What is the typical cause and development of osteomyelitis of the skull?

How Skull Osteomyelitis Develops

Skull osteomyelitis develops through three primary mechanisms: direct extension from adjacent infections (particularly otitis externa progressing to skull base involvement), hematogenous seeding from distant bacteremia, or direct inoculation from trauma or neurosurgical procedures. 1, 2, 3

Primary Pathways of Development

1. Extension from Otitis Externa (Most Common for Skull Base)

• Necrotizing otitis externa (NOE) in diabetic or immunocompromised patients represents the classic pathway to skull base osteomyelitis (SBO). 1
• The infection begins as otitis externa in the external auditory canal, typically caused by Pseudomonas aeruginosa or Staphylococcus aureus. 1
• In susceptible hosts (poorly controlled diabetes, immunosuppression), the infection becomes fulminant and extends beyond the external auditory canal into the skull base bone. 1
• This progression carries high morbidity and mortality, with potential involvement of cranial nerves and vascular structures. 1

2. Extension from Paranasal Sinus Infection

• Sinusitis can lead to skull osteomyelitis through progression of septic thrombi through the valveless diploic veins that penetrate the dura, or through direct extension of osteomyelitis. 1
• Frontal sinusitis most commonly causes intracranial complications and skull involvement. 1
• Sphenoid and ethmoid sinusitis can lead to central skull base osteomyelitis, though this is rare in children (1-3% of sinonasal diseases). 1
• Fungal sinusitis, particularly acute invasive fungal sinusitis in immunocompromised patients, can progress to skull base osteomyelitis with mortality rates of 50-80%. 1

3. Hematogenous Seeding

• Distant bacteremia can seed the skull bone through hematogenous spread, similar to the mechanism in vertebral osteomyelitis. 4, 2
• Recent bloodstream infections, particularly S. aureus bacteremia, represent a significant risk factor. 4
• The infection typically begins with septic emboli lodging in the bone vasculature. 4

4. Direct Inoculation (Post-Traumatic or Post-Surgical)

• Neurosurgical procedures that breach the skull can introduce pathogens directly into the bone. 3
• Craniotomy, subdural hematoma evacuation, and other skull-penetrating procedures create risk for osteomyelitis. 3
• In these cases, typical cutaneous flora such as S. aureus or coagulase-negative staphylococci are the usual pathogens. 3
• Polymicrobial infections can occur, occasionally including unusual organisms like E. coli. 3

Key Microbiology

• Staphylococcus aureus (21%) and Pseudomonas aeruginosa (19%) are the two most common causative pathogens in central skull base osteomyelitis. 2
• Fungal pathogens, particularly zygomycetes (55% of fungal cases), occur more frequently in immunocompromised patients and carry worse prognosis. 5
• Gram-negative bacteria occur more frequently in skull osteomyelitis than in the past. 6

Clinical Presentation Patterns

• Headaches and cranial nerve palsies are the most common presenting symptoms, with cranial nerves VI (31%), IX (29%), and X (29%) most frequently affected. 2
• Bacterial skull base osteomyelitis more frequently presents with deafness, ear pain, or ear discharge, while fungal SBO presents with sinonasal pain, facial/periorbital swelling, and nasal symptoms. 5
• Median time to presentation is longer in bacterial SBO (26.3 weeks) compared to fungal SBO (8.1 weeks). 5

Critical Risk Factors

• Diabetes mellitus (57% of cases) and chronic otitis externa (33%) are the most frequent co-morbidities. 2
• Immunosuppression is present in 24% of cases and represents a significant risk factor for mortality, particularly in fungal infections. 2, 5
• Advanced age, long-term steroid use, liver failure, and renal failure increase risk. 4

Common Pitfalls

• Diagnosis is often delayed by several months due to insidious onset and nonspecific symptoms. 4, 7
• Radiographic changes (moth-eaten appearance) may not be recognized for several months after infection onset. 7
• Distinguishing fungal from bacterial etiology is critical as it has significant therapeutic implications; early diagnostic sampling (bone biopsy) is essential in patients at increased risk of fungal SBO. 5