Exam Detail:

Key Revision Focus: Cierny-Mader Classification (essential for viva), Biofilm mechanism (glycocalyx), Sequestrum vs Involucrum, Dead Space Management options, Antibiotic cement preparation. High-yield for FRCS Basic Science viva.

1. Clinical Overview

Osteomyelitis is an inflammatory process of bone and marrow caused by an infectious organism, leading to bone destruction and potential necrosis. It remains one of the most challenging conditions in orthopaedic surgery due to the unique physiology of bone and the protective mechanisms of pathogens, specifically biofilm formation.

Clinical Pearl:

The Law of Bone Infection: "Antibiotics cannot sterilize dead bone." Surgical debridement of necrotic bone (sequestrum) is the cornerstone of treatment for chronic osteomyelitis. Systemic antibiotics are adjunctive, not curative, in the presence of dead bone.

Key Concepts

1. Biofilm: The primary reason for treatment failure. Bacteria adhere to implant/bone and secrete a glycocalyx matrix (EPS), rendering them 100-1000x more resistant to antibiotics.
2. Sequestrum: A segment of necrotic bone separated from living bone by granulation tissue. It acts as a nidus for persistent infection.
3. Involucrum: A sheath of new periosteal bone formation surrounding a sequestrum.
4. Cloaca: A channel/sinus tract in the bone (often through the involucrum) allowing pus/debris to discharge.
5. Brodie's Abscess: A subacute osteomyelitis, classically a lytic lesion with a sclerotic rim in the metaphysis (distal tibia is common).
6. Classification: Cierny-Mader is the clinically relevant system guiding treatment (Host status + Anatomic involvement).
7. Probe-to-Bone Test: High Positive Predictive Value (PPV) for osteomyelitis in diabetic foot ulcers.
8. Dead Space: Following debridement, the resulting void must be managed (beads, muscle flap, bone graft) to prevent recurrence.
9. Marjolin's Ulcer: Malignant transformation (Squamous Cell Carcinoma) in a chronic sinus tract.
10. Hematogenous vs Contiguous: Pediatric is often hematogenous (metaphyseal); Adult is often contiguous (post-trauma, diabetic).

Clinical Pearls

• Probe-to-Bone: If you can probe to bone in a diabetic ulcer with a metal instrument, the probability of osteomyelitis is >85%.
• ESR/CRP: Useful for monitoring response to therapy, not specific for diagnosis.
• MRI: The gold standard imaging modality (high sensitivity for marrow edema).
• Culture: Sinus tract swabs are notoriously unreliable (concordance with deep bone culture is <50%). Always get deep bone biopsy/tissue.
• Antibiotics: Rifampicin is unique as it can penetrate biofilm (activity against Staph aureus), but never use as monotherapy due to rapid resistance.
• Debridement: Must be executed to the "Paprika Sign" (punctate bleeding from viable Haversian canals).

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2. Epidemiology

Osteomyelitis is a significant burden on healthcare systems, associated with high morbidity and cost.

• Incidence:
  • Post-traumatic: 10-25% of open fractures (increases with Gustilo grade).
  • Prosthetic Joint Infection (PJI): 1-2% of primary arthroplasties.
  • Vertebral Osteomyelitis: 2-4% of all cases (increasing with age/IVDU).
• Demographics:
  • Children: Hematogenous seeding (metaphysis of long bones). Boys > Girls.
  • Adults: Contiguous spread (diabetic foot, trauma, surgery). >50 years.
  • IV Drug Users: Prone to atypical locations (SC joint, spine) and organisms (Pseudomonas, Candida).

Risk Factors (The 'Compromised Host')

The Cierny-Mader B-Host factors are critical for prognosis:

• Systemic (Bs):
  • Diabetes Mellitus (most common).
  • Smoking (nicotine vasoconstriction).
  • Malnutrition (Albumin <35).
  • Immunosuppression (Steroids, Chemo, HIV).
  • Renal/Liver failure.
  • Advanced Age.
• Local (Bl):
  • Chronic lymphedema/venous stasis.
  • Major vessel compromise (PVD).
  • Extensive scarring/radiation fibrosis.
  • Small vessel disease.
  • Neuropathy (Charcot).

