PCR (rapid result) - Histology showing granulomatous inflammation **Management of Skeletal TB:** - **Antituberculous therapy**: RIPE regimen (Rifampicin, Isoniazid, Pyrazinamide, Ethambutol) - Duration: 9-12 months for bone TB - Surgery: Reserved for abscess drainage, debridement, instability - Less aggressive surgery than pyogenic (tends to heal with medical therapy) **Key Differences in Surgical Approach:** | Pyogenic | Tuberculous | |----------|-------------| | Aggressive debridement essential | More conservative approach | | Antibiotic-loaded cement useful | Not typically used | | Shorter antibiotic course | 9-12 months antituberculous therapy | > **Consultant Tip:** In patients from TB-endemic areas, always send tissue for AFB and TB PCR. The absence of the penumbra sign on MRI should raise suspicion for tuberculosis over pyogenic infection. --- ## Key Teaching Points ### Pattern Recognition **This pattern suggests Brodie's Abscess:** - Young patient with subacute limb pain - Minimal systemic symptoms despite prolonged course - Normal or mildly elevated inflammatory markers - Well-defined metaphyseal lytic lesion - Sclerotic rim on radiograph - **Penumbra sign** on MRI **Distinguish from Acute Osteomyelitis:** | Feature | Acute | Subacute (Brodie's) | |---------|-------|---------------------| | Duration | Days | Weeks to months | | Fever | Present | Usually absent | | Inflammatory markers | Markedly elevated | Normal or mildly elevated | | X-ray | May be normal initially | Sclerotic rim present | | Management urgency | Emergency | Can be planned | ### Critical Management Points 1. **Penumbra sign** on MRI is highly specific for Brodie's abscess 2. **Biopsy before treatment** - rules out tumour, identifies organism 3. **Surgical debridement is essential** - antibiotics alone insufficient 4. **Culture-negative is common** (30-50%) - treat empirically 5. **6-12 weeks antibiotics** - shorter courses have higher recurrence 6. **Consider TB** in patients from endemic regions --- ## Common Examiner Follow-ups **Q: "What is the penumbra sign and what causes it?"** The penumbra sign is a rim of high T1 signal surrounding the abscess cavity on MRI. It is caused by: - Vascular granulation tissue rich in haemoglobin breakdown products - The paramagnetic effect of methaemoglobin creates T1 shortening - Present in pyogenic infections - Absent in tuberculosis (caseous necrosis lacks vascularity) - Absent in tumours Sensitivity ~75%, specificity ~95% for pyogenic osteomyelitis. --- **Q: "Why are inflammatory markers often normal in Brodie's abscess?"** Inflammatory markers are normal or mildly elevated because: - Host immune response has successfully contained the infection - The abscess cavity is walled off from systemic circulation - Low-grade, indolent infection with balance between organism and host - No systemic inflammatory response despite local infection This differentiates from acute osteomyelitis where WCC, CRP, and ESR are markedly elevated. --- **Q: "What is the culture-negative rate and how does this affect management?"** Culture-negative rate in Brodie's abscess is 30-50%, due to: - Prior antibiotic therapy - Delayed or inadequate transport - Low bacterial load - Fastidious organisms Management when culture-negative: - Continue empirical anti-staphylococcal antibiotics - Histology confirms infection (acute/chronic inflammation, necrosis) - Consider broadening coverage if no response - Extended tissue cultures (hold for 14 days for slow-growing organisms) --- **Q: "When would you consider bone grafting the cavity?"** Bone grafting considerations: | Factor | Graft Indicated | No Graft Needed | |--------|-----------------|-----------------| | Cavity size | >3cm diameter | <3cm | | Location | Structural area | Non-weight-bearing | | Bone stock | Poor remaining bone | Good remaining bone | | Contamination | Clean after debridement | Ongoing contamination | Options include: - Autograft (iliac crest) - Antibiotic-impregnated bone substitute - Calcium sulphate with antibiotics Most Brodie's abscesses heal without grafting if adequately debrided. --- ## Related Topics - Acute Osteomyelitis - Chronic Osteomyelitis - Skeletal Tuberculosis - Eosinophilic Granuloma - Metaphyseal Bone Lesions - Antibiotic Therapy in Bone Infection