Organism Prevalence

• Staphylococcus aureus: By far the most common (>50-70% of cases).
• MRSA: Increasing prevalence, especially in nosocomial/chronic cases.
• Coagulase-negative Staph (Staph epi): Common in implants/hardware.
• Pseudomonas aeruginosa: Puncture wounds through shoe (sneaker foam), IVDU.
• Salmonella: Sickle Cell Disease (though Staph is still #1, Salmonella is uniquely high).
• Kingella kingae: Young children (<3 years).
• Propionibacterium acnes: Shoulder surgery (post-arthroscopy/arthroplasty).

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3. Pathophysiology

The development of osteomyelitis involves a battle between the host immune system, the vascular supply, and the bacterial virulence factors.

The "Biofilm" Concept

Understanding biofilm is essential for modern management.

• Planktonic: Free-floating bacteria (susceptible to antibiotics/host defense).
• Sessile (Biofilm): Bacteria adhere to a surface (necrotic bone or metal).
  • Phase 1 (Attachment): Rapid, reversible Van der Waals forces. Then irreversible receptor binding (fibronectin/collagen).
  • Phase 2 (Aggregation): Bacteria multiply and secrete Exopolysaccharide Matrix (EPS) or glycocalyx.
  • Phase 3 (Maturation): Organized structure with water channels for nutrient delivery. Quorum sensing regulates growth.
  • Phase 4 (Detachment): Planktonic showers released to spread infection (causing acute sepsis spikes).
• Resistance: Biofilm bacteria are metabolically inactive (senescent), making them resistant to antibiotics that target cell wall synthesis or replication. The EPS blocks antibody/leukocyte penetration.

Mechanism of Bone Destruction

Step 1: Inoculation & Inflammation

• Bacteria enter (hematogenous or direct).
• PMN leukocytes arrive, releasing enzymes/cytokines creating pus.
• Intra-osseous pressure rises within the rigid bony canal.

Step 2: Ischemia & Necrosis

• Increased pressure compresses blood vessels (Volkmann's canals).
• Vascular thrombosis occurs.
• Bone death ensues creating the Sequestrum (dead bone).
• Sequestrum acts as a foreign body, harbouring bacteria away from blood supply (antibiotics cannot reach).

Step 3: New Bone Formation

• Periosteum is elevated by pus.
• New bone forms on the underside of the periosteum: Involucrum.
• This creates a shell around the infection.

Step 4: Chronicity

• Pus ruptures through the involucrum (through a Cloaca).
• Tracks to skin surface (Sinus tract).
• Cycle continues until dead bone is removed.

Classifications

1. Cierny-Mader Classification (The Gold Standard)

Based on Anatomy + Host Physiology. Guides treatability.

Anatomic Type	Description	Surgical Strategy
Type I	Medullary. Hematogenous. Endosteal only.	Intramedullary reaming/antibiotics.
Type II	Superficial. Surface of bone. Continuity of coverage defect.	Soft tissue coverage + superficial decortication.
Type III	Localized. Full cortical thickness but stable. Sequestrum.	Sequestrectomy + dead space management. Stable.
Type IV	Diffuse. Through-and-through instability.	Segmental resection + stabilization (ExFix/Nail) + reconstruction.

Physiological Class	Description	Clinical Implication
A Host	Normal host. Good immune system/vascularity.	Candidate for limb salvage/reconstruction.
B Host	Compromised (Local or Systemic).	Treatment carries higher risk/fail rate.
Bs	Systemic (Smoker, DM, Immunosuppressed).	Optimization required.
Bl	Local (PVD, Lymphedema, Scarring).	High risk of wound failure.
C Host	Treatment worse than the disease.	Palliative tx or Amputation. Curative surgery too risky.

2. Waldvogel Classification (Older system)

• Hematogenous: Kids, vertebrae.
• Contiguous: Trauma, surgery.
• Chronic: Necrotic bone present.

3. Lew and Waldvogel Duration

• Acute: < 2 weeks.
• Subacute: weeks to months.
• Chronic: > 6 weeks (or presence of sequestrum/radiographic changes).

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4. Clinical Presentation

Presentation varies significantly between acute and chronic forms.

Acute Osteomyelitis

• Symptoms: Severe pain, deep aching, refusal to bear weight (antalgic).
• Systemic: High fevers, rigors, malaise, sepsis.
• Local: Erythema, warmth, exquisite point tenderness over the metaphysis.
• Children: "Pseudoparalysis" in infants. Refusal to move limb.

Chronic Osteomyelitis

• Symptoms: Often low-grade pain or painless discharging sinus.
• History: Previous fracture, surgery, or acute episode "treated" years ago.
• Local:
  • Sinus Tract: Persistent drainage. Pathognomonic if draining for months.
  • Woody Induration: Check soft tissues.
  • Scarring: 'Water-can' skin perineum implies massive deep infection.
• Red Flag: Check for squamous cell CA (Marjolin Ulcer) at the sinus edge (everted edge, bleeding).

Special Scenarios

• Diabetic Foot: Often no pain (neuropathy), no fever. "Sausage toe". Deep ulcer.
• Vertebral: Back pain (worse at night/rest). Neurological deficit (epidural abscess).
• Puncture Wound: Pseudomonas. Pain returns after initial improvement.

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5. Clinical Examination

Structured approach required (Look, Feel, Move, Special Tests).

1. Look:
   • Skin quality: Atrophic, shiny, scarred?
   • Sinus tracts: Number, location, quality of discharge (purulent, serous, granular).
   • Deformity: Angular deformity implies bone loss or physeal damage.
2. Feel:
   • Probe-to-Bone (PTB): Use a sterile metal probe in the ulcer. Hard stop = Bone. Soft stop = Soft tissue. PTB+ has >85% PPV for osteomyelitis.
   • Temperature: Compare to contralateral side.
   • Pulses: CRITICAL. Palpate DP/PT. If absent -> ABPI/Doppler. Essential for ascertaining "B-Host" status.
   • Sensation: Monofilament testing (Neuropathy).
3. Move:
   • Adjacent joints. Stiffness suggests arthritis or tenodesis from scarring.
   • Pathological movement (pseudarthrosis) implies Type IV (Instability).
4. Neuro:
   • Document status pre-debridement.

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6. Investigations

Laboratory

• WBC: Often normal in chronic/diabetic osteomyelitis. Elevated in acute.
• ESR/CRP: almost always elevated.
  • CRP: Responds fast (half-life 19 hrs). Good for monitoring treatment.
  • ESR: Slow response.
• Nutritional Screen: Albumin, Pre-albumin, Transferrin. (Low albumin <35 increases failure risk).
• HbA1c: Diabetic control.
• Blood Cultures: Positive in 50% of acute hematogenous. Low yield in chronic.

Imaging

1. X-ray:
   • Usually normal for first 10-14 days.
   • Acute: Soft tissue swelling -> Permeative lysis -> Periosteal reaction (Codman's triangle/Onion-skinning).
   • Chronic: Sequestrum (dense island), Involucrum (thickened cortex), Cloaca.
   • Brodie's Abscess: Lytic lesion with sclerotic rim.
2. MRI (Gold Standard):
   • Sensitivity 99%, Specificity 80%.
   • T1: Low signal (Dark) replacement of bright marrow fat. Confluent T1 hypointensity is key.
   • T2/STIR: High signal (Bright) edema/fluid.
   • Rim Sign: Low signal rim around an abscess (Penumbra sign).
3. CT Scan:
   • Best for bony anatomy.
   • Identifying Sequestrum vs Involucrum.
   • Surgical planning for resection.
4. Nuclear Medicine:
   • Bone Scan (Tc-99): Sensitive but not specific (lights up for fracture, tumor, arthritis). Triphasic scan helps.
   • WBC Scan (Indium-111 or Tc-99 HMPAO): More specific. Leucocytes tagged.
   • Combined Scan: Bone scan + WBC scan. "Concordant" (hot on both) = Infection.
5. Biopsy (Microbiology):
   • The Gold Standard Diagnosis.
   • Deep bone curettage/biopsy sent for MC&S and Histology (acute/chronic inflammation).
   • Stop antibiotics 2 weeks prior if possible.
   • Send 3-5 separate samples with clean instruments each time.
   • Sonication of hardware can increase yield.

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7. Management

Management depends on the Cierny-Mader Host type.

• A Host: Aggressive curative surgery.
• B Host: Optimize host first, then surgery. Or suppressive hierarchy.
• C Host: Palliative/Suppressive or Amputation. Do NOT operate for cure.

ASCII Algorithm:

          Suspicion of OSTEOMYELITIS
                      ↓
┌──────────────────────────────────────────────┐
│           WORKUP & STAGING                   │
│ - MRI / X-ray + CRP/ESR                      │
│ - Cierny-Mader Host Class (A / B / C)        │
│ - Biopsy (if stable) - Culture guided        │
└──────────────────────────────────────────────┘
                      ↓
┌──────────────────────────────────────────────┐
│           DECISION MATRIX                    │
├──────────────────────┬───────────────────────┤
│    ACUTE (<2 wks)    │    CHRONIC (>6 wks)   │
│  (No dead bone yet)  │      (Dead Bone)      │
└──────────┬───────────┴───────────┬───────────┘
           ↓                       ↓
┌──────────────────────┐  ┌────────────────────┐
│  High Dose IV ABx    │  │   Is Host C?       │
│  (Empiric → Target)  ├─Yes→ Suppressive ABx  │
│      6 Weeks         │  │    Or Amputation   │
└──────────┬───────────┘  └────────┬───────────┘
           ↓                       ↓ No (A/B)
    Failure/Abscess?      ┌────────────────────┐
           ↓              │   SURGICAL CURE    │
    Surgical Drain        │ 1. Radical Debride │
                          │ 2. Dead Space Mgt  │
                          │ 3. Soft Tissue Cov │
                          │ 4. Stability       │
                          │ 5. Systemic ABx    │
                          └────────────────────┘

1. Surgical Debridement (The Engine of Cure)

• Principle: "You must remove all dead bone." Antibiotics don't work on sequestrum.
• Technique: Resect back to Paprika Sign (punctate bleeding cortical bone).
• Margins: Take cultures from the margin to ensure clean cut.
• Stability: If resection causes instability (Type IV), stabilize with ExFix (Ilizarov/TSF ideal as outside infection zone).

2. Dead Space Management

Leaving a void (dead space) allows hematoma -> culture medium -> recurrence. The void MUST be filled.

• Option A: Antibiotic Beads (PMMA):
  • High local concentration (100x MIC). Low systemic toxicity.
  • Use Heat Stable antibiotics: Vancomycin (powder), Tobramycin/Gentamycin (liquid).
  • Ratio: 4g Vanc per 40g Cement (High dose for beads).
  • Non-absorbable (needs removal) usually.
• Option B: Muscle Flap:
  • Brings blood supply/antibiotics to the bed. Fills space.
• Option C: Papineau Technique:
  • Open cancellous bone grafting. Wound left open. Beads layered. Granulation grows over.
• Option D: Masquelet Technique (Induced Membrane):
  • Stage 1: Debride + Insert Cement Spacer -> Close wound.
  • Wait 6-8 weeks: A biological membrane forms around cement (rich in VEGF/BMPs).
  • Stage 2: Open membrane, remove cement, fill with bone graft, close membrane.

3. Systemic Antibiotics

• Start IV, switch to PO when CRP drops/clinical improvement.
• Duration: Traditionally 4-6 weeks (bone revascularization time).
• OVIVA Trial (2019): Oral vs IV Antibiotics. Result: Oral non-inferior to IV for first 6 weeks if specific bacterium targeted. Changed practice significantly (less PICC lines).
• Rifampicin: Add for Vitallium/Staph infections (biofilm penetration).

4. Hyperbaric Oxygen (HBO)

• adjunctive for refractory cases (Cierny-Mader B-hosts). Increases oxygen tension in tissues promoting neutrophil function/angiogenesis.

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8. Complications

• Recurrence: 20-30% rate, often years later. "Once an osteo, always an osteo".
• Pathologic Fracture: Weakened bone post-debridement.
• Growth Arrest: If physis involved in children (limb length processing).
• Amputation: If recurrence fails or biologic cost to patient too high.
• Squamous Cell Carcinoma (Marjolin's Ulcer):
  • Malignancy arising in chronic sinus tract (>10-20 years).
  • Aggressive. Requires wide excision/amputation.
• Amyloidosis: Secondary AA amyloidosis (rare now) from chronic inflammation.
• DVT/PE: High risk due to immobility + inflammation.

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9. Prognosis & Outcomes

• Cure Rates:
  • Cierny I (Medullary): >95% cure.
  • Cierny III/IV (Complex): 70-80% cure with aggressive management.
• OVIVA Trial: Challenged the dogma of IV antibiotics. Oral is viable.
• Predictors of Failure:
  • Smokers.
  • Retained hardware.
  • Inadequate debridement (Surgeon factor).
  • Gram-negative organisms/Polymicrobial.

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10. Evidence & Guidelines

Guidelines

• IDSA Guidelines (2015): Diagnosis and Treatment of Native Vertebral Osteomyelitis.
• NICE Guidelines: Diabetic foot problems: prevention and management (NG19). PTB test recommended.

Landmark Trials

• OVIVA (Oral vs IV Antibiotics) [2019]: n=1054. 1-year failure rate 13.2% (IV) vs 14.6% (Oral). P = non-significant. Conclusion: Oral therapy non-inferior for complex orthopaedic infection. [PMID: 30703429]
• Cierny & Mader (1985): Established the classification system. n=200+. showed physiologic status (Host A/B) more important than defect size. [PMID: 4044199]
• Masquelet (2010): Description of induced membrane technique for large bone defects. 90% union rate. [PMID: 20138258]

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11. Patient Explanation

What is Osteomyelitis?

It is a deep infection of the bone. Unlike skin infections, bone infections are very hard to treat because bone has a poor blood supply, and bacteria can "hide" inside dead bone where antibiotics cannot reach.

Why do I need surgery?

Antibiotics travel in the blood. If parts of the bone are dead (sequestrum), they have no blood flow, so the medicine cannot get there. The bacteria survive in these dead areas. Surgery is needed to physically remove the dead bone and clean the area. This is like removing a splinter—the wound won't heal until the splinter is out.

What is the treatment plan?

1. Surgery: We will clean out the infection and remove dead bone.
2. Space Management: We might put antibiotic beads or a spacer in the hole.
3. Antibiotics: You will need strong antibiotics (pills or drip) for 6 weeks.
4. Recovery: It is a long road. Recurrence can happen, and you need to stop smoking and control sugar (if diabetic) to help healing.

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12. References

1. Cierny G 3rd, Mader JT, Penninck JJ. A clinical staging system for adult osteomyelitis. Clin Orthop Relat Res. 2003 Sep;(414):7-24. [PMID: 12975574] (Classic Paper - reprint of 1985).
2. Li HK, Rombach I, Zambellas R, et al. Oral versus Intravenous Antibiotics for Bone and Joint Infection. N Engl J Med. 2019 Jan 31;380(5):425-436. [PMID: 30703429] (OVIVA Trial).
3. Masquelet AC. Induced membrane technique: pearls and pitfalls. J Orthop Trauma. 2017 Oct;31 Suppl 5:S36-S38. [PMID: 28938399]
4. Lew DP, Waldvogel FA. Osteomyelitis. Lancet. 2004 Jul 24-30;364(9431):369-79. [PMID: 15276398]
5. Calhoun JH, Manring MM. Adult osteomyelitis. Infect Dis Clin North Am. 2005 Dec;19(4):765-86. [PMID: 16297731]
6. Zimmerli W. Vertebral osteomyelitis. N Engl J Med. 2010 Mar 18;362(11):1022-9. [PMID: 20237348]
7. Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms: a common cause of persistent infections. Science. 1999 May 21;284(5418):1318-22. [PMID: 10334980]
8. Parsons B, Strauss E. Surgical management of chronic osteomyelitis. Am J Surg. 2004 Jul;188(1A Suppl):57-66. [PMID: 15308133]
9. Simpson AH, Deakin M, Latham JM. Chronic osteomyelitis. The effect of the extent of surgical resection on infection-free survival. J Bone Joint Surg Br. 2001 Apr;83(3):403-7. [PMID: 11341427]
10. Conterno LO, Tiskievicz F. Antibiotics for treating chronic osteomyelitis in adults. Cochrane Database Syst Rev. 2013 Sep 7;(9):CD004439. [PMID: 24014191]
11. Tice AD, Hoaglund PA, Shoultz DA. Risk factors and treatment outcomes in osteomyelitis. J Antimicrob Chemother. 2003 Jun;51(6):1261-8. [PMID: 12716788]
12. Lavery LA, Armstrong DG, Peters EJ, et al. Probe-to-bone test for diagnosing diabetic foot osteomyelitis: reliable or relic? Diabetes Care. 2007 Feb;30(2):270-4. [PMID: 17259493]
13. Marais LC, et al. The management of chronic osteomyelitis: Part I - Diagnostic work-up and surgical principles. SA Orthop J. 2014;13(2):42-48.
14. Mader JT, et al. Staging and staging application in osteomyelitis. Clin Infect Dis. 1997 Dec;25(6):1303-9. [PMID: 9431369]
15. Walter G, Kemmerer M, Kappler C, et al. Treatment algorithms for chronic osteomyelitis. Dtsch Arztebl Int. 2012 Apr;109(14):257-64. [PMID: 22536302]

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13. Examination Focus

Common Exam Questions (FRCS/Boards)

1. classify Osteomyelitis? (Answer: Cierny-Mader. Describe Anatomic I-IV and Host A/B/C. Do NOT use Waldvogel unless asked).
2. What is a Biofilm? (Answer: Sessile colony, Glycocalyx matrix, Quorum sensing, 1000x antibiotic resistance).
3. How do you treat a Type III, Host B chronic osteomyelitis? (Answer: Optimize host factors Bs/Bl -> Sequestrectomy -> Dead space management -> Culture-specific ABx).
4. Discuss the OVIVA trial. (Answer: Oral non-inferior to IV for bone infection. Allows earlier discharge/fewer line complications).
5. What is the 'Paprika Sign'? (Answer: Viable cortical bleeding looking like paprika on pink meat. Endpoint of debridement).

Viva "Buzzwords"

• "Sequestrum and Involucrum"
• "Paprika Sign"
• "Biofilm Glycocalyx"
• "Cierny-Mader Classification"
• "Dead Space Management"
• "Probe-to-Bone Test"

Common Pitfalls

• Failing to mention host optimization: Operating on a smoker/uncontrolled diabetic (HbA1c >8%) leads to recurrence. Mention "Host Optimization" first.
• Assuming IV is better than Oral: Shows lack of current literature knowledge (OVIVA).
• Relying on swabbing sinus tract: Mention "Deep bone biopsy/curettage samples